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The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. Since 2004, Diagenode has accumulated shearing expertise to design the Bioruptor® Pico and guarantee the best experience with the sample preparation for number of applications -- in various fields of studies including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.
The Bioruptor Pico shearing accessories and consumables have been developed to allow flexibility in sample volumes (20 µl - 2 ml) and a fast parallel processing of samples (up to 16 samples simultaneously). The built-in cooling system (Bioruptor® Cooler) ensures high precision temperature control. The user-friendly interface has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control.
In addition, Diagenode provides fully-validated tubes that remain budget-friendly with low operating cost (< 1€/$/DNA sample) and shearing kits for best sample quality.
Application versatility:
Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA
By combining antibody-targeted controlled cleavage by MNase and NGS, CUT&RUN sequencing can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.
Explore the Bioruptor Pico now.
| Name | Catalog number | Throughput |
| Tube holder for 0.2 ml tubes | B01201144 | 16 samples |
| Tube holder for 0.65 ml tubes | B01201143 | 12 samples |
| Tube holder for 1.5 ml tubes | B01201140 | 6 samples |
| 15 ml sonication accessories | B01200016 | 6 samples |
| Name | Catalog Number |
| 0.2 ml Pico Microtubes | C30010020 |
| 0.65 ml Pico Microtubes | C30010011 |
| 1.5 ml Pico Microtubes | C30010016 |
| 15 ml Pico Tubes | C30010017 |
| 15 ml Pico Tubes & sonication beads | C01020031 |
| DNA shearing guide DNA shearing for Next-Generation Sequencing with the Bioruptor Pico | Download |
Diagenode has optimized a range of solutions for successful chromatin preparation. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.
For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.
| SAMPLE TYPE | SAMPLE INPUT | KIT | SDS CONCENTRATION |
NUCLEI ISOLATION |
||
|---|---|---|---|---|---|---|
 |
CELLS
|
< 100,000 | Chromatin EasyShear Kit High SDS |
1% |  |
|
|
CELLS
|
> 100,000 | Chromatin EasyShear Kit Ultra Low SDS |
< 0.1% |  |
||
|
TISSUE
|
Chromatin EasyShear Kit Ultra Low SDS |
< 0.1% | |
|||
|
PLANT TISSUE
|
Chromatin EasyShear Kit for Plant |
0.5% | |
|||
|
FFPE SAMPLES
|
Chromatin EasyShear Kit Low SDS |
0.2% | |
|||
 |
||||||
|
CELLS
|
Chromatin EasyShear Kit Low SDS |
0.2% | |
|||
|
TISSUE
|
||||||
|
FFPE SAMPLES
|
||||||
| Chromatin Shearing Guide PROTOCOL Guide for successful chromatin preparation using the Bioruptor Pico | Download |
| DNA shearing guide PROTOCOL DNA shearing for Next-Generation Sequencing with the Bioruptor Pico | Download |
| Which tubes for Bioruptor® Pico DOCUMENT | Download |
| Unlock Low-Input 3D Genome Analysis with the Arima-HiC Kit APPLICATION NOTE By combining the optimized chemistry of the Arima-HiC kit along with new low input protocols, the... | Download |
| Datasheet of Bioruptor tubes DATASHEET Datasheet of Diagenode tubes for Bioruptor Pico and Bioruptor Plus. | Download |
| Critical steps for Bioruptor® maintenance and efficient shearing DOCUMENT | Download |
Notice (8): Undefined index: SafetySheet [APP/View/Products/view.ctp, line 641]Code Context<?phpif (sizeof($product['SafetySheet']) > 0) {$viewFile = '/home/website-server/www/app/View/Products/view.ctp' $dataForView = array( 'language' => 'en', 'noindex' => 'noindex', 'meta_keywords' => '', 'meta_description' => 'Bioruptor® Pico sonication device', 'meta_title' => 'Bioruptor® Pico sonication device', 'product' => array( 'Product' => array( 'id' => '3046', 'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa 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53 => array( [maximum depth reached] ), (int) 54 => array( [maximum depth reached] ), (int) 55 => array( [maximum depth reached] ), (int) 56 => array( [maximum depth reached] ), (int) 57 => array( [maximum depth reached] ), (int) 58 => array( [maximum depth reached] ), (int) 59 => array( [maximum depth reached] ), (int) 60 => array( [maximum depth reached] ), (int) 61 => array( [maximum depth reached] ), (int) 62 => array( [maximum depth reached] ), (int) 63 => array( [maximum depth reached] ), (int) 64 => array( [maximum depth reached] ), (int) 65 => array( [maximum depth reached] ), (int) 66 => array( [maximum depth reached] ), (int) 67 => array( [maximum depth reached] ), (int) 68 => array( [maximum depth reached] ) ), 'Testimonial' => array(), 'Area' => array() ) ) $language = 'en' $noindex = 'noindex' $meta_keywords = '' $meta_description = 'Bioruptor® Pico sonication device' $meta_title = 'Bioruptor® Pico sonication device' $product = array( 'Product' => array( 'id' => '3046', 'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa 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Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>®</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>®</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>®</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div> <div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 µl volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.1 ml Bioruptor® Microtubes (Cat. No. B01200041). <strong>Panel B, 100 µl volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.65 ml Bioruptor® Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 µl volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016). Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37°C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 µl of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div> <div class="small-12 medium-12 large-12 columns"><br /><br /></div> <div class="small-12 medium-12 large-12 columns"> <p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p> </div> <div class="small-12 medium-12 large-12 columns"> <div class="page" title="Page 7"> <table> <tbody> <tr valign="middle"> <td></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>SDS concentration</strong></p> </td> <td style="text-align: center;"> <p>< 0.1%</p> </td> <td style="text-align: center;"> <p>0.2%</p> </td> <td style="text-align: center;"> <p>1%</p> </td> <td style="text-align: center;"> <p>0.5%</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Nuclei isolation</strong></p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>No</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Allows for shearing of... cells/tissue</strong></p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>up to 25 g of tissue</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Corresponding to shearing buffers from</strong></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p> <p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p> </td> </tr> </tbody> </table> <p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor® Pico</span></a></em></p> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'chromatin-shearing', 'meta_keywords' => 'Chromatin shearing,Chromatin Immunoprecipitation,Bioruptor,Sonication,Sonicator', 'meta_description' => 'Diagenode's Bioruptor® is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.', 'meta_title' => 'Chromatin shearing using Bioruptor® sonication device | Diagenode', 'modified' => '2017-11-15 10:14:02', 'created' => '2015-03-05 15:56:30', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3', 'position' => '10', 'parent_id' => null, 'name' => '次世代シーケンシング', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2 style="font-size: 22px;">DNA断片化、ライブラリー調製、自動化：NGSのワンストップショップ</h2> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-12 medium-12 large-12 columns"> <h4>1. 断片化装置を選択してください：150 bp〜75 kbの範囲でDNAを断片化します。</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-pico-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/bioruptor_pico.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/megaruptor2-1-unit"><img src="https://www.diagenode.com/img/product/shearing_technologies/B06010001_megaruptor2.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-one-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/br-one-profil.png" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns">5μlまで断片化：150 bp〜2 kb<br />NGS DNAライブラリー調製およびFFPE核酸抽出に最適で、</td> <td class="small-4 medium-4 large-4 columns">2 kb〜75 kbの範囲をできます。<br />メイトペアライブラリー調製および長いフラグメントDNAシーケンシングに最適で、この軽量デスクトップデバイスで</td> <td class="small-4 medium-4 large-4 columns">20または50μlの断片化が可能です。</td> </tr> </tbody> </table> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-8 medium-8 large-8 columns"> <h4>2. 最適化されたライブラリー調整キットを選択してください。</h4> </th> <th class="small-4 medium-4 large-4 columns"> <h4>3. ライブラリー前処理自動化を選択して、比類のないデータ再現性を実感</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><img src="https://www.diagenode.com/img/product/kits/microPlex_library_preparation.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns"><img src="https://www.diagenode.com/img/product/kits/box_kit.jpg" style="display: block; margin-left: auto; margin-right: auto;" height="173" width="250" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/sx-8g-ip-star-compact-automated-system-1-unit"><img src="https://www.diagenode.com/img/product/automation/B03000002%20_ipstar_compact.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">50pgの低入力：MicroPlex Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">5ng以上：iDeal Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">Achieve great NGS data easily</td> </tr> </tbody> </table> </div> </div> <blockquote> <div class="row"> <div class="small-12 medium-12 large-12 columns"><span class="label" style="margin-bottom: 16px; margin-left: -22px; font-size: 15px;">DiagenodeがNGS研究にぴったりなプロバイダーである理由</span> <p>Diagenodeは15年以上もエピジェネティクス研究に専念、専門としています。 ChIP研究クロマチン用のユニークな断片化システムの開発から始まり、 専門知識を活かし、5μlのせん断体積まで可能で、NGS DNAライブラリーの調製に最適な最先端DNA断片化装置の開発にたどり着きました。 我々は以来、ChIP-seq、Methyl-seq、NGSライブラリー調製用キットを研究開発し、業界をリードする免疫沈降研究と同様に、ライブラリー調製を自動化および完結させる独自の自動化システムを開発にも成功しました。</p> <ul> <li>信頼されるせん断装置</li> <li>様々なインプットからのライブラリ作成キット</li> <li>独自の自動化デバイス</li> </ul> </div> </div> </blockquote> <div class="row"> <div class="small-12 columns"> <ul class="accordion" data-accordion=""> <li class="accordion-navigation"><a href="#panel1a">次世代シーケンシングへの理解とその専門知識</a> <div id="panel1a" class="content"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p><strong>次世代シーケンシング (NGS)</strong> ）は、著しいスケールとハイスループットでシーケンシングを行い、1日に数十億もの塩基生成を可能にします。 NGSのハイスループットは迅速でありながら正確で、再現性のあるデータセットを実現し、さらにシーケンシング費用を削減します。 NGSは、ゲノムシーケンシング、ゲノム再シーケンシング、デノボシーケンシング、トランスクリプトームシーケンシング、その他にDNA-タンパク質相互作用の検出やエピゲノムなどを示します。 指数関数的に増加するシーケンシングデータの需要は、計算分析の障害や解釈、データストレージなどの課題を解決します。</p> <p>アプリケーションおよび出発物質に応じて、数百万から数十億の鋳型DNA分子を大規模に並行してシーケンシングすることが可能です。その為に、異なる化学物質を使用するいくつかの市販のNGSプラットフォームを利用することができます。 NGSプラットフォームの種類によっては、事前準備とライブラリー作成が必要です。</p> <p>NGSにとっても、特にデータ処理と分析に関した大きな課題はあります。第3世代技術はゲノミクス研究にさらに革命を起こすであろうと大きく期待されています。</p> </div> </div> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <p><strong>NGS アプリケーション</strong></p> <ul> <li>全ゲノム配列決定</li> <li>デノボシーケンシング</li> <li>標的配列</li> <li>Exomeシーケンシング</li> <li>トランスクリプトーム配列決定</li> <li>ゲノム配列決定</li> <li>ミトコンドリア配列決定</li> <li>DNA-タンパク質相互作用（ChIP-seq</li> <li>バリアント検出</li> <li>ゲノム仕上げ</li> </ul> </div> <div class="small-6 medium-6 large-6 columns"> <p><strong>研究分野におけるNGS:</strong></p> <ul> <li>腫瘍学</li> <li>リプロダクティブ・ヘルス</li> <li>法医学ゲノミクス</li> <li>アグリゲノミックス</li> <li>複雑な病気</li> <li>微生物ゲノミクス</li> <li>食品・環境ゲノミクス</li> <li>創薬ゲノミクス - パーソナライズド・メディカル</li> </ul> </div> <div class="small-12 medium-12 large-12 columns"> <p><strong>NGSの用語</strong></p> <dl> <dt>リード（読み取り）</dt> <dd>この装置から得られた連続した単一のストレッチ</dd> <dt>断片リード</dt> <dd>フラグメントライブラリからの読み込み。 シーケンシングプラットフォームに応じて、読み取りは通常約100〜300bp。</dd> <dt>断片ペアエンドリード</dt> <dd>断片ライブラリーからDNA断片の各末端2つの読み取り。</dd> <dt>メイトペアリード</dt> <dd>大きなDNA断片（通常は予め定義されたサイズ範囲）の各末端から2つの読み取り。</dd> <dt>カバレッジ（例）</dt> <dd>30×適用範囲とは、参照ゲノム中の各塩基対が平均30回の読み取りを示す。</dd> </dl> </div> </div> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2>NGSプラットフォーム</h2> <h3><a href="http://www.illumina.com" target="_blank">イルミナ</a></h3> <p>イルミナは、クローン的に増幅された鋳型DNA（クラスター）上に位置する、蛍光標識された可逆的鎖ターミネーターヌクレオチドを用いた配列別合成技術を使用。 DNAクラスターは、ガラスフローセルの表面上に固定化され、 ワークフローは、4つのヌクレオチド（それぞれ異なる蛍光色素で標識された）の組み込み、4色イメージング、色素や末端基の切断、取り込み、イメージングなどを繰り返します。フローセルは大規模な並列配列決定を受ける。 この方法により、単一蛍光標識されたヌクレオチドの制御添加によるモノヌクレオチドのエラーを回避する可能性があります。 読み取りの長さは、通常約100〜150 bpです。</p> <h3><a href="http://www.lifetechnologies.com" target="_blank">イオン トレント</a></h3> <p>イオントレントは、半導体技術チップを用いて、合成中にヌクレオチドを取り込む際に放出されたプロトンを検出します。 これは、イオン球粒子と呼ばれるビーズの表面にエマルションPCR（emPCR）を使用し、リンクされた特定のアダプターを用いてDNA断片を増幅します。 各ビーズは1種類のDNA断片で覆われていて、異なるDNA断片を有するビーズは次いで、チップの陽子感知ウェル内に配置されます。 チップには一度に4つのヌクレオチドのうちの1つが浸水し、このプロセスは異なるヌクレオチドで15秒ごとに繰り返されます。 配列決定の間に4つの塩基の各々が1つずつ導入されます、組み込みの場合はプロトンが放出され、電圧信号が取り込みに比例して検出されます。.</p> <h3><a href="http://www.pacificbiosciences.com" target="_blank">パシフィック バイオサイエンス</a></h3> <p>パシフィックバイオサイエンスでは、20kbを超える塩基対の読み取りも、単一分子リアルタイム（SMRT）シーケンシングによる構造および細胞タイプの変化を観察することができます。 このプラットフォームでは、超長鎖二本鎖DNA（dsDNA）断片が、Megaruptor（登録商標）のようなDiagenode装置を用いたランダムシアリングまたは目的の標的領域の増幅によって生成されます。 SMRTbellライブラリーは、ユニバーサルヘアピンアダプターをDNA断片の各末端に連結することによって生成します。 サイズ選択条件による洗浄ステップの後、配列決定プライマーをSMRTbellテンプレートにアニーリングし、鋳型DNAに結合したDNAポリメラーゼを含む配列決定を、蛍光標識ヌクレオチドの存在下で開始。 各塩基が取り込まれると、異なる蛍光のパルスをリアルタイムで検出します。</p> <h3><a href="https://nanoporetech.com" target="_blank">オックスフォード ナノポア</a></h3> <p>Oxford Nanoporeは、単一のDNA分子配列決定に基づく技術を開発します。その技術により生物学的分子、すなわちDNAが一群の電気抵抗性高分子膜として位置するナノスケールの孔（ナノ細孔）またはその近くを通過し、イオン電流が変化します。 この変化に関する情報は、例えば4つのヌクレオチド（AまたはG r CまたはT）ならびに修飾されたヌクレオチドすべてを区別することによって分子情報に訳されます。 シーケンシングミニオンデバイスのフローセルは、数百個のナノポアチャネルのセンサアレイを含みます。 DNAサンプルは、Diagenode社のMegaruptor（登録商標）を用いてランダムシアリングによって生成され得る超長鎖DNAフラグメントが必要です。</p> <h3><a href="http://www.lifetechnologies.com/be/en/home/life-science/sequencing/next-generation-sequencing/solid-next-generation-sequencing.html" target="_blank">SOLiD</a></h3> <p>SOLiDは、ユニークな化学作用により、何千という個々のDNA分子の同時配列決定を可能にします。 それは、アダプター対ライブラリーのフラグメントが適切で、せん断されたゲノムDNAへのアダプターのライゲーションによるライブラリー作製から始まります。 次のステップでは、エマルジョンPCR（emPCR）を実施して、ビーズの表面上の個々の鋳型DNA分子をクローン的に増幅。 emPCRでは、個々の鋳型DNAをPCR試薬と混合し、水中油型エマルジョン内の疎水性シェルで囲まれた水性液滴内のプライマーコートビーズを、配列決定のためにロードするスライドガラスの表面にランダムに付着。 この技術は、シークエンシングプライマーへのライゲーションで競合する4つの蛍光標識されたジ塩基プローブのセットを使用します。</p> <h3><a href="http://454.com/products/technology.asp" target="_blank">454</a></h3> <p>454は、大規模並列パイロシーケンシングを利用しています。 始めに全ゲノムDNAまたは標的遺伝子断片の300〜800bp断片のライブラリー調製します。 次に、DNAフラグメントへのアダプターの付着および単一のDNA鎖の分離。 その後アダプターに連結されたDNAフラグメントをエマルジョンベースのクローン増幅（emPCR）で処理し、DNAライブラリーフラグメントをミクロンサイズのビーズ上に配置します。 各DNA結合ビーズを光ファイバーチップ上のウェルに入れ、器具に挿入します。 4つのDNAヌクレオチドは、配列決定操作中に固定された順序で連続して加えられ、並行して配列決定されます。</p> </div> </div> </div> </li> </ul> </div> </div>', 'in_footer' => true, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'next-generation-sequencing', 'meta_keywords' => 'Next-generation sequencing,NGS,Whole genome sequencing,NGS platforms,DNA/RNA shearing', 'meta_description' => 'Diagenode offers kits and DNA/RNA shearing technology prior to next-generation sequencing, many Next-generation sequencing platforms require preparation of the DNA.', 'meta_title' => 'Next-generation sequencing (NGS) Applications and Methods | Diagenode', 'modified' => '2018-07-26 05:24:29', 'created' => '2015-04-01 22:47:04', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '13', 'position' => '10', 'parent_id' => '3', 'name' => 'DNA/RNA shearing', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns">In recent years, advances in Next-Generation Sequencing (NGS) have revolutionized genomics and biology. This growth has fueled demands on upstream techniques for optimal sample preparation and genomic library construction. One of the most critical aspects of optimal library preparation is the quality of the DNA to be sequenced. The DNA must first be effectively and consistently sheared into the appropriate fragment size (depending on the sequencing platform) to enable sensitive and reliable NGS results. The <strong>Bioruptor</strong><sup>®</sup> <strong>Pico</strong> and the <strong>Megaruptor</strong><sup>®</sup> provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows. Follow our guidelines and find the good parameters for your expected DNA size: <a href="https://pybrevet.typeform.com/to/o8cQfM">DNA shearing with the Bioruptor<sup>®</sup></a>.</div> </div> <p></p> <div class="row"> <div class="small-7 medium-7 large-7 columns text-center"><img src="https://www.diagenode.com/img/applications/true-flexibility-with-br-ngs.jpg" /></div> <div class="small-5 medium-5 large-5 columns"><small><strong>Programmable DNA size distribution and high reproducibility with Bioruptor<sup>®</sup> Pico using 0.65 (panel A) or 0.1 ml (panel B) microtubes</strong>. <b>Panel A:</b> 200 bp after 13 cycles (13 sec ON/OFF) using 100 µl volume. Average size: 204; CV%:1.89%). <b>Panel B:</b> 200 bp after 20 cycles (30 sec ON/OFF) using 10 µl volume. (Average size: 215 bp; CV%: 6.6%). <b>Panel A & B:</b> peak electropherogram view. <b>Panel C & D:</b> virtual gel view.</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-10 medium-10 large-10 columns text-center end small-offset-1"><img src="https://www.diagenode.com/img/applications/megaruptor-short-frag.jpg" /></div> <div class="small-12 medium-12 large-12 columns"><small><strong> Reproducible and narrow DNA size distribution with Megaruptor® using short fragment size Hydropores Validation using two different DNA sources and two different methods of analysis. A:</strong> Shearing of lambda phage genomic DNA (20 ng/μl; 150 μl/sample) sheared at different speed settings and analyzed on 1% agarose gel. <strong>B:</strong> Bioanalyzer profiles of human genomic DNA (20 ng/μl; 150 μl/sample) sheared at different software settings of 2 and 5 kb. Three independent experiments were run for each setting. (Agilent DNA 12000 kit was used for separation and fragment sizing).</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-4 medium-4 large-4 columns text-center"><img src="https://www.diagenode.com/img/applications/megaruptor-long-frag.jpg" /></div> <div class="small-8 medium-8 large-8 columns"><small><strong> Demonstrated shearing to fragment sizes between 15 kb and 75 kb with Megaruptor® using long fragment size Hydropores. </strong>Image shows DNA size distribution of human genomic DNA sheared with long fragment Hydropores. DNA was analyzed by pulsed field gel electrophoresis (PFGE) in 1% agarose gel and a mean size of smears was estimated using Image Lab 4.1 software.<br /> * indicates unsheared DNA </small></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'dna-rna-shearing', 'meta_keywords' => 'DNA/RNA shearing,Bioruptor® Pico,Megaruptor®,Next-Generation Sequencing ', 'meta_description' => 'Bioruptor® Pico and the Megaruptor® provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows.', 'meta_title' => 'DNA shearing & RNA shearing for Next-Generation Sequencing (NGS) | Diagenode', 'modified' => '2017-12-08 14:44:11', 'created' => '2014-10-29 12:45:41', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '17', 'position' => '10', 'parent_id' => '4', 'name' => 'Protein extraction', 'description' => '<div class="row"> <div class="large-12 columns">Various biochemical and analytical techniques require the extraction of protein from tissues or mammalian, yeast and bacterial cells. Obtaining high quality and yields of proteins is important for further downstream protein characterization such as in PAGE, western blotting, mass spectrometry or protein purification. The efficient disruption and homogenization of tissues and cultured cells obtained in just one step using <strong>Diagenode's Bioruptor</strong><sup>®</sup> deliver high quality protein.</div> </div> <p></p> <div class="row"> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_standard_plus.png" /> <p><small>Western blot analysis of GAPDH and HSP90 proteins in tissues (various mouse tissues) and cultured cell extracts (HeLA).</small></p> </div> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_pico.png" /> <p><small>Western blot analysis of GAPDH and ß-tubulin proteins in tissues (mouse liver) and cultured cell extracts (HeLA).</small></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'protein-extraction', 'meta_keywords' => 'Protein extraction,Bioruptor,Sonication,Protein Analysis', 'meta_description' => 'Diagenode provides efficient disruption and homogenization of tissues and cultured cells obtained in just one step using Bioruptor® deliver high quality protein.', 'meta_title' => 'Protein extraction using Bioruptor® Sonication device | Diagenode', 'modified' => '2017-10-16 14:39:42', 'created' => '2014-07-02 04:41:03', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '6', 'position' => '10', 'parent_id' => '1', 'name' => 'メチル化DNA結合タンパク質', 'description' => '<div class="row"> <div class="large-12 columns">MBD方法は、メチル化DNAに対するH6-GST-MBD融合タンパク質の非常に高い親和性に基づいています。 このタンパク質は、N末端His6タグを含むグルタチオン-S-トランスフェラーゼ（GST）とのC末端融合物として、ヒトMeCP2のメチル結合ドメイン（MBD）を含有します。 このH6-GST-MBD融合タンパク質を用いて、メチル化CpGを含むDNAを特異的に単離する事が可能です。<br /><br />DiagenodeのMethylCap®キットは、二本鎖DNAの高濃縮と、メチル化CpG密度の関数における微分分画を可能にします。 分画はサンプルの複雑さを軽減し、次世代のシーケンシングを容易にします。 MethylCapアッセイに先立ち、DNAを最初に抽出し、Picoruptorソニケーターを用いて断片化します。<br /> <h3>概要</h3> <p class="text-center"><br /><img src="https://www.diagenode.com/img/applications/methyl_binding_domain_overview.jpg" /></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'methylbinding-domain-protein', 'meta_keywords' => 'Epigenetic,Methylbinding Domain Protein,MBD,DNA methylation,DNA replication,MethylCap,MethylCap assay,', 'meta_description' => 'Methylbinding Domain Protein(MBD) approach is based on the very high affinity of a H6-GST-MBD fusion protein for methylated DNA. This protein consists of the methyl binding domain (MBD) of human MeCP2, as a C-terminal fusion with Glutathione-S-transferase', 'meta_title' => 'Epigenetic Methylbinding Domain Protein(MBD) - DNA methylation | Diagenode', 'modified' => '2019-03-22 12:32:12', 'created' => '2015-06-02 17:05:42', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '9', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-seq', 'description' => '<div class="row"> <div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div> <div class="large-12 columns"></div> <h5 class="large-12 columns"><strong></strong></h5> <h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div> <div class="large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by sonication to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with <strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: Reverse cross-links, elute, and purify </li> <li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify IP'd material</li> <li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chromatin-immunoprecipitation-sequencing', 'meta_keywords' => 'Chromatin Immunoprecipitation Sequencing,ChIP-Seq,ChIP-seq grade antibodies,DNA purification,qPCR,Shearing of chromatin', 'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing', 'meta_title' => 'Chromatin Immunoprecipitation - ChIP-seq Kits - Dna methylation | Diagenode', 'modified' => '2017-11-14 09:57:16', 'created' => '2015-04-12 18:08:46', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '11', 'position' => '10', 'parent_id' => '3', 'name' => 'FFPE DNA extraction', 'description' => '<div class="row"> <div class="large-12 columns">Diagenode's high yields FFPE DNA extraction using Bioruptor<sup><span>®</span></sup> is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no toxic reagents, digest tissues, and purify DNA with high yields and low sample degradation. The DNA can then be analyzed by traditional methods or can be sheared with the Bioruptor<sup>®</sup> Pico ultrasonicator for downstream NGS library prep using the MicroPlex Library Preparation Kit.</div> <div class="small-12 medium-12 large-12 columns text-center"><img src="https://www.diagenode.com/img/applications/ffpe_workflow.png" /></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'ffpe-dna-extraction', 'meta_keywords' => 'FFPE DNA extraction,Next-Gen Sequencing,Bioruptor® ultrasonicator', 'meta_description' => 'Diagenode's high yields FFPE DNA extraction using Bioruptor is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no tox', 'meta_title' => 'FFPE DNA extraction using Bioruptor® ultrasonicator | Diagenode', 'modified' => '2017-10-16 14:34:57', 'created' => '2014-10-01 01:24:40', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '10', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-qPCR', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns text-justify"> <p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p> <p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p> </div> <div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div> <div class="small-12 medium-12 large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li> <li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chip-qpcr', 'meta_keywords' => 'Chromatin immunoprecipitation,ChIP Quantitative PCR,polymerase chain reaction (PCR)', 'meta_description' => 'Diagenode's ChIP qPCR kits can be used to quantify enriched DNA after chromatin immunoprecipitation. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of', 'meta_title' => 'ChIP Quantitative PCR (ChIP-qPCR) | Diagenode', 'modified' => '2018-01-09 16:46:56', 'created' => '2014-12-11 00:22:08', 'ProductsApplication' => array( [maximum depth reached] ) ) ), 'Category' => array( (int) 0 => array( 'id' => '6', 'position' => '1', 'parent_id' => '1', 'name' => 'Bioruptor<sup>®</sup>', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"><br /> <p><span>Diagenode focuses on state-of-the-art preparation of high quality biological and chemical samples by developing the industry’s most advanced water bath sonicators and hydrodynamic devices. Our instruments are ideal for a number of applications in various fields of studies including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</span></p> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor/TAB-BR-comparaison.pdf" target="_blank"><img src="https://www.diagenode.com/img/bouton-comparaison.png" /></a></p> </div> <!-- <center> <div class="small-12 medium-4 large-4 columns"> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img 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crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script>// <![CDATA[ (function (d) { var js, id = "genially-embed-js", ref = d.getElementsByTagName("script")[0]; if (d.getElementById(id)) { return; } js = d.createElement("script"); js.id = id; js.async = true; js.src = "https://view.genial.ly/static/embed/embed.js"; ref.parentNode.insertBefore(js, ref); }(document)); // ]]></script> </div> </div>--> <p><span> <br /></span></p> <div class="spacer"></div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">Reproductibility is our priority</h2> </div> </div> <div><img src="https://www.diagenode.com/img/shearing/reproductibility.png" alt="reproductibility" /> <p class="bottom_note"></p> </div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">An affordable instrument for wide range of applications</h2> </div> </div> <p style="text-align: center;">Designed for any researchers, the Bioruptor gives the user the right level of flexibility.</p> <table style="width: 972px;"> <tbody> <tr style="height: 56px;"> <th style="width: 380px; height: 56px;"></th> <th class="text-center" style="width: 126px; height: 56px;">Bioruptor</th> <th class="text-center" style="width: 141px; height: 56px;">Cup Horn Sonicators</th> <th class="text-center" style="width: 156px; height: 56px;">Focused <br />ultra-sonicators</th> <th class="text-center" style="width: 155px; height: 56px;">Multi Sample Sonicator</th> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Instrument pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Consumables pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Range of applications</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Scalable and sample volume flexibility</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Throughput</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> </tbody> </table> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;"></h2> <h2 style="text-align: center;">Bioruptor ultrasonication for best results in:</h2> <p><b><span>✓ Chromatin shearing</span><span> </span><span style="font-weight: 400;">- Industry leader in accurate and tight fragment ranges</span></b></p> <p><b><span>✓ DNA shearing</span><span> </span><span style="font-weight: 400;">- Excellent results for optimal fragment lengths in NGS library prep</span></b></p> <p><b><span>✓<span> </span></span>Protein aggregation studies </b><span style="font-weight: 400;">- Standardizing seeding with the robust Bioruptor.<br /></span><i><span style="font-weight: 400;">Read the app note by Dr. Kelvin Luk at the University of Pennsylvania </span></i><a href="https://www.diagenode.com/en/documents/standardizing-seeding-experiments-for-the-understanding-of-parkinson-disease" style="color: #13b29c;"><i><span style="font-weight: 400;">“Standardizing seeding experiments using the Bioruptor® for the understanding of the neuronal alpha-synuclein pathology”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>3D genome analysis with Hi-C</b><span style="font-weight: 400;"> - Preparing chromatin libraries with high-quality sonication.<br /></span><i><span style="font-weight: 400;">Read the app note, “</span></i><a href="https://www.diagenode.com/en/documents/applicationnote-arima-low-input" style="color: #13b29c;"><i><span style="font-weight: 400;">Unlock Low-Input 3D Genome Analysis with the Arima-HiC Kit”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>Mass spectrometry</b> <b>and increasing protein identification</b><span style="font-weight: 400;">- Sample preparation using Preomics iST and Bioruptor sonication.<br /></span><i><span style="font-weight: 400;">Read the app note “</span></i><a href="https://www.diagenode.com/en/documents/wp-ist-adaptators" style="color: #13b29c;"><i><span style="font-weight: 400;">Increase your iST ultrasonication throughput with the new Bioruptor® Pico cartridge holder”</span></i></a></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>Cell lysis, liposome prep, protein extraction, RNA extraction and more</b></span></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>CUT&RUN –Sonication of input DNA (for enrichment comparison) for NGS</b></span></p> </div> </div> <p><a href="https://www.diagenode.com/en/categories/bioruptor-maintenance"><img src="https://www.diagenode.com/img/banners/maintenance-banner-br.png" /></a></p> <p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" 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When studying samples that are difficult to obtain or grow, low input solutions can help you understand genome structure across a new range of low input samples. In addition, the Diagenode Bioruptor Pico assures that chromatin is sheared to optimal fragment lengths.</span></p>', 'image_id' => '247', 'type' => 'Application Note', 'url' => 'files/application_notes/ApplicationNote-Arima-Low-Input.pdf', 'slug' => 'applicationnote-arima-low-input', 'meta_keywords' => 'application note arima low input', 'meta_description' => 'application note arima low input', 'modified' => '2021-02-09 09:55:59', 'created' => '2021-02-09 09:55:59', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1074', 'name' => 'Datasheet of Bioruptor tubes', 'description' => '<p>Datasheet of Diagenode tubes for Bioruptor Pico and Bioruptor Plus.</p>', 'image_id' => null, 'type' => 'Datasheet', 'url' => 'files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf', 'slug' => 'tds-bioruptor-tubes', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2022-02-23 12:21:44', 'created' => '2020-03-23 10:41:46', 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'modified' => '2020-01-10 10:53:08', 'created' => '2020-01-10 10:53:08', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '1805', 'name' => 'product/shearing_technologies/B01080000-3.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:46', 'created' => '2020-01-10 10:53:46', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1806', 'name' => 'product/shearing_technologies/B01080000-4.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:56', 'created' => '2020-01-10 10:53:56', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1807', 'name' => 'product/shearing_technologies/B01080000-5.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:54:06', 'created' => '2020-01-10 10:54:06', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => '2018-02-14 15:41:46', 'ProductsImage' => array( [maximum depth reached] ) ) ), 'Promotion' => array(), 'Protocol' => array( (int) 0 => array( 'id' => '73', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:16:00', 'created' => '0000-00-00 00:00:00', 'ProductsProtocol' => array( [maximum depth reached] ) ) ), 'Publication' => array( (int) 0 => array( 'id' => '4881', 'name' => 'LEO1 Is Required for Efficient Entry into Quiescence, Control of H3K9 Methylation and Gene Expression in Human Fibroblasts', 'authors' => 'Laurent M. et al.', 'description' => '<p><span>(1) Background: The LEO1 (Left open reading frame 1) protein is a conserved subunit of the PAF1C complex (RNA polymerase II-associated factor 1 complex). PAF1C has well-established mechanistic functions in elongation of transcription and RNA processing. We previously showed, in fission yeast, that LEO1 controls histone H3K9 methylation levels by affecting the turnover of histone H3 in chromatin, and that it is essential for the proper regulation of gene expression during cellular quiescence. Human fibroblasts enter a reversible quiescence state upon serum deprivation in the growth media. Here we investigate the function of LEO1 in human fibroblasts. (2) Methods: We knocked out the </span><span class="html-italic">LEO1</span><span><span> </span>gene using CRISPR/Cas9 methodology in human fibroblasts and verified that the LEO1 protein was undetectable by Western blot. We characterized the phenotype of the<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout cells with FACS analysis and cell growth assays. We used RNA-sequencing using spike-in controls to measure gene expression and spike-in controlled ChIP-sequencing experiments to measure the histone modification H3K9me2 genome-wide. (3) Results: Gene expression levels are altered in quiescent cells, however factors controlling chromatin and gene expression changes in quiescent human cells are largely unknown. The<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout fibroblasts are viable but have reduced metabolic activity compared to wild-type cells.<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells showed a slower entry into quiescence and a different morphology compared to wild-type cells. Gene expression was generally reduced in quiescent wild-type cells. The downregulated genes included genes involved in cell proliferation. A small number of genes were upregulated in quiescent wild-type cells including several genes involved in ERK1/ERK2 and Wnt signaling. In quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells, many genes were mis-regulated compared to wild-type cells. This included genes involved in Calcium ion transport and cell morphogenesis. Finally, spike-in controlled ChIP-sequencing experiments demonstrated that the histone modification H3K9me2 levels are globally increased in quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells. (4) Conclusions: Thus, LEO1 is important for proper entry into cellular quiescence, control of H3K9me2 levels, and gene expression in human fibroblasts.</span></p>', 'date' => '2023-11-17', 'pmid' => 'https://www.mdpi.com/2218-273X/13/11/1662', 'doi' => 'https://doi.org/10.3390/biom13111662', 'modified' => '2023-11-21 12:01:53', 'created' => '2023-11-21 12:01:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '4845', 'name' => 'DeSUMOylation of chromatin-bound proteins limits the rapidtranscriptional reprogramming induced by daunorubicin in acute myeloidleukemias.', 'authors' => 'Boulanger M. et al.', 'description' => '<p>Genotoxicants have been used for decades as front-line therapies against cancer on the basis of their DNA-damaging actions. However, some of their non-DNA-damaging effects are also instrumental for killing dividing cells. We report here that the anthracycline Daunorubicin (DNR), one of the main drugs used to treat Acute Myeloid Leukemia (AML), induces rapid (3 h) and broad transcriptional changes in AML cells. The regulated genes are particularly enriched in genes controlling cell proliferation and death, as well as inflammation and immunity. These transcriptional changes are preceded by DNR-dependent deSUMOylation of chromatin proteins, in particular at active promoters and enhancers. Surprisingly, inhibition of SUMOylation with ML-792 (SUMO E1 inhibitor), dampens DNR-induced transcriptional reprogramming. Quantitative proteomics shows that the proteins deSUMOylated in response to DNR are mostly transcription factors, transcriptional co-regulators and chromatin organizers. Among them, the CCCTC-binding factor CTCF is highly enriched at SUMO-binding sites found in cis-regulatory regions. This is notably the case at the promoter of the DNR-induced NFKB2 gene. DNR leads to a reconfiguration of chromatin loops engaging CTCF- and SUMO-bound NFKB2 promoter with a distal cis-regulatory region and inhibition of SUMOylation with ML-792 prevents these changes.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37462077', 'doi' => '10.1093/nar/gkad581', 'modified' => '2023-08-01 14:16:43', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '4846', 'name' => 'RNA polymerase II CTD is dispensable for transcription and requiredfor termination in human cells.', 'authors' => 'Yahia Y. et al.', 'description' => '<p>The largest subunit of RNA polymerase (Pol) II harbors an evolutionarily conserved C-terminal domain (CTD), composed of heptapeptide repeats, central to the transcriptional process. Here, we analyze the transcriptional phenotypes of a CTD-Δ5 mutant that carries a large CTD truncation in human cells. Our data show that this mutant can transcribe genes in living cells but displays a pervasive phenotype with impaired termination, similar to but more severe than previously characterized mutations of CTD tyrosine residues. The CTD-Δ5 mutant does not interact with the Mediator and Integrator complexes involved in the activation of transcription and processing of RNAs. Examination of long-distance interactions and CTCF-binding patterns in CTD-Δ5 mutant cells reveals no changes in TAD domains or borders. Our data demonstrate that the CTD is largely dispensable for the act of transcription in living cells. We propose a model in which CTD-depleted Pol II has a lower entry rate onto DNA but becomes pervasive once engaged in transcription, resulting in a defect in termination.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37424514', 'doi' => '10.15252/embr.202256150', 'modified' => '2023-08-01 14:17:54', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '4793', 'name' => 'Targeting lymphoid-derived IL-17 signaling to delay skin aging.', 'authors' => 'Paloma S. et al.', 'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, γδ T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-κB in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218', 'doi' => '10.1038/s43587-023-00431-z', 'modified' => '2023-06-14 15:56:56', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '4796', 'name' => 'Nicotinamide N-methyltransferase sustains a core epigenetic programthat promotes metastatic colonization in breast cancer.', 'authors' => 'Couto J.P. et al.', 'description' => '<p><span>Metastatic colonization of distant organs accounts for over 90% of deaths related to solid cancers, yet the molecular determinants of metastasis remain poorly understood. Here, we unveil a mechanism of colonization in the aggressive basal-like subtype of breast cancer that is driven by the NAD</span><sup>+</sup><span><span> </span>metabolic enzyme nicotinamide N-methyltransferase (NNMT). We demonstrate that NNMT imprints a basal genetic program into cancer cells, enhancing their plasticity. In line, NNMT expression is associated with poor clinical outcomes in patients with breast cancer. Accordingly, ablation of NNMT dramatically suppresses metastasis formation in pre-clinical mouse models. Mechanistically, NNMT depletion results in a methyl overflow that increases histone H3K9 trimethylation (H3K9me3) and DNA methylation at the promoters of PR/SET Domain-5 (PRDM5) and extracellular matrix-related genes. PRDM5 emerged in this study as a pro-metastatic gene acting via induction of cancer-cell intrinsic transcription of collagens. Depletion of PRDM5 in tumor cells decreases COL1A1 deposition and impairs metastatic colonization of the lungs. These findings reveal a critical activity of the NNMT-PRDM5-COL1A1 axis for cancer cell plasticity and metastasis in basal-like breast cancer.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37259596', 'doi' => '10.15252/embj.2022112559', 'modified' => '2023-06-15 08:35:19', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '4812', 'name' => 'SOX expression in prostate cancer drives resistance to nuclear hormonereceptor signaling inhibition through the WEE1/CDK1 signaling axis.', 'authors' => 'Williams A. et al.', 'description' => '<p><span>The development of androgen receptor signaling inhibitor (ARSI) drug resistance in prostate cancer (PC) remains therapeutically challenging. Our group has described the role of sex determining region Y-box 2 (SOX2) overexpression in ARSI-resistant PC. Continuing this work, we report that NR3C1, the gene encoding glucocorticoid receptor (GR), is a novel SOX2 target in PC, positively regulating its expression. Similar to ARSI treatment, SOX2-positive PC cells are insensitive to GR signaling inhibition using a GR modulating therapy. To understand SOX2-mediated nuclear hormone receptor signaling inhibitor (NHRSI) insensitivity, we performed RNA-seq in SOX2-positive and -negative PC cells following NHRSI treatment. RNA-seq prioritized differentially regulated genes mediating the cell cycle, including G2 checkpoint WEE1 Kinase (WEE1) and cyclin-dependent kinase 1 (CDK1). Additionally, WEE1 and CDK1 were differentially expressed in PC patient tumors dichotomized by high vs low SOX2 gene expression. Importantly, pharmacological targeting of WEE1 (WEE1i) in combination with an ARSI or GR modulator re-sensitizes SOX2-positive PC cells to nuclear hormone receptor signaling inhibition in vitro, and WEE1i combined with ARSI significantly slowed tumor growth in vivo. Collectively, our data suggest SOX2 predicts NHRSI resistance, and simultaneously indicates the addition of WEE1i to improve therapeutic efficacy of NHRSIs in SOX2-positive PC.</span></p>', 'date' => '2023-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37169162', 'doi' => '10.1016/j.canlet.2023.216209', 'modified' => '2023-06-15 08:58:59', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '4787', 'name' => 'The Effect of Metformin and Carbohydrate-Controlled Diet onDNA Methylation and Gene Expression in the Endometrium of Womenwith Polycystic Ovary Syndrome.', 'authors' => 'Garcia-Gomez E. et al.', 'description' => '<p>Polycystic ovary syndrome (PCOS) is an endocrine disease associated with infertility and metabolic disorders in reproductive-aged women. In this study, we evaluated the expression of eight genes related to endometrial function and their DNA methylation levels in the endometrium of PCOS patients and women without the disease (control group). In addition, eight of the PCOS patients underwent intervention with metformin (1500 mg/day) and a carbohydrate-controlled diet (type and quantity) for three months. Clinical and metabolic parameters were determined, and RT-qPCR and MeDIP-qPCR were used to evaluate gene expression and DNA methylation levels, respectively. Decreased expression levels of , , and genes and increased DNA methylation levels of the promoter were found in the endometrium of PCOS patients compared to controls. After metformin and nutritional intervention, some metabolic and clinical variables improved in PCOS patients. This intervention was associated with increased expression of , , and genes and reduced DNA methylation levels of the promoter in the endometrium of PCOS women. Our preliminary findings suggest that metformin and a carbohydrate-controlled diet improve endometrial function in PCOS patients, partly by modulating DNA methylation of the gene promoter and the expression of genes implicated in endometrial receptivity and insulin signaling.</p>', 'date' => '2023-04-01', 'pmid' => 'https://doi.org/10.3390%2Fijms24076857', 'doi' => '10.3390/ijms24076857', 'modified' => '2023-06-12 08:58:33', 'created' => '2023-05-05 12:34:24', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '4763', 'name' => 'Chromatin profiling identifies transcriptional readthrough as a conservedmechanism for piRNA biogenesis in mosquitoes.', 'authors' => 'Qu J. et al.', 'description' => '<p>The piRNA pathway in mosquitoes differs substantially from other model organisms, with an expanded PIWI gene family and functions in antiviral defense. Here, we define core piRNA clusters as genomic loci that show ubiquitous piRNA expression in both somatic and germline tissues. These core piRNA clusters are enriched for non-retroviral endogenous viral elements (nrEVEs) in antisense orientation and depend on key biogenesis factors, Veneno, Tejas, Yb, and Shutdown. Combined transcriptome and chromatin state analyses identify transcriptional readthrough as a conserved mechanism for cluster-derived piRNA biogenesis in the vector mosquitoes Aedes aegypti, Aedes albopictus, Culex quinquefasciatus, and Anopheles gambiae. Comparative analyses between the two Aedes species suggest that piRNA clusters function as traps for nrEVEs, allowing adaptation to environmental challenges such as virus infection. Our systematic transcriptome and chromatin state analyses lay the foundation for studies of gene regulation, genome evolution, and piRNA function in these important vector species.</p>', 'date' => '2023-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36930642', 'doi' => '10.1016/j.celrep.2023.112257', 'modified' => '2023-04-17 09:12:37', 'created' => '2023-04-14 13:41:22', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 8 => array( 'id' => '4720', 'name' => 'Activation of AKT induces EZH2-mediated β-catenin trimethylation incolorectal cancer.', 'authors' => 'Ghobashi A. H. et al.', 'description' => '<p>Colorectal cancer (CRC) develops in part through the deregulation of different signaling pathways, including activation of the WNT/β-catenin and PI3K/AKT pathways. Enhancer of zeste homolog 2 (EZH2) is a lysine methyltransferase that is involved in regulating stem cell development and differentiation and is overexpressed in CRC. However, depending on the study EZH2 has been found to be both positively and negatively correlated with the survival of CRC patients suggesting that EZH2's role in CRC may be context specific. In this study, we explored how PI3K/AKT activation alters EZH2's role in CRC. We found that activation of AKT by PTEN knockdown or by hydrogen peroxide treatment induced EZH2 phosphorylation at serine 21. Phosphorylation of EZH2 resulted in EZH2-mediated methylation of β-catenin and an associated increased interaction between β-catenin, TCF1, and RNA polymerase II. AKT activation increased β-catenin's enrichment across the genome and EZH2 inhibition reduced this enrichment by reducing the methylation of β-catenin. Furthermore, PTEN knockdown increased the expression of epithelial-mesenchymal transition (EMT)-related genes, and somewhat unexpectedly EZH2 inhibition further increased the expression of these genes. Consistent with these findings, EZH2 inhibition enhanced the migratory phenotype of PTEN knockdown cells. Overall, we demonstrated that EZH2 modulates AKT-induced changes in gene expression through the AKT/EZH2/ β-catenin axis in CRC with active PI3K/AKT signaling. Therefore, it is important to consider the use of EZH2 inhibitors in CRC with caution as these inhibitors will inhibit EZH2-mediated methylation of histone and non-histone targets such as β-catenin, which can have tumor-promoting effects.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1101%2F2023.01.31.526429', 'doi' => '10.1101/2023.01.31.526429', 'modified' => '2023-03-28 09:13:16', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 9 => array( 'id' => '4667', 'name' => 'Detailed molecular and epigenetic characterization of the Pig IPECJ2and Chicken SL-29 cell lines', 'authors' => 'de Vos J. et al.', 'description' => '<p>The pig IPECJ2 and chicken SL-29 cell lines are of interest because of their untransformed nature and wide use in functional studies. Molecular characterization of these cell lines is important to gain insight into possible molecular aberrations. The aims of this paper are providing a molecular and epigenetic characterization of the IPEC-J2 and SL-29 cell lines and providing a cell-line reference for the FAANG community, and future biomedical research. Whole genome sequencing , gene expression, DNA methylation , chromatin accessibility and ChIP-seq of four histone marks (H3K4me1, H3K4me3, H3K27ac, H3K27me3) and an insulator (CTCF) are used to achieve these aims. Heteroploidy (aneuploidy) of various chromosomes was observed from whole genome sequencing analysis in both cell lines. Furthermore, higher gene expression for genes located on chromosomes with aneuploidy in comparison to diploid chromosomes was observed. Regulatory complexity of gene expression, DNA methylation and chromatin accessibility was investigated through an integrative approach.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.isci.2023.106252', 'doi' => '10.1016/j.isci.2023.106252', 'modified' => '2023-04-07 16:52:26', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 10 => array( 'id' => '4673', 'name' => 'Signal-induced enhancer activation requires Ku70 to readtopoisomerase1-DNA covalent complexes.', 'authors' => 'Tan Y. et al.', 'description' => '<p>Enhancer activation serves as the main mechanism regulating signal-dependent transcriptional programs, ensuring cellular plasticity, yet central questions persist regarding their mechanism of activation. Here, by successfully mapping topoisomerase I-DNA covalent complexes genome-wide, we find that most, if not all, acutely activated enhancers, including those induced by 17β-estradiol, dihydrotestosterone, tumor necrosis factor alpha and neuronal depolarization, are hotspots for topoisomerase I-DNA covalent complexes, functioning as epigenomic signatures read by the classic DNA damage sensor protein, Ku70. Ku70 in turn nucleates a heterochromatin protein 1 gamma (HP1γ)-mediator subunit Med26 complex to facilitate acute, but not chronic, transcriptional activation programs. Together, our data uncover a broad, unappreciated transcriptional code, required for most, if not all, acute signal-dependent enhancer activation events in both mitotic and postmitotic cells.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36747093', 'doi' => '10.1038/s41594-022-00883-8', 'modified' => '2023-04-14 09:24:10', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 11 => array( 'id' => '4668', 'name' => 'Cotranscriptional demethylation induces global loss of H3K4me2 fromactive genes in Arabidopsis', 'authors' => 'Mori S. et al.', 'description' => '<p>Based on studies of animals and yeasts, methylation of histone H3 lysine 4 (H3K4me1/2/3, for mono-, di-, and tri-methylation, respectively) is regarded as the key epigenetic modification of transcriptionally active genes. In plants, however, H3K4me2 correlates negatively with transcription, and the regulatory mechanisms of this counterintuitive H3K4me2 distribution in plants remain largely unexplored. A previous genetic screen for factors regulating plant regeneration identified Arabidopsis LYSINE-SPECIFIC DEMETHYLASE 1-LIKE 3 (LDL3), which is a major H3K4me2 demethylase. Here, we show that LDL3-mediated H3K4me2 demethylation depends on the transcription elongation factor Paf1C and phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII). In addition, LDL3 binds to phosphorylated RNAPII. These results suggest that LDL3 is recruited to transcribed genes by binding to elongating RNAPII and demethylates H3K4me2 cotranscriptionally. Importantly, the negative correlation between H3K4me2 and transcription is disrupted in the ldl3 mutant, demonstrating the genome-wide impacts of the transcription-driven LDL3 pathway to control H3K4me2 in plants. Our findings implicate H3K4me2 in plants as chromatin memory for transcriptionally repressive states, which ensures robust gene control.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.02.17.528985v1', 'doi' => '10.1101/2023.02.17.528985', 'modified' => '2023-04-14 09:31:55', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 12 => array( 'id' => '4670', 'name' => 'Epigenetic regulation of plastin 3 expression by the macrosatelliteDXZ4 and the transcriptional regulator CHD4.', 'authors' => 'Strathmann E. A. et al.', 'description' => '<p>Dysregulated Plastin 3 (PLS3) levels associate with a wide range of skeletal and neuromuscular disorders and the most common types of solid and hematopoietic cancer. Most importantly, PLS3 overexpression protects against spinal muscular atrophy. Despite its crucial role in F-actin dynamics in healthy cells and its involvement in many diseases, the mechanisms that regulate PLS3 expression are unknown. Interestingly, PLS3 is an X-linked gene and all asymptomatic SMN1-deleted individuals in SMA-discordant families who exhibit PLS3 upregulation are female, suggesting that PLS3 may escape X chromosome inactivation. To elucidate mechanisms contributing to PLS3 regulation, we performed a multi-omics analysis in two SMA-discordant families using lymphoblastoid cell lines and iPSC-derived spinal motor neurons originated from fibroblasts. We show that PLS3 tissue-specifically escapes X-inactivation. PLS3 is located ∼500 kb proximal to the DXZ4 macrosatellite, which is essential for X chromosome inactivation. By applying molecular combing in a total of 25 lymphoblastoid cell lines (asymptomatic individuals, individuals with SMA, control subjects) with variable PLS3 expression, we found a significant correlation between the copy number of DXZ4 monomers and PLS3 levels. Additionally, we identified chromodomain helicase DNA binding protein 4 (CHD4) as an epigenetic transcriptional regulator of PLS3 and validated co-regulation of the two genes by siRNA-mediated knock-down and overexpression of CHD4. We show that CHD4 binds the PLS3 promoter by performing chromatin immunoprecipitation and that CHD4/NuRD activates the transcription of PLS3 by dual-luciferase promoter assays. Thus, we provide evidence for a multilevel epigenetic regulation of PLS3 that may help to understand the protective or disease-associated PLS3 dysregulation.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.ajhg.2023.02.004', 'doi' => '10.1016/j.ajhg.2023.02.004', 'modified' => '2023-04-14 09:36:04', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 13 => array( 'id' => '4672', 'name' => 'A dataset of definitive endoderm and hepatocyte differentiations fromhuman induced pluripotent stem cells.', 'authors' => 'Tanaka Y. et al.', 'description' => '<p>Hepatocytes are a major parenchymal cell type in the liver and play an essential role in liver function. Hepatocyte-like cells can be differentiated in vitro from induced pluripotent stem cells (iPSCs) via definitive endoderm (DE)-like cells and hepatoblast-like cells. Here, we explored the in vitro differentiation time-course of hepatocyte-like cells. We performed methylome and transcriptome analyses for hepatocyte-like cell differentiation. We also analyzed DE-like cell differentiation by methylome, transcriptome, chromatin accessibility, and GATA6 binding profiles, using finer time-course samples. In this manuscript, we provide a detailed description of the dataset and the technical validations. Our data may be valuable for the analysis of the molecular mechanisms underlying hepatocyte and DE differentiations.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36788249', 'doi' => '10.1038/s41597-023-02001-9', 'modified' => '2023-04-14 09:41:29', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 14 => array( 'id' => '4643', 'name' => 'The mineralocorticoid receptor modulates timing and location of genomicbinding by glucocorticoid receptor in response to synthetic glucocorticoidsin keratinocytes.', 'authors' => 'Carceller-Zazo E. et al.', 'description' => '<p>Glucocorticoids (GCs) exert potent antiproliferative and anti-inflammatory properties, explaining their therapeutic efficacy for skin diseases. GCs act by binding to the GC receptor (GR) and the mineralocorticoid receptor (MR), co-expressed in classical and non-classical targets including keratinocytes. Using knockout mice, we previously demonstrated that GR and MR exert essential nonoverlapping functions in skin homeostasis. These closely related receptors may homo- or heterodimerize to regulate transcription, and theoretically bind identical GC-response elements (GRE). We assessed the contribution of MR to GR genomic binding and the transcriptional response to the synthetic GC dexamethasone (Dex) using control (CO) and MR knockout (MR ) keratinocytes. GR chromatin immunoprecipitation (ChIP)-seq identified peaks common and unique to both genotypes upon Dex treatment (1 h). GREs, AP-1, TEAD, and p53 motifs were enriched in CO and MR peaks. However, GR genomic binding was 35\% reduced in MR , with significantly decreased GRE enrichment, and reduced nuclear GR. Surface plasmon resonance determined steady state affinity constants, suggesting preferred dimer formation as MR-MR > GR-MR ~ GR-GR; however, kinetic studies demonstrated that GR-containing dimers had the longest lifetimes. Despite GR-binding differences, RNA-seq identified largely similar subsets of differentially expressed genes in both genotypes upon Dex treatment (3 h). However, time-course experiments showed gene-dependent differences in the magnitude of expression, which correlated with earlier and more pronounced GR binding to GRE sites unique to CO including near Nr3c1. Our data show that endogenous MR has an impact on the kinetics and differential genomic binding of GR, affecting the time-course, specificity, and magnitude of GC transcriptional responses in keratinocytes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36527388', 'doi' => '10.1096/fj.202201199RR', 'modified' => '2023-03-28 08:55:08', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 15 => array( 'id' => '4605', 'name' => 'Gene Regulatory Interactions at Lamina-Associated Domains', 'authors' => 'Madsen-Østerbye J. et al.', 'description' => '<p>The nuclear lamina provides a repressive chromatin environment at the nuclear periphery. However, whereas most genes in lamina-associated domains (LADs) are inactive, over ten percent reside in local euchromatic contexts and are expressed. How these genes are regulated and whether they are able to interact with regulatory elements remain unclear. Here, we integrate publicly available enhancer-capture Hi-C data with our own chromatin state and transcriptomic datasets to show that inferred enhancers of active genes in LADs are able to form connections with other enhancers within LADs and outside LADs. Fluorescence in situ hybridization analyses show proximity changes between differentially expressed genes in LADs and distant enhancers upon the induction of adipogenic differentiation. We also provide evidence of involvement of lamin A/C, but not lamin B1, in repressing genes at the border of an in-LAD active region within a topological domain. Our data favor a model where the spatial topology of chromatin at the nuclear lamina is compatible with gene expression in this dynamic nuclear compartment.</p>', 'date' => '2023-01-01', 'pmid' => 'https://doi.org/10.3390%2Fgenes14020334', 'doi' => '10.3390/genes14020334', 'modified' => '2023-04-04 08:57:32', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 16 => array( 'id' => '4578', 'name' => 'The aryl hydrocarbon receptor cell intrinsically promotes resident memoryCD8 T cell differentiation and function.', 'authors' => 'Dean J. W. et al.', 'description' => '<p>The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4 T cells; however, its cell-intrinsic role in CD8 T cells remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8 T cell (T) differentiation and function. Genetic ablation of Ahr in mouse CD8 T cells leads to increased CD127KLRG1 short-lived effector cells and CD44CD62L T central memory cells but reduced granzyme-B-producing CD69CD103 T cells. Genome-wide analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8 T cell population, revealed by single-cell RNA-seq, is diminished upon Ahr deletion, compromising anti-tumor immunity. Human intestinal intraepithelial CD8 T cells also highly express AHR that regulates in vitro T differentiation and granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8 T cell immunity.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36640340', 'doi' => '10.1016/j.celrep.2022.111963', 'modified' => '2023-04-11 10:14:26', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 17 => array( 'id' => '4577', 'name' => 'Impact of Fetal Exposure to Endocrine Disrupting ChemicalMixtures on FOXA3 Gene and Protein Expression in Adult RatTestes.', 'authors' => 'Walker C. et al.', 'description' => '<p>Perinatal exposure to endocrine disrupting chemicals (EDCs) has been shown to affect male reproductive functions. However, the effects on male reproduction of exposure to EDC mixtures at doses relevant to humans have not been fully characterized. In previous studies, we found that in utero exposure to mixtures of the plasticizer di(2-ethylhexyl) phthalate (DEHP) and the soy-based phytoestrogen genistein (Gen) induced abnormal testis development in rats. In the present study, we investigated the molecular basis of these effects in adult testes from the offspring of pregnant SD rats gavaged with corn oil or Gen + DEHP mixtures at 0.1 or 10 mg/kg/day. Testicular transcriptomes were determined by microarray and RNA-seq analyses. A protein analysis was performed on paraffin and frozen testis sections, mainly by immunofluorescence. The transcription factor forkhead box protein 3 (FOXA3), a key regulator of Leydig cell function, was identified as the most significantly downregulated gene in testes from rats exposed in utero to Gen + DEHP mixtures. FOXA3 protein levels were decreased in testicular interstitium at a dose previously found to reduce testosterone levels, suggesting a primary effect of fetal exposure to Gen + DEHP on adult Leydig cells, rather than on spermatids and Sertoli cells, also expressing FOXA3. Thus, FOXA3 downregulation in adult testes following fetal exposure to Gen + DEHP may contribute to adverse male reproductive outcomes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36674726', 'doi' => '10.3390/ijms24021211', 'modified' => '2023-04-11 10:18:58', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 18 => array( 'id' => '4721', 'name' => 'Transfer of blocker-based qPCR reactions for DNA methylation analysisinto a microfluidic LoC system using thermal modeling.', 'authors' => 'Kärcher J.et al.', 'description' => '<p>Changes in the DNA methylation landscape are associated with many diseases like cancer. Therefore, DNA methylation analysis is of great interest for molecular diagnostics and can be applied, e.g., for minimally invasive diagnostics in liquid biopsy samples like blood plasma. Sensitive detection of local methylation, which occurs in various cancer types, can be achieved with quantitative HeavyMethyl-PCR using oligonucleotides that block the amplification of unmethylated DNA. A transfer of these quantitative PCRs (qPCRs) into point-of-care (PoC) devices like microfluidic Lab-on-Chip (LoC) cartridges can be challenging as LoC systems show significantly different thermal properties than qPCR cyclers. We demonstrate how an adequate thermal model of the specific LoC system can help us to identify a suitable thermal profile, even for complex HeavyMethyl qPCRs, with reduced experimental effort. Using a simulation-based approach, we demonstrate a proof-of-principle for the successful LoC transfer of colorectal /-qPCR from Epi Procolon® colorectal carcinoma test, by avoidance of oligonucleotide interactions.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36506005', 'doi' => '10.1063/5.0108374', 'modified' => '2023-03-28 09:15:30', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 19 => array( 'id' => '4575', 'name' => 'Intranasal administration of Acinetobacter lwoffii in a murine model ofasthma induces IL-6-mediated protection associated with cecal microbiotachanges.', 'authors' => 'Alashkar A. B. et al.', 'description' => '<p>BACKGROUND: Early-life exposure to certain environmental bacteria including Acinetobacter lwoffii (AL) has been implicated in protection from chronic inflammatory diseases including asthma later in life. However, the underlying mechanisms at the immune-microbe interface remain largely unknown. METHODS: The effects of repeated intranasal AL exposure on local and systemic innate immune responses were investigated in wild-type and Il6 , Il10 , and Il17 mice exposed to ovalbumin-induced allergic airway inflammation. Those investigations were expanded by microbiome analyses. To assess for AL-associated changes in gene expression, the picture arising from animal data was supplemented by in vitro experiments of macrophage and T-cell responses, yielding expression and epigenetic data. RESULTS: The asthma preventive effect of AL was confirmed in the lung. Repeated intranasal AL administration triggered a proinflammatory immune response particularly characterized by elevated levels of IL-6, and consequently, IL-6 induced IL-10 production in CD4 T-cells. Both IL-6 and IL-10, but not IL-17, were required for asthma protection. AL had a profound impact on the gene regulatory landscape of CD4 T-cells which could be largely recapitulated by recombinant IL-6. AL administration also induced marked changes in the gastrointestinal microbiome but not in the lung microbiome. By comparing the effects on the microbiota according to mouse genotype and AL-treatment status, we have identified microbial taxa that were associated with either disease protection or activity. CONCLUSION: These experiments provide a novel mechanism of Acinetobacter lwoffii-induced asthma protection operating through IL-6-mediated epigenetic activation of IL-10 production and with associated effects on the intestinal microbiome.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36458896', 'doi' => '10.1111/all.15606', 'modified' => '2023-04-11 10:23:07', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 20 => array( 'id' => '4574', 'name' => 'Trichoderma root colonization triggers epigenetic changes in jasmonic andsalicylic acid pathway-related genes.', 'authors' => 'Agostini R. B. et al.', 'description' => '<p>Beneficial interactions between plant-roots and Trichoderma spp. lead to a local and systemic enhancement of the plant immune system through a mechanism known as priming of defenses. In recent reports, we outlined a repertoire of genes and proteins differentially regulated in distant tissues of maize plants previously inoculated with Trichoderma atroviride. To further investigate the mechanisms involved in the systemic activation of plant responses, we continued evaluating the regulatory aspects of a selected group of genes when priming is triggered in maize plants. We conducted a time-course expression experiment from the beginning of the interaction between T. atroviride and maize roots, along plant vegetative growth and during Colletotrichum graminicola leaf infection. In addition to gene expression studies, the levels of jasmonic and salicylic acid were determined in the same samples for a comprehensive understanding of the gene expression results. Lastly, chromatin structure and modification assays were designed to evaluate the role of epigenetic marks during the long-lasting activation of the primed state of maize plants. The overall analysis of the results allowed us to shed some light on the interplay between the phytohormones and epigenetic regulatory events in the systemic and long-lasting regulation of maize plant defenses after Trichoderma inoculation.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36575905', 'doi' => '10.1093/jxb/erac518', 'modified' => '2023-04-14 09:08:14', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 21 => array( 'id' => '4474', 'name' => 'DNA sequence and chromatin modifiers cooperate to confer epigeneticbistability at imprinting control regions.', 'authors' => 'Butz S. et al.', 'description' => '<p>Genomic imprinting is regulated by parental-specific DNA methylation of imprinting control regions (ICRs). Despite an identical DNA sequence, ICRs can exist in two distinct epigenetic states that are memorized throughout unlimited cell divisions and reset during germline formation. Here, we systematically study the genetic and epigenetic determinants of this epigenetic bistability. By iterative integration of ICRs and related DNA sequences to an ectopic location in the mouse genome, we first identify the DNA sequence features required for maintenance of epigenetic states in embryonic stem cells. The autonomous regulatory properties of ICRs further enabled us to create DNA-methylation-sensitive reporters and to screen for key components involved in regulating their epigenetic memory. Besides DNMT1, UHRF1 and ZFP57, we identify factors that prevent switching from methylated to unmethylated states and show that two of these candidates, ATF7IP and ZMYM2, are important for the stability of DNA and H3K9 methylation at ICRs in embryonic stem cells.</p>', 'date' => '2022-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36333500', 'doi' => '10.1038/s41588-022-01210-z', 'modified' => '2022-11-18 12:20:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 22 => array( 'id' => '4493', 'name' => 'Smc5/6 silences episomal transcription by a three-step function.', 'authors' => 'Abdul F. et al.', 'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36097294', 'doi' => '10.1038/s41594-022-00829-0', 'modified' => '2022-11-18 12:41:42', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 23 => array( 'id' => '4495', 'name' => 'Exploration of nuclear body-enhanced sumoylation reveals that PMLrepresses 2-cell features of embryonic stem cells.', 'authors' => 'Tessier S. et al.', 'description' => '<p>Membrane-less organelles are condensates formed by phase separation whose functions often remain enigmatic. Upon oxidative stress, PML scaffolds Nuclear Bodies (NBs) to regulate senescence or metabolic adaptation. PML NBs recruit many partner proteins, but the actual biochemical mechanism underlying their pleiotropic functions remains elusive. Similarly, PML role in embryonic stem cell (ESC) and retro-element biology is unsettled. Here we demonstrate that PML is essential for oxidative stress-driven partner SUMO2/3 conjugation in mouse ESCs (mESCs) or leukemia, a process often followed by their poly-ubiquitination and degradation. Functionally, PML is required for stress responses in mESCs. Differential proteomics unravel the KAP1 complex as a PML NB-dependent SUMO2-target in arsenic-treated APL mice or mESCs. PML-driven KAP1 sumoylation enables activation of this key epigenetic repressor implicated in retro-element silencing. Accordingly, Pml mESCs re-express transposable elements and display 2-Cell-Like features, the latter enforced by PML-controlled SUMO2-conjugation of DPPA2. Thus, PML orchestrates mESC state by coordinating SUMO2-conjugation of different transcriptional regulators, raising new hypotheses about PML roles in cancer.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36175410', 'doi' => '10.1038/s41467-022-33147-6', 'modified' => '2022-11-21 10:21:48', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 24 => array( 'id' => '4502', 'name' => 'Loss of epigenetic regulation disrupts lineage integrity, inducesaberrant alveogenesis and promotes breast cancer.', 'authors' => 'Langille E. et al.', 'description' => '<p>Systematically investigating the scores of genes mutated in cancer and discerning disease drivers from inconsequential bystanders is a prerequisite for Precision Medicine but remains challenging. Here, we developed a somatic CRISPR/Cas9 mutagenesis screen to study 215 recurrent 'long-tail' breast cancer genes, which revealed epigenetic regulation as a major tumor suppressive mechanism. We report that components of the BAP1 and the COMPASS-like complexes, including KMT2C/D, KDM6A, BAP1 and ASXL1/2 ("EpiDrivers"), cooperate with PIK3CAH1047R to transform mouse and human breast epithelial cells. Mechanistically, we find that activation of PIK3CAH1047R and concomitant EpiDriver loss triggered an alveolar-like lineage conversion of basal mammary epithelial cells and accelerated formation of luminal-like tumors, suggesting a basal origin for luminal tumors. EpiDrivers mutations are found in ~39\% of human breast cancers and ~50\% of ductal-carcinoma-in-situ express casein suggesting that lineage infidelity and alveogenic mimicry may significantly contribute to early steps of breast cancer etiology.</p>', 'date' => '2022-09-01', 'pmid' => 'https://aacrjournals.org/cancerdiscovery/article-abstract/doi/10.1158/2159-8290.CD-21-0865/709222/Loss-of-epigenetic-regulation-disrupts-lineage?redirectedFrom=fulltext', 'doi' => '10.1158/2159-8290.CD-21-0865', 'modified' => '2022-11-21 10:34:24', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 25 => array( 'id' => '4449', 'name' => 'RAD51 protects human cells from transcription-replication conflicts.', 'authors' => 'Bhowmick R. et al.', 'description' => '<p>Oncogene activation during tumorigenesis promotes DNA replication stress (RS), which subsequently drives the formation of cancer-associated chromosomal rearrangements. Many episodes of physiological RS likely arise due to conflicts between the DNA replication and transcription machineries operating simultaneously at the same loci. One role of the RAD51 recombinase in human cells is to protect replication forks undergoing RS. Here, we have identified a key role for RAD51 in preventing transcription-replication conflicts (TRCs) from triggering replication fork breakage. The genomic regions most affected by RAD51 deficiency are characterized by being replicated and transcribed in early S-phase and show significant overlap with loci prone to cancer-associated amplification. Consistent with a role for RAD51 in protecting against transcription-replication conflicts, many of the adverse effects of RAD51 depletion are ameliorated by inhibiting early S-phase transcription. We propose a model whereby RAD51 suppresses fork breakage and subsequent inadvertent amplification of genomic loci prone to experiencing TRCs.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36002000', 'doi' => '10.1016/j.molcel.2022.07.010', 'modified' => '2022-10-14 16:44:54', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 26 => array( 'id' => '4511', 'name' => 'The Arabidopsis APOLO and human UPAT sequence-unrelated longnoncoding RNAs can modulate DNA and histone methylation machineries inplants.', 'authors' => 'Fonouni-Farde C. et al.', 'description' => '<p>BACKGROUND: RNA-DNA hybrid (R-loop)-associated long noncoding RNAs (lncRNAs), including the Arabidopsis lncRNA AUXIN-REGULATED PROMOTER LOOP (APOLO), are emerging as important regulators of three-dimensional chromatin conformation and gene transcriptional activity. RESULTS: Here, we show that in addition to the PRC1-component LIKE HETEROCHROMATIN PROTEIN 1 (LHP1), APOLO interacts with the methylcytosine-binding protein VARIANT IN METHYLATION 1 (VIM1), a conserved homolog of the mammalian DNA methylation regulator UBIQUITIN-LIKE CONTAINING PHD AND RING FINGER DOMAINS 1 (UHRF1). The APOLO-VIM1-LHP1 complex directly regulates the transcription of the auxin biosynthesis gene YUCCA2 by dynamically determining DNA methylation and H3K27me3 deposition over its promoter during the plant thermomorphogenic response. Strikingly, we demonstrate that the lncRNA UHRF1 Protein Associated Transcript (UPAT), a direct interactor of UHRF1 in humans, can be recognized by VIM1 and LHP1 in plant cells, despite the lack of sequence homology between UPAT and APOLO. In addition, we show that increased levels of APOLO or UPAT hamper VIM1 and LHP1 binding to YUCCA2 promoter and globally alter the Arabidopsis transcriptome in a similar manner. CONCLUSIONS: Collectively, our results uncover a new mechanism in which a plant lncRNA coordinates Polycomb action and DNA methylation through the interaction with VIM1, and indicates that evolutionary unrelated lncRNAs with potentially conserved structures may exert similar functions by interacting with homolog partners.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36038910', 'doi' => '10.1186/s13059-022-02750-7', 'modified' => '2022-11-21 10:43:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 27 => array( 'id' => '4552', 'name' => 'Prolonged FOS activity disrupts a global myogenic transcriptionalprogram by altering 3D chromatin architecture in primary muscleprogenitor cells.', 'authors' => 'Barutcu A Rasim et al.', 'description' => '<p>BACKGROUND: The AP-1 transcription factor, FBJ osteosarcoma oncogene (FOS), is induced in adult muscle satellite cells (SCs) within hours following muscle damage and is required for effective stem cell activation and muscle repair. However, why FOS is rapidly downregulated before SCs enter cell cycle as progenitor cells (i.e., transiently expressed) remains unclear. Further, whether boosting FOS levels in the proliferating progeny of SCs can enhance their myogenic properties needs further evaluation. METHODS: We established an inducible, FOS expression system to evaluate the impact of persistent FOS activity in muscle progenitor cells ex vivo. We performed various assays to measure cellular proliferation and differentiation, as well as uncover changes in RNA levels and three-dimensional (3D) chromatin interactions. RESULTS: Persistent FOS activity in primary muscle progenitor cells severely antagonizes their ability to differentiate and form myotubes within the first 2 weeks in culture. RNA-seq analysis revealed that ectopic FOS activity in muscle progenitor cells suppressed a global pro-myogenic transcriptional program, while activating a stress-induced, mitogen-activated protein kinase (MAPK) transcriptional signature. Additionally, we observed various FOS-dependent, chromosomal re-organization events in A/B compartments, topologically associated domains (TADs), and genomic loops near FOS-regulated genes. CONCLUSIONS: Our results suggest that elevated FOS activity in recently activated muscle progenitor cells perturbs cellular differentiation by altering the 3D chromosome organization near critical pro-myogenic genes. This work highlights the crucial importance of tightly controlling FOS expression in the muscle lineage and suggests that in states of chronic stress or disease, persistent FOS activity in muscle precursor cells may disrupt the muscle-forming process.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35971133', 'doi' => '10.1186/s13395-022-00303-x', 'modified' => '2022-11-24 10:11:55', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 28 => array( 'id' => '4452', 'name' => 'Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.', 'authors' => 'Schomann T. et al.', 'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>', 'date' => '2022-07-01', 'pmid' => 'https://doi.org/10.3390%2Fbiom12081048', 'doi' => '10.3390/biom12081048', 'modified' => '2022-10-21 09:33:25', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 29 => array( 'id' => '4446', 'name' => 'Variation in PU.1 binding and chromatin looping at neutrophil enhancersinfluences autoimmune disease susceptibility', 'authors' => 'Watt S. et al. ', 'description' => '<p>Neutrophils play fundamental roles in innate inflammatory response, shape adaptive immunity1, and have been identified as a potentially causal cell type underpinning genetic associations with immune system traits and diseases2,3 The majority of these variants are non-coding and the underlying mechanisms are not fully understood. Here, we profiled the binding of one of the principal myeloid transcriptional regulators, PU.1, in primary neutrophils across nearly a hundred volunteers, and elucidate the coordinated genetic effects of PU.1 binding variation, local chromatin state, promoter-enhancer interactions and gene expression. We show that PU.1 binding and the associated chain of molecular changes underlie genetically-driven differences in cell count and autoimmune disease susceptibility. Our results advance interpretation for genetic loci associated with neutrophil biology and immune disease.</p>', 'date' => '2022-05-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/620260v1.abstract', 'doi' => '10.1101/620260', 'modified' => '2022-10-14 16:39:03', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 30 => array( 'id' => '4217', 'name' => 'CREBBP/EP300 acetyltransferase inhibition disrupts FOXA1-bound enhancers to inhibit the proliferation of ER+ breast cancer cells.', 'authors' => 'Bommi-Reddy A. et al.', 'description' => '<p><span>Therapeutic targeting of the estrogen receptor (ER) is a clinically validated approach for estrogen receptor positive breast cancer (ER+ BC), but sustained response is limited by acquired resistance. Targeting the transcriptional coactivators required for estrogen receptor activity represents an alternative approach that is not subject to the same limitations as targeting estrogen receptor itself. In this report we demonstrate that the acetyltransferase activity of coactivator paralogs CREBBP/EP300 represents a promising therapeutic target in ER+ BC. Using the potent and selective inhibitor CPI-1612, we show that CREBBP/EP300 acetyltransferase inhibition potently suppresses in vitro and in vivo growth of breast cancer cell line models and acts in a manner orthogonal to directly targeting ER. CREBBP/EP300 acetyltransferase inhibition suppresses ER-dependent transcription by targeting lineage-specific enhancers defined by the pioneer transcription factor FOXA1. These results validate CREBBP/EP300 acetyltransferase activity as a viable target for clinical development in ER+ breast cancer.</span></p>', 'date' => '2022-03-30', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/35353838/', 'doi' => '10.1371/journal.pone.0262378', 'modified' => '2022-04-12 10:56:54', 'created' => '2022-04-12 10:56:54', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 31 => array( 'id' => '4407', 'name' => 'Transient regulation of focal adhesion via Tensin3 is required fornascent oligodendrocyte differentiation', 'authors' => 'Merour E. et al.', 'description' => '<p>The differentiation of oligodendroglia from oligodendrocyte precursor cells (OPCs) to complex and extensive myelinating oligodendrocytes (OLs) is a multistep process that involves largescale morphological changes with significant strain on the cytoskeleton. While key chromatin and transcriptional regulators of differentiation have been identified, their target genes responsible for the morphological changes occurring during OL myelination are still largely unknown. Here, we show that the regulator of focal adhesion, Tensin3 (Tns3), is a direct target gene of Olig2, Chd7, and Chd8, transcriptional regulators of OL differentiation. Tns3 is transiently upregulated and localized to cell processes of immature OLs, together with integrin-β1, a key mediator of survival at this transient stage. Constitutive Tns3 loss-of-function leads to reduced viability in mouse and humans, with surviving knockout mice still expressing Tns3 in oligodendroglia. Acute deletion of Tns3 in vivo, either in postnatal neural stem cells (NSCs) or in OPCs, leads to a two-fold reduction in OL numbers. We find that the transient upregulation of Tns3 is required to protect differentiating OPCs and immature OLs from cell death by preventing the upregulation of p53, a key regulator of apoptosis. Altogether, our findings reveal a specific time window during which transcriptional upregulation of Tns3 in immature OLs is required for OL differentiation likely by mediating integrin-β1 survival signaling to the actin cytoskeleton as OL undergo the large morphological changes required for their terminal differentiation.</p>', 'date' => '2022-02-01', 'pmid' => 'https://doi.org/10.1101%2F2022.02.25.481980', 'doi' => '10.1101/2022.02.25.481980', 'modified' => '2022-08-11 15:05:41', 'created' => '2022-08-11 12:14:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 32 => array( 'id' => '4238', 'name' => 'The long noncoding RNA H19 regulates tumor plasticity inneuroendocrine prostate cancer', 'authors' => 'Singh N. et al.', 'description' => '<p>Neuroendocrine (NE) prostate cancer (NEPC) is a lethal subtype of castration-resistant prostate cancer (PCa) arising either de novo or from transdifferentiated prostate adenocarcinoma following androgen deprivation therapy (ADT). Extensive computational analysis has identified a high degree of association between the long noncoding RNA (lncRNA) H19 and NEPC, with the longest isoform highly expressed in NEPC. H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown). It contributes to treatment resistance, with the knockdown of H19 re-sensitizing PCa to ADT. It is also essential for the proliferation and invasion of NEPC. H19 levels are negatively regulated by androgen signaling via androgen receptor (AR). When androgen is absent SOX2 levels increase, driving H19 transcription and facilitating transdifferentiation. H19 facilitates the PRC2 complex in regulating methylation changes at H3K27me3/H3K4me3 histone sites of AR-driven and NEPC-related genes. Additionally, this lncRNA induces alterations in genome-wide DNA methylation on CpG sites, further regulating genes associated with the NEPC phenotype. Our clinical data identify H19 as a candidate diagnostic marker and predictive marker of NEPC with elevated H19 levels associated with an increased probability of biochemical recurrence and metastatic disease in patients receiving ADT. Here we report H19 as an early upstream regulator of cell fate, plasticity, and treatment resistance in NEPC that can reverse/transform cells to a treatable form of PCa once therapeutically deactivated.</p>', 'date' => '2021-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34934057', 'doi' => '10.1038/s41467-021-26901-9', 'modified' => '2022-05-19 17:06:50', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 33 => array( 'id' => '4239', 'name' => 'Epromoters function as a hub to recruit key transcription factorsrequired for the inflammatory response', 'authors' => 'Santiago-Algarra D. et al. ', 'description' => '<p>Gene expression is controlled by the involvement of gene-proximal (promoters) and distal (enhancers) regulatory elements. Our previous results demonstrated that a subset of gene promoters, termed Epromoters, work as bona fide enhancers and regulate distal gene expression. Here, we hypothesized that Epromoters play a key role in the coordination of rapid gene induction during the inflammatory response. Using a high-throughput reporter assay we explored the function of Epromoters in response to type I interferon. We find that clusters of IFNa-induced genes are frequently associated with Epromoters and that these regulatory elements preferentially recruit the STAT1/2 and IRF transcription factors and distally regulate the activation of interferon-response genes. Consistently, we identified and validated the involvement of Epromoter-containing clusters in the regulation of LPS-stimulated macrophages. Our findings suggest that Epromoters function as a local hub recruiting the key TFs required for coordinated regulation of gene clusters during the inflammatory response.</p>', 'date' => '2021-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34795220', 'doi' => '10.1038/s41467-021-26861-0', 'modified' => '2022-05-19 17:10:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 34 => array( 'id' => '4231', 'name' => 'Differential contribution to gene expression prediction of histonemodifications at enhancers or promoters.', 'authors' => 'González-Ramírez M. et al.', 'description' => '<p>The ChIP-seq signal of histone modifications at promoters is a good predictor of gene expression in different cellular contexts, but whether this is also true at enhancers is not clear. To address this issue, we develop quantitative models to characterize the relationship of gene expression with histone modifications at enhancers or promoters. We use embryonic stem cells (ESCs), which contain a full spectrum of active and repressed (poised) enhancers, to train predictive models. As many poised enhancers in ESCs switch towards an active state during differentiation, predictive models can also be trained on poised enhancers throughout differentiation and in development. Remarkably, we determine that histone modifications at enhancers, as well as promoters, are predictive of gene expression in ESCs and throughout differentiation and development. Importantly, we demonstrate that their contribution to the predictive models varies depending on their location in enhancers or promoters. Moreover, we use a local regression (LOESS) to normalize sequencing data from different sources, which allows us to apply predictive models trained in a specific cellular context to a different one. We conclude that the relationship between gene expression and histone modifications at enhancers is universal and different from promoters. Our study provides new insight into how histone modifications relate to gene expression based on their location in enhancers or promoters.</p>', 'date' => '2021-09-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473698/', 'doi' => '10.1371/journal.pcbi.1009368', 'modified' => '2022-05-19 16:50:59', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 35 => array( 'id' => '4315', 'name' => 'Atg7 deficiency in microglia drives an altered transcriptomic profileassociated with an impaired neuroinflammatory response', 'authors' => 'Friess L. et al.', 'description' => '<p>Microglia, resident immunocompetent cells of the central nervous system, can display a range of reaction states and thereby exhibit distinct biological functions across development, adulthood and under disease conditions. Distinct gene expression profiles are reported to define each of these microglial reaction states. Hence, the identification of modulators of selective microglial transcriptomic signature, which have the potential to regulate unique microglial function has gained interest. Here, we report the identification of ATG7 (Autophagy-related 7) as a selective modulator of an NF-κB-dependent transcriptional program controlling the pro-inflammatory response of microglia. We also uncover that microglial Atg7-deficiency was associated with reduced microglia-mediated neurotoxicity, and thus a loss of biological function associated with the pro-inflammatory microglial reactive state. Further, we show that Atg7-deficiency in microglia did not impact on their ability to respond to alternative stimulus, such as one driving them towards an anti-inflammatory/tumor supportive phenotype. The identification of distinct regulators, such as Atg7, controlling specific microglial transcriptional programs could lead to developing novel therapeutic strategies aiming to manipulate selected microglial phenotypes, instead of the whole microglial population with is associated with several pitfalls. Supplementary Information The online version contains supplementary material available at 10.1186/s13041-021-00794-7.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34082793', 'doi' => '10.1186/s13041-021-00794-7', 'modified' => '2022-08-02 16:47:13', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 36 => array( 'id' => '4349', 'name' => 'Lasp1 regulates adherens junction dynamics and fibroblast transformationin destructive arthritis', 'authors' => 'Beckmann D. et al.', 'description' => '<p>The LIM and SH3 domain protein 1 (Lasp1) was originally cloned from metastatic breast cancer and characterised as an adaptor molecule associated with tumourigenesis and cancer cell invasion. However, the regulation of Lasp1 and its function in the aggressive transformation of cells is unclear. Here we use integrative epigenomic profiling of invasive fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA) and from mouse models of the disease, to identify Lasp1 as an epigenomically co-modified region in chronic inflammatory arthritis and a functionally important binding partner of the Cadherin-11/β-Catenin complex in zipper-like cell-to-cell contacts. In vitro, loss or blocking of Lasp1 alters pathological tissue formation, migratory behaviour and platelet-derived growth factor response of arthritic FLS. In arthritic human TNF transgenic mice, deletion of Lasp1 reduces arthritic joint destruction. Therefore, we show a function of Lasp1 in cellular junction formation and inflammatory tissue remodelling and identify Lasp1 as a potential target for treating inflammatory joint disorders associated with aggressive cellular transformation.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34131132', 'doi' => '10.1038/s41467-021-23706-8', 'modified' => '2022-08-03 17:02:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 37 => array( 'id' => '4136', 'name' => 'The lncRNA and the transcription factor WRKY42 target common cell wallEXTENSIN encoding genes to trigger root hair cell elongation.', 'authors' => 'Pacheco, J. M. et al.', 'description' => '<p>Plant long noncoding RNAs (lncRNAs) are key chromatin dynamics regulators, directing the transcriptional programs driving a wide variety of developmental outputs. Recently, we uncovered how the lncRNA () directly recognizes the locus encoding the root hair (RH) master regulator () modulating its transcriptional activation and leading to low temperature-induced RH elongation. We further demonstrated that interacts with the transcription factor WRKY42 in a novel ribonucleoprotein complex shaping epigenetic environment and integrating signals governing RH growth and development. In this work, we expand this model showing that is able to bind and positively control the expression of several cell wall EXTENSIN (EXT) encoding genes, including , a key regulator for RH growth. Interestingly, emerged as a novel common target of and WRKY42. Furthermore, we showed that the ROS homeostasis-related gene is deregulated upon overexpression, likely through the RHD6-RSL4 pathway, and that is required for low temperature-dependent enhancement of RH growth. Collectively, our results uncover an intricate regulatory network involving the /WRKY42 hub in the control of master and effector genes during RH development.</p>', 'date' => '2021-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33944666', 'doi' => '10.1080/15592324.2021.1920191', 'modified' => '2021-12-13 09:06:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 38 => array( 'id' => '4143', 'name' => 'Placental uptake and metabolism of 25(OH)Vitamin D determines itsactivity within the fetoplacental unit', 'authors' => 'Ashley, B. et al.', 'description' => '<p>Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes, but the underlying mechanisms have not been elucidated. Using physiological human placental perfusion approaches and intact villous explants we demonstrate a role for the placenta in regulating the relationships between maternal 25(OH)D concentrations and fetal physiology. Here, we demonstrate active placental uptake of 25(OH)D3 by endocytosis and placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the fetal and maternal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than solely the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer, including transcriptional activation and inflammatory responses. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta; with widespread effects on the placenta itself. These data show complex and synergistic interplay between vitamin D and the placenta, and inform possible interventions to optimise placental function to better support fetal growth and the maternal adaptations to pregnancy.</p>', 'date' => '2021-05-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.01.431439', 'doi' => '10.1101/2021.03.01.431439', 'modified' => '2021-12-13 09:29:25', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 39 => array( 'id' => '4147', 'name' => 'Waves of sumoylation support transcription dynamics during adipocytedifferentiation', 'authors' => 'Zhao, X. et al.', 'description' => '<p>Tight control of gene expression networks required for adipose tissue formation and plasticity is essential for adaptation to energy needs and environmental cues. However, little is known about the mechanisms that orchestrate the dramatic transcriptional changes leading to adipocyte differentiation. We investigated the regulation of nascent transcription by the sumoylation pathway during adipocyte differentiation using SLAMseq and ChIPseq. We discovered that the sumoylation pathway has a dual function in differentiation; it supports the initial downregulation of pre-adipocyte-specific genes, while it promotes the establishment of the mature adipocyte transcriptional program. By characterizing sumoylome dynamics in differentiating adipocytes by mass spectrometry, we found that sumoylation of specific transcription factors like Pparγ/RXR and their co-factors is associated with the transcription of adipogenic genes. Our data demonstrate that the sumoylation pathway coordinates the rewiring of transcriptional networks required for formation of functional adipocytes. This study also provides an in-depth resource of gene transcription dynamics, SUMO-regulated genes and sumoylation sites during adipogenesis.</p>', 'date' => '2021-04-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.20.432084', 'doi' => '10.1101/2021.02.20.432084', 'modified' => '2021-12-14 09:23:28', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 40 => array( 'id' => '4171', 'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.', 'authors' => 'Ryan, Genevieve E. et al.', 'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse LβT2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733', 'doi' => '10.1016/j.mce.2021.111286', 'modified' => '2021-12-21 15:57:35', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 41 => array( 'id' => '4181', 'name' => 'Genetic perturbation of PU.1 binding and chromatin looping at neutrophilenhancers associates with autoimmune disease.', 'authors' => 'Watt, Stephen et al.', 'description' => '<p>Neutrophils play fundamental roles in innate immune response, shape adaptive immunity, and are a potentially causal cell type underpinning genetic associations with immune system traits and diseases. Here, we profile the binding of myeloid master regulator PU.1 in primary neutrophils across nearly a hundred volunteers. We show that variants associated with differential PU.1 binding underlie genetically-driven differences in cell count and susceptibility to autoimmune and inflammatory diseases. We integrate these results with other multi-individual genomic readouts, revealing coordinated effects of PU.1 binding variants on the local chromatin state, enhancer-promoter contacts and downstream gene expression, and providing a functional interpretation for 27 genes underlying immune traits. Collectively, these results demonstrate the functional role of PU.1 and its target enhancers in neutrophil transcriptional control and immune disease susceptibility.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863903', 'doi' => '10.1038/s41467-021-22548-8', 'modified' => '2021-12-21 16:50:30', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 42 => array( 'id' => '4126', 'name' => 'Fra-1 regulates its target genes via binding to remote enhancers withoutexerting major control on chromatin architecture in triple negative breastcancers.', 'authors' => 'Bejjani, Fabienne and Tolza, Claire and Boulanger, Mathias and Downes,Damien and Romero, Raphaël and Maqbool, Muhammad Ahmad and Zine ElAabidine, Amal and Andrau, Jean-Christophe and Lebre, Sophie and Brehelin,Laurent and Parrinello, Hughes and Rohmer,', 'description' => '<p>The ubiquitous family of dimeric transcription factors AP-1 is made up of Fos and Jun family proteins. It has long been thought to operate principally at gene promoters and how it controls transcription is still ill-understood. The Fos family protein Fra-1 is overexpressed in triple negative breast cancers (TNBCs) where it contributes to tumor aggressiveness. To address its transcriptional actions in TNBCs, we combined transcriptomics, ChIP-seqs, machine learning and NG Capture-C. Additionally, we studied its Fos family kin Fra-2 also expressed in TNBCs, albeit much less. Consistently with their pleiotropic effects, Fra-1 and Fra-2 up- and downregulate individually, together or redundantly many genes associated with a wide range of biological processes. Target gene regulation is principally due to binding of Fra-1 and Fra-2 at regulatory elements located distantly from cognate promoters where Fra-1 modulates the recruitment of the transcriptional co-regulator p300/CBP and where differences in AP-1 variant motif recognition can underlie preferential Fra-1- or Fra-2 bindings. Our work also shows no major role for Fra-1 in chromatin architecture control at target gene loci, but suggests collaboration between Fra-1-bound and -unbound enhancers within chromatin hubs sometimes including promoters for other Fra-1-regulated genes. Our work impacts our view of AP-1.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33533919', 'doi' => '10.1093/nar/gkab053', 'modified' => '2021-12-07 10:09:23', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 43 => array( 'id' => '4139', 'name' => 'Cell-specific alterations inPitx1regulatory landscape activation caused bythe loss of a single enhancer', 'authors' => 'Rouco, R. et al.', 'description' => '<p>Most developmental genes rely on multiple transcriptional enhancers for their accurate expression during embryogenesis. Because enhancers may have partially redundant activities, the loss of one of them often leads to a partial loss of gene expression and concurrent moderate phenotypic outcome, if any. While such a phenomenon has been observed in many instances, the nature of the underlying mechanisms remains elusive. We used the Pitx1 testbed locus to characterize in detail the regulatory and cellular identity alterations following the deletion in vivo of one of its enhancers (Pen), which normally accounts for 30 percent of Pitx1 expression in hindlimb buds. By combining single cell transcriptomics and a novel in embryo cell tracing approach, we observed that this global decrease in Pitx1 expression results from both an increase in the number of non- or low-expressing cells, and a decrease in the number of high-expressing cells. We found that the over-representation of Pitx1 non/low-expressing cells originates from a failure of the Pitx1 locus to coordinate enhancer activities and 3D chromatin changes. The resulting increase in Pitx1 non/low-expressing cells eventually affects the proximal limb more severely than the distal limb, leading to a clubfoot phenotype likely produced through a localized heterochrony and concurrent loss of irregular connective tissue. This data suggests that, in some cases, redundant enhancers may be used to locally enforce a robust activation of their host regulatory landscapes.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.10.434611', 'doi' => '10.1101/2021.03.10.434611', 'modified' => '2021-12-13 09:18:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 44 => array( 'id' => '4141', 'name' => 'Transgenic mice for in vivo epigenome editing with CRISPR-based systems', 'authors' => 'Gemberling, M. et al.', 'description' => '<p>The discovery, characterization, and adaptation of the RNA-guided clustered regularly interspersed short palindromic repeat (CRISPR)-Cas9 system has greatly increased the ease with which genome and epigenome editing can be performed. Fusion of chromatin-modifying domains to the nuclease-deactivated form of Cas9 (dCas9) has enabled targeted gene activation or repression in both cultured cells and in vivo in animal models. However, delivery of the large dCas9 fusion proteins to target cell types and tissues is an obstacle to widespread adoption of these tools for in vivo studies. Here we describe the generation and validation of two conditional transgenic mouse lines for targeted gene regulation, Rosa26:LSL-dCas9-p300 for gene activation and Rosa26:LSL-dCas9-KRAB for gene repression. Using the dCas9p300 and dCas9KRAB transgenic mice we demonstrate activation or repression of genes in both the brain and liver in vivo, and T cells and fibroblasts ex vivo. We show gene regulation and targeted epigenetic modification with gRNAs targeting either transcriptional start sites (TSS) or distal enhancer elements, as well as corresponding changes to downstream phenotypes. These mouse lines are convenient and valuable tools for facile, temporally controlled, and tissue-restricted epigenome editing and manipulation of gene expression in vivo.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.08.434430', 'doi' => '10.1101/2021.03.08.434430', 'modified' => '2021-12-13 09:23:10', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 45 => array( 'id' => '4163', 'name' => 'Transcriptional programming drives Ibrutinib-resistance evolution in mantlecell lymphoma.', 'authors' => 'Zhao, Xiaohong et al.', 'description' => '<p>Ibrutinib, a bruton's tyrosine kinase (BTK) inhibitor, provokes robust clinical responses in aggressive mantle cell lymphoma (MCL), yet many patients relapse with lethal Ibrutinib-resistant (IR) disease. Here, using genomic, chemical proteomic, and drug screen profiling, we report that enhancer remodeling-mediated transcriptional activation and adaptive signaling changes drive the aggressive phenotypes of IR. Accordingly, IR MCL cells are vulnerable to inhibitors of the transcriptional machinery and especially so to inhibitors of cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the positive transcription elongation factor b (P-TEFb) of RNA polymerase II (RNAPII). Further, CDK9 inhibition disables reprogrammed signaling circuits and prevents the emergence of IR in MCL. Finally, and importantly, we find that a robust and facile ex vivo image-based functional drug screening platform can predict clinical therapeutic responses of IR MCL and identify vulnerabilities that can be targeted to disable the evolution of IR.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33730585', 'doi' => '10.1016/j.celrep.2021.108870', 'modified' => '2021-12-21 15:28:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 46 => array( 'id' => '4119', 'name' => 'Coordinated changes in gene expression, H1 variant distribution and genome3D conformation in response to H1 depletion', 'authors' => 'Serna-Pujol, Nuria and Salinas-Pena, Monica and Mugianesi, Francesca and LeDily, François and Marti-Renom, Marc A. and Jordan, Albert', 'description' => '<p>Up to seven members of the histone H1 family may contribute to chromatin compaction and its regulation in human somatic cells. In breast cancer cells, knock-down of multiple H1 variants deregulates many genes, promotes the appearance of genome-wide accessibility sites and triggers an interferon response via activation of heterochromatic repeats. However, how these changes in the expression profile relate to the re-distribution of H1 variants as well as to genome conformational changes have not been yet studied. Here, we combined ChIP-seq of five endogenous H1 variants with Chromosome Conformation Capture analysis in wild-type and H1 knock-down T47D cells. The results indicate that H1 variants coexist in the genome in two large groups depending on the local DNA GC content and that their distribution is robust with respect to multiple H1 depletion. Despite the small changes in H1 variants distribution, knock-down of H1 translated into more isolated but de-compacted chromatin structures at the scale of Topologically Associating Domains or TADs. Such changes in TAD structure correlated with a coordinated gene expression response of their resident genes. This is the first report describing simultaneous profiling of five endogenous H1 variants within a cell line and giving functional evidence of genome topology alterations upon H1 depletion in human cancer cells.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.12.429879', 'doi' => '10.1101/2021.02.12.429879', 'modified' => '2021-12-07 09:43:11', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 47 => array( 'id' => '4144', 'name' => 'REPROGRAMMING CBX8-PRC1 FUNCTION WITH A POSITIVE ALLOSTERICMODULATOR', 'authors' => 'Suh, J. L. et al.', 'description' => '<p>Canonical targeting of Polycomb Repressive Complex 1 (PRC1) to repress developmental genes is mediated by cell type-specific, paralogous chromobox (CBX) proteins (CBX2, 4, 6, 7 and 8). Based on their central role in silencing and their misregulation associated with human disease including cancer, CBX proteins are attractive targets for small molecule chemical probe development. Here, we have used a quantitative and target-specific cellular assay to discover a potent positive allosteric modulator (PAM) of CBX8. The PAM activity of UNC7040 antagonizes H3K27me3 binding by CBX8 while increasing interactions with nucleic acids and participation in variant PRC1. We show that treatment with UNC7040 leads to efficient PRC1 chromatin eviction, loss of silencing and reduced proliferation across different cancer cell lines. Our discovery and characterization of UNC7040 not only revealed the most cellularly potent CBX8-specific chemical probe to date, but also corroborates a mechanism of polycomb regulation by non-histone lysine methylated interaction partners.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.23.432388', 'doi' => '10.1101/2021.02.23.432388', 'modified' => '2021-12-13 09:35:04', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 48 => array( 'id' => '4145', 'name' => 'Germline activity of the heat shock factor HSF-1 programs theinsulin-receptor daf-2 in C. elegans', 'authors' => 'Das, S. et al.', 'description' => '<p>The mechanisms by which maternal stress alters offspring phenotypes remain poorly understood. Here we report that the heat shock transcription factor HSF-1, activated in the C. elegans maternal germline upon stress, epigenetically programs the insulin-like receptor daf-2 by increasing repressive H3K9me2 levels throughout the daf-2 gene. This increase occurs by the recruitment of the C. elegans SETDB1 homolog MET-2 by HSF-1. Increased H3K9me2 levels at daf-2 persist in offspring to downregulate daf-2, activate the C. elegans FOXO ortholog DAF-16 and enhance offspring stress resilience. Thus, HSF-1 activity in the mother promotes the early life programming of the insulin/IGF-1 signaling (IIS) pathway and determines the strategy of stress resilience in progeny.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.22.432344', 'doi' => '10.1101/2021.02.22.432344', 'modified' => '2021-12-14 09:13:54', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 49 => array( 'id' => '4151', 'name' => 'The epigenetic landscape in purified myonuclei from fast and slow muscles', 'authors' => 'Bengtsen, M. et al.', 'description' => '<p>Muscle cells have different phenotypes adapted to different usage and can be grossly divided into fast/glycolytic and slow/oxidative types. While most muscles contain a mixture of such fiber types, we aimed at providing a genome-wide analysis of chromatin environment by ChIP-Seq in two muscle extremes, the almost completely fast/glycolytic extensor digitorum longus (EDL) and slow/oxidative soleus muscles. Muscle is a heterogeneous tissue where less than 60\% of the nuclei are inside muscle fibers. Since cellular homogeneity is critical in epigenome-wide association studies we devised a new method for purifying skeletal muscle nuclei from whole tissue based on the nuclear envelope protein Pericentriolar material 1 (PCM1) being a specific marker for myonuclei. Using antibody labeling and a magnetic-assisted sorting approach we were able to sort out myonuclei with 95\% purity. The sorting eliminated influence from other cell types in the tissue and improved the myo-specific signal. A genome-wide comparison of the epigenetic landscape in EDL and soleus reflected the functional properties of the two muscles each with a distinct regulatory program involving distal enhancers, including a glycolytic super-enhancer in the EDL. The two muscles are also regulated by different sets of transcription factors; e.g. in soleus binding sites for MEF2C, NFATC2 and PPARA were enriched, while in EDL MYOD1 and SOX1 binding sites were found to be overrepresented. In addition, novel factors for muscle regulation such as MAF, ZFX and ZBTB14 were identified.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.04.429545', 'doi' => '10.1101/2021.02.04.429545', 'modified' => '2021-12-14 09:40:02', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 50 => array( 'id' => '4166', 'name' => 'The glucocorticoid receptor recruits the COMPASS complex to regulateinflammatory transcription at macrophage enhancers.', 'authors' => 'Greulich, Franziska et al.', 'description' => '<p>Glucocorticoids (GCs) are effective anti-inflammatory drugs; yet, their mechanisms of action are poorly understood. GCs bind to the glucocorticoid receptor (GR), a ligand-gated transcription factor controlling gene expression in numerous cell types. Here, we characterize GR's protein interactome and find the SETD1A (SET domain containing 1A)/COMPASS (complex of proteins associated with Set1) histone H3 lysine 4 (H3K4) methyltransferase complex highly enriched in activated mouse macrophages. We show that SETD1A/COMPASS is recruited by GR to specific cis-regulatory elements, coinciding with H3K4 methylation dynamics at subsets of sites, upon treatment with lipopolysaccharide (LPS) and GCs. By chromatin immunoprecipitation sequencing (ChIP-seq) and RNA-seq, we identify subsets of GR target loci that display SETD1A occupancy, H3K4 mono-, di-, or tri-methylation patterns, and transcriptional changes. However, our data on methylation status and COMPASS recruitment suggest that SETD1A has additional transcriptional functions. Setd1a loss-of-function studies reveal that SETD1A/COMPASS is required for GR-controlled transcription of subsets of macrophage target genes. We demonstrate that the SETD1A/COMPASS complex cooperates with GR to mediate anti-inflammatory effects.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33567280', 'doi' => '10.1016/j.celrep.2021.108742', 'modified' => '2021-12-21 15:42:49', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 51 => array( 'id' => '4185', 'name' => 'A distinct metabolic response characterizes sensitivity to EZH2inhibition in multiple myeloma.', 'authors' => 'Nylund P. et al.', 'description' => '<p>Multiple myeloma (MM) is a heterogeneous haematological disease that remains clinically challenging. Increased activity of the epigenetic silencer EZH2 is a common feature in patients with poor prognosis. Previous findings have demonstrated that metabolic profiles can be sensitive markers for response to treatment in cancer. While EZH2 inhibition (EZH2i) has proven efficient in inducing cell death in a number of human MM cell lines, we hereby identified a subset of cell lines that despite a global loss of H3K27me3, remains viable after EZH2i. By coupling liquid chromatography-mass spectrometry with gene and miRNA expression profiling, we found that sensitivity to EZH2i correlated with distinct metabolic signatures resulting from a dysregulation of genes involved in methionine cycling. Specifically, EZH2i resulted in a miRNA-mediated downregulation of methionine cycling-associated genes in responsive cells. This induced metabolite accumulation and DNA damage, leading to G2 arrest and apoptosis. Altogether, we unveiled that sensitivity to EZH2i in human MM cell lines is associated with a specific metabolic and gene expression profile post-treatment.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33579905', 'doi' => '10.1038/s41419-021-03447-8', 'modified' => '2022-01-05 14:59:39', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 52 => array( 'id' => '4108', 'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma', 'authors' => 'Laubscher et. al.', 'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that </span><em>SMARCA4</em><span><span> </span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span> </span></span><em>de novo</em><span><span> </span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>', 'date' => '2021-01-07', 'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1', 'doi' => ' 10.21203/rs.3.rs-131009/v1', 'modified' => '2021-07-07 11:52:23', 'created' => '2021-07-07 06:38:34', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 53 => array( 'id' => '4098', 'name' => 'A Tumor Suppressor Enhancer of PTEN in T-cell development and leukemia', 'authors' => 'L. Tottone at al.', 'description' => '<p>Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss of expression of PTEN is associated with the pathogenesis of various cancers, including T-cell leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts with the <em>PTEN</em> promoter in multiple hematopoietic populations, including T-cells, and acts as a hub of relevant transcription factors in T-ALL. Consistently, loss of PE leads to reduced <em>PTEN</em> levels in T-ALL cells. Moreover, PE-null mice show reduced <em>Pten</em> levels in thymocytes and accelerated development of NOTCH1-induced T-ALL. Furthermore, secondary loss of PE in established leukemias leads to accelerated progression and a gene expression signature driven by <em>Pten</em> loss. Finally, we uncovered recurrent deletions encompassing PE in T-ALL, which are associated with decreased <em>PTEN</em> levels. Altogether, our results identify PE as the first long-range tumor suppressor enhancer directly implicated in cancer.</p>', 'date' => '2021-01-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33458694/', 'doi' => '10.1158/2643-3230.BCD-20-0201 ', 'modified' => '2021-05-04 09:51:10', 'created' => '2021-05-04 09:51:10', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 54 => array( 'id' => '4157', 'name' => 'Stronger induction of trained immunity by mucosal BCG or MTBVAC vaccination compared to standard intradermal vaccination.', 'authors' => 'Vierboom, M.P.M. et al. ', 'description' => '<p>BCG vaccination can strengthen protection against pathogens through the induction of epigenetic and metabolic reprogramming of innate immune cells, a process called trained immunity. We and others recently demonstrated that mucosal or intravenous BCG better protects rhesus macaques from infection and TB disease than standard intradermal vaccination, correlating with local adaptive immune signatures. In line with prior mouse data, here, we show in rhesus macaques that intravenous BCG enhances innate cytokine production associated with changes in H3K27 acetylation typical of trained immunity. Alternative delivery of BCG does not alter the cytokine production of unfractionated bronchial lavage cells. However, mucosal but not intradermal vaccination, either with BCG or the -derived candidate MTBVAC, enhances innate cytokine production by blood- and bone marrow-derived monocytes associated with metabolic rewiring, typical of trained immunity. These results provide support to strategies for improving TB vaccination and, more broadly, modulating innate immunity via mucosal surfaces.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33521699', 'doi' => '10.1016/j.xcrm.2020.100185', 'modified' => '2021-12-16 10:50:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 55 => array( 'id' => '4193', 'name' => 'Postoperative abdominal sepsis induces selective and persistent changes inCTCF binding within the MHC-II region of human monocytes.', 'authors' => 'Siegler B. et al.', 'description' => '<p>BACKGROUND: Postoperative abdominal infections belong to the most common triggers of sepsis and septic shock in intensive care units worldwide. While monocytes play a central role in mediating the initial host response to infections, sepsis-induced immune dysregulation is characterized by a defective antigen presentation to T-cells via loss of Major Histocompatibility Complex Class II DR (HLA-DR) surface expression. Here, we hypothesized a sepsis-induced differential occupancy of the CCCTC-Binding Factor (CTCF), an architectural protein and superordinate regulator of transcription, inside the Major Histocompatibility Complex Class II (MHC-II) region in patients with postoperative sepsis, contributing to an altered monocytic transcriptional response during critical illness. RESULTS: Compared to a matched surgical control cohort, postoperative sepsis was associated with selective and enduring increase in CTCF binding within the MHC-II. In detail, increased CTCF binding was detected at four sites adjacent to classical HLA class II genes coding for proteins expressed on monocyte surface. Gene expression analysis revealed a sepsis-associated decreased transcription of (i) the classical HLA genes HLA-DRA, HLA-DRB1, HLA-DPA1 and HLA-DPB1 and (ii) the gene of the MHC-II master regulator, CIITA (Class II Major Histocompatibility Complex Transactivator). Increased CTCF binding persisted in all sepsis patients, while transcriptional recovery CIITA was exclusively found in long-term survivors. CONCLUSION: Our experiments demonstrate differential and persisting alterations of CTCF occupancy within the MHC-II, accompanied by selective changes in the expression of spatially related HLA class II genes, indicating an important role of CTCF in modulating the transcriptional response of immunocompromised human monocytes during critical illness.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33939725', 'doi' => '10.1371/journal.pone.0250818', 'modified' => '2022-01-06 14:22:15', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 56 => array( 'id' => '4204', 'name' => 'S-adenosyl-l-homocysteine hydrolase links methionine metabolism to thecircadian clock and chromatin remodeling.', 'authors' => 'Greco C. M. et al. ', 'description' => '<p>Circadian gene expression driven by transcription activators CLOCK and BMAL1 is intimately associated with dynamic chromatin remodeling. However, how cellular metabolism directs circadian chromatin remodeling is virtually unexplored. We report that the S-adenosylhomocysteine (SAH) hydrolyzing enzyme adenosylhomocysteinase (AHCY) cyclically associates to CLOCK-BMAL1 at chromatin sites and promotes circadian transcriptional activity. SAH is a potent feedback inhibitor of S-adenosylmethionine (SAM)-dependent methyltransferases, and timely hydrolysis of SAH by AHCY is critical to sustain methylation reactions. We show that AHCY is essential for cyclic H3K4 trimethylation, genome-wide recruitment of BMAL1 to chromatin, and subsequent circadian transcription. Depletion or targeted pharmacological inhibition of AHCY in mammalian cells markedly decreases the amplitude of circadian gene expression. In mice, pharmacological inhibition of AHCY in the hypothalamus alters circadian locomotor activity and rhythmic transcription within the suprachiasmatic nucleus. These results reveal a previously unappreciated connection between cellular metabolism, chromatin dynamics, and circadian regulation.</p>', 'date' => '2020-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33328229', 'doi' => '10.1126/sciadv.abc5629', 'modified' => '2022-01-06 14:59:48', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 57 => array( 'id' => '4040', 'name' => 'Genomic profiling of T-cell activation suggests increased sensitivity ofmemory T cells to CD28 costimulation.', 'authors' => 'Glinos, Dafni A and Soskic, Blagoje and Williams, Cayman and Kennedy, Alanand Jostins, Luke and Sansom, David M and Trynka, Gosia', 'description' => '<p>T-cell activation is a critical driver of immune responses. The CD28 costimulation is an essential regulator of CD4 T-cell responses, however, its relative importance in naive and memory T cells is not fully understood. Using different model systems, we observe that human memory T cells are more sensitive to CD28 costimulation than naive T cells. To deconvolute how the T-cell receptor (TCR) and CD28 orchestrate activation of human T cells, we stimulate cells using varying intensities of TCR and CD28 and profiled gene expression. We show that genes involved in cell cycle progression and division are CD28-driven in memory cells, but under TCR control in naive cells. We further demonstrate that T-helper differentiation and cytokine expression are controlled by CD28. Using chromatin accessibility profiling, we observe that AP1 transcriptional regulation is enriched when both TCR and CD28 are engaged, whereas open chromatin near CD28-sensitive genes is enriched for NF-kB motifs. Lastly, we show that CD28-sensitive genes are enriched in GWAS regions associated with immune diseases, implicating a role for CD28 in disease development. Our study provides important insights into the differential role of costimulation in naive and memory T-cell responses and disease susceptibility.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33223527', 'doi' => '10.1038/s41435-020-00118-0', 'modified' => '2021-02-19 12:08:04', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 58 => array( 'id' => '4060', 'name' => 'A genetic variant controls interferon-β gene expression in human myeloidcells by preventing C/EBP-β binding on a conserved enhancer.', 'authors' => 'Assouvie, Anaïs and Rotival, Maxime and Hamroune, Juliette and Busso,Didier and Romeo, Paul-Henri and Quintana-Murci, Lluis and Rousselet,Germain', 'description' => '<p>Interferon β (IFN-β) is a cytokine that induces a global antiviral proteome, and regulates the adaptive immune response to infections and tumors. Its effects strongly depend on its level and timing of expression. Therefore, the transcription of its coding gene IFNB1 is strictly controlled. We have previously shown that in mice, the TRIM33 protein restrains Ifnb1 transcription in activated myeloid cells through an upstream inhibitory sequence called ICE. Here, we show that the deregulation of Ifnb1 expression observed in murine Trim33-/- macrophages correlates with abnormal looping of both ICE and the Ifnb1 gene to a 100 kb downstream region overlapping the Ptplad2/Hacd4 gene. This region is a predicted myeloid super-enhancer in which we could characterize 3 myeloid-specific active enhancers, one of which (E5) increases the response of the Ifnb1 promoter to activation. In humans, the orthologous region contains several single nucleotide polymorphisms (SNPs) known to be associated with decreased expression of IFNB1 in activated monocytes, and loops to the IFNB1 gene. The strongest association is found for the rs12553564 SNP, located in the E5 orthologous region. The minor allele of rs12553564 disrupts a conserved C/EBP-β binding motif, prevents binding of C/EBP-β, and abolishes the activation-induced enhancer activity of E5. Altogether, these results establish a link between a genetic variant preventing binding of a transcription factor and a higher order phenotype, and suggest that the frequent minor allele (around 30\% worldwide) might be associated with phenotypes regulated by IFN-β expression in myeloid cells.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147208', 'doi' => '10.1371/journal.pgen.1009090', 'modified' => '2021-02-19 17:29:34', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 59 => array( 'id' => '4084', 'name' => 'BCG Vaccination Induces Long-Term Functional Reprogramming of HumanNeutrophils.', 'authors' => 'Moorlag, Simone J C F M and Rodriguez-Rosales, Yessica Alina and Gillard,Joshua and Fanucchi, Stephanie and Theunissen, Kate and Novakovic, Borisand de Bont, Cynthia M and Negishi, Yutaka and Fok, Ezio T and Kalafati,Lydia and Verginis, Panayotis and M', 'description' => '<p>The tuberculosis vaccine bacillus Calmette-Guérin (BCG) protects against some heterologous infections, probably via induction of non-specific innate immune memory in monocytes and natural killer (NK) cells, a process known as trained immunity. Recent studies have revealed that the induction of trained immunity is associated with a bias toward granulopoiesis in bone marrow hematopoietic progenitor cells, but it is unknown whether BCG vaccination also leads to functional reprogramming of mature neutrophils. Here, we show that BCG vaccination of healthy humans induces long-lasting changes in neutrophil phenotype, characterized by increased expression of activation markers and antimicrobial function. The enhanced function of human neutrophils persists for at least 3 months after vaccination and is associated with genome-wide epigenetic modifications in trimethylation at histone 3 lysine 4. Functional reprogramming of neutrophils by the induction of trained immunity might offer novel therapeutic strategies in clinical conditions that could benefit from modulation of neutrophil effector function.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33207187', 'doi' => '10.1016/j.celrep.2020.108387', 'modified' => '2021-03-15 17:07:29', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 60 => array( 'id' => '4086', 'name' => 'Macrophage Immune Memory Controls Endometriosis in Mice and Humans.', 'authors' => 'Jeljeli, Mohamed and Riccio, Luiza G C and Chouzenoux, Sandrine and Moresi,Fabiana and Toullec, Laurie and Doridot, Ludivine and Nicco, Carole andBourdon, Mathilde and Marcellin, Louis and Santulli, Pietro and Abrão,Mauricio S and Chapron, Charles and ', 'description' => '<p>Endometriosis is a frequent, chronic, inflammatory gynecological disease characterized by the presence of ectopic endometrial tissue causing pain and infertility. Macrophages have a central role in lesion establishment and maintenance by driving chronic inflammation and tissue remodeling. Macrophages can be reprogrammed to acquire memory-like characteristics after antigenic challenge to reinforce or inhibit a subsequent immune response, a phenomenon termed "trained immunity." Here, whereas bacille Calmette-Guérin (BCG) training enhances the lesion growth in a mice model of endometriosis, tolerization with repeated low doses of lipopolysaccharide (LPS) or adoptive transfer of LPS-tolerized macrophages elicits a suppressor effect. LPS-tolerized human macrophages mitigate the fibro-inflammatory phenotype of endometriotic cells in an interleukin-10 (IL-10)-dependent manner. A history of severe Gram-negative infection is associated with reduced infertility duration and alleviated symptoms, in contrast to patients with Gram-positive infection history. Thus, the manipulation of innate immune memory may be effective in dampening hyper-inflammatory conditions, opening the way to promising therapeutic approaches.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147452', 'doi' => '10.1016/j.celrep.2020.108325', 'modified' => '2021-03-15 17:14:08', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 61 => array( 'id' => '4050', 'name' => 'UTX/KDM6A suppresses AP-1 and a gliogenesis program during neuraldifferentiation of human pluripotent stem cells.', 'authors' => 'Xu, Beisi and Mulvey, Brett and Salie, Muneeb and Yang, Xiaoyang andMatsui, Yurika and Nityanandam, Anjana and Fan, Yiping and Peng, Jamy C', 'description' => '<p>BACKGROUND: UTX/KDM6A is known to interact and influence multiple different chromatin modifiers to promote an open chromatin environment to facilitate gene activation, but its molecular activities in developmental gene regulation remain unclear. RESULTS: We report that in human neural stem cells, UTX binding correlates with both promotion and suppression of gene expression. These activities enable UTX to modulate neural stem cell self-renewal, promote neurogenesis, and suppress gliogenesis. In neural stem cells, UTX has a less influence over histone H3 lysine 27 and lysine 4 methylation but more predominantly affects histone H3 lysine 27 acetylation and chromatin accessibility. Furthermore, UTX suppresses components of AP-1 and, in turn, a gliogenesis program. CONCLUSIONS: Our findings revealed that UTX coordinates dualistic gene regulation to govern neural stem cell properties and neurogenesis-gliogenesis switch.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32977832', 'doi' => '10.1186/s13072-020-00359-3', 'modified' => '2021-02-19 14:46:42', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 62 => array( 'id' => '4091', 'name' => 'Epigenetic regulation of the lineage specificity of primary human dermallymphatic and blood vascular endothelial cells.', 'authors' => 'Tacconi, Carlotta and He, Yuliang and Ducoli, Luca and Detmar, Michael', 'description' => '<p>Lymphatic and blood vascular endothelial cells (ECs) share several molecular and developmental features. However, these two cell types possess distinct phenotypic signatures, reflecting their different biological functions. Despite significant advances in elucidating how the specification of lymphatic and blood vascular ECs is regulated at the transcriptional level during development, the key molecular mechanisms governing their lineage identity under physiological or pathological conditions remain poorly understood. To explore the epigenomic signatures in the maintenance of EC lineage specificity, we compared the transcriptomic landscapes, histone composition (H3K4me3 and H3K27me3) and DNA methylomes of cultured matched human primary dermal lymphatic and blood vascular ECs. Our findings reveal that blood vascular lineage genes manifest a more 'repressed' histone composition in lymphatic ECs, whereas DNA methylation at promoters is less linked to the differential transcriptomes of lymphatic versus blood vascular ECs. Meta-analyses identified two transcriptional regulators, BCL6 and MEF2C, which potentially govern endothelial lineage specificity. Notably, the blood vascular endothelial lineage markers CD34, ESAM and FLT1 and the lymphatic endothelial lineage markers PROX1, PDPN and FLT4 exhibited highly differential epigenetic profiles and responded in distinct manners to epigenetic drug treatments. The perturbation of histone and DNA methylation selectively promoted the expression of blood vascular endothelial markers in lymphatic endothelial cells, but not vice versa. Overall, our study reveals that the fine regulation of lymphatic and blood vascular endothelial transcriptomes is maintained via several epigenetic mechanisms, which are crucial to the maintenance of endothelial cell identity.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32918672', 'doi' => '10.1007/s10456-020-09743-9', 'modified' => '2021-03-17 17:09:36', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 63 => array( 'id' => '4010', 'name' => 'Combined treatment with CBP and BET inhibitors reverses inadvertentactivation of detrimental super enhancer programs in DIPG cells.', 'authors' => 'Wiese, M and Hamdan, FH and Kubiak, K and Diederichs, C and Gielen, GHand Nussbaumer, G and Carcaboso, AM and Hulleman, E and Johnsen, SA andKramm, CM', 'description' => '<p>Diffuse intrinsic pontine gliomas (DIPG) are the most aggressive brain tumors in children with 5-year survival rates of only 2%. About 85% of all DIPG are characterized by a lysine-to-methionine substitution in histone 3, which leads to global H3K27 hypomethylation accompanied by H3K27 hyperacetylation. Hyperacetylation in DIPG favors the action of the Bromodomain and Extra-Terminal (BET) protein BRD4, and leads to the reprogramming of the enhancer landscape contributing to the activation of DIPG super enhancer-driven oncogenes. The activity of the acetyltransferase CREB-binding protein (CBP) is enhanced by BRD4 and associated with acetylation of nucleosomes at super enhancers (SE). In addition, CBP contributes to transcriptional activation through its function as a scaffold and protein bridge. Monotherapy with either a CBP (ICG-001) or BET inhibitor (JQ1) led to the reduction of tumor-related characteristics. Interestingly, combined treatment induced strong cytotoxic effects in H3.3K27M-mutated DIPG cell lines. RNA sequencing and chromatin immunoprecipitation revealed that these effects were caused by the inactivation of DIPG SE-controlled tumor-related genes. However, single treatment with ICG-001 or JQ1, respectively, led to activation of a subgroup of detrimental super enhancers. Combinatorial treatment reversed the inadvertent activation of these super enhancers and rescued the effect of ICG-001 and JQ1 single treatment on enhancer-driven oncogenes in H3K27M-mutated DIPG, but not in H3 wild-type pedHGG cells. In conclusion, combinatorial treatment with CBP and BET inhibitors is highly efficient in H3K27M-mutant DIPG due to reversal of inadvertent activation of detrimental SE programs in comparison with monotherapy.</p>', 'date' => '2020-08-21', 'pmid' => 'http://www.pubmed.gov/32826850', 'doi' => '10.1038/s41419-020-02800-7', 'modified' => '2020-12-18 13:25:09', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 64 => array( 'id' => '4028', 'name' => 'Methylation in pericytes after acute injury promotes chronic kidneydisease.', 'authors' => 'Chou, YH and Pan, SY and Shao, YH and Shih, HM and Wei, SY andLai, CF and Chiang, WC and Schrimpf, C and Yang, KC and Lai, LC andChen, YM and Chu, TS and Lin, SL', 'description' => '<p>The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury-induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-β1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD.</p>', 'date' => '2020-08-04', 'pmid' => 'http://www.pubmed.gov/32749240', 'doi' => '10.1172/JCI135773.', 'modified' => '2020-12-18 13:25:55', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 65 => array( 'id' => '4011', 'name' => 'Exploring the virulence gene interactome with CRISPR/dCas9 in the humanmalaria parasite.', 'authors' => 'Bryant, JM and Baumgarten, S and Dingli, F and Loew, D and Sinha, A andClaës, A and Preiser, PR and Dedon, PC and Scherf, A', 'description' => '<p>Mutually exclusive expression of the var multigene family is key to immune evasion and pathogenesis in Plasmodium falciparum, but few factors have been shown to play a direct role. We adapted a CRISPR-based proteomics approach to identify novel factors associated with var genes in their natural chromatin context. Catalytically inactive Cas9 ("dCas9") was targeted to var gene regulatory elements, immunoprecipitated, and analyzed with mass spectrometry. Known and novel factors were enriched including structural proteins, DNA helicases, and chromatin remodelers. Functional characterization of PfISWI, an evolutionarily divergent putative chromatin remodeler enriched at the var gene promoter, revealed a role in transcriptional activation. Proteomics of PfISWI identified several proteins enriched at the var gene promoter such as acetyl-CoA synthetase, a putative MORC protein, and an ApiAP2 transcription factor. These findings validate the CRISPR/dCas9 proteomics method and define a new var gene-associated chromatin complex. This study establishes a tool for targeted chromatin purification of unaltered genomic loci and identifies novel chromatin-associated factors potentially involved in transcriptional control and/or chromatin organization of virulence genes in the human malaria parasite.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32816370', 'doi' => 'https://dx.doi.org/10.15252%2Fmsb.20209569', 'modified' => '2020-12-18 13:26:33', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 66 => array( 'id' => '4019', 'name' => 'Targeted bisulfite sequencing for biomarker discovery.', 'authors' => 'Morselli, M and Farrell, C and Rubbi, L and Fehling, HL and Henkhaus, Rand Pellegrini, M', 'description' => '<p>Cytosine methylation is one of the best studied epigenetic modifications. In mammals, DNA methylation patterns vary among cells and is mainly found in the CpG context. DNA methylation is involved in important processes during development and differentiation and its dysregulation can lead to or is associated with diseases, such as cancer, loss-of-imprinting syndromes and neurological disorders. It has been also shown that DNA methylation at the cellular, tissue and organism level varies with age. To overcome the costs of Whole-Genome Bisulfite Sequencing, the gold standard method to detect 5-methylcytosines at a single base resolution, DNA methylation arrays have been developed and extensively used. This method allows one to assess the status of a fraction of the CpG sites present in the genome of an organism. In order to combine the relatively low cost of Methylation Arrays and digital signals of bisulfite sequencing, we developed a Targeted Bisulfite Sequencing method that can be applied to biomarker discovery for virtually any phenotype. Here we describe a comprehensive step-by-step protocol to build a DNA methylation-based epigenetic clock.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32755621', 'doi' => '10.1016/j.ymeth.2020.07.006', 'modified' => '2020-12-18 13:27:14', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 67 => array( 'id' => '4031', 'name' => 'Battle of the sex chromosomes: competition between X- and Y-chromosomeencoded proteins for partner interaction and chromatin occupancy drivesmulti-copy gene expression and evolution in muroid rodents.', 'authors' => 'Moretti, C and Blanco, M and Ialy-Radio, C and Serrentino, ME and Gobé,C and Friedman, R and Battail, C and Leduc, M and Ward, MA and Vaiman, Dand Tores, F and Cocquet, J', 'description' => '<p>Transmission distorters (TDs) are genetic elements that favor their own transmission to the detriments of others. Slx/Slxl1 (Sycp3-like-X-linked and Slx-like1) and Sly (Sycp3-like-Y-linked) are TDs which have been co-amplified on the X and Y chromosomes of Mus species. They are involved in an intragenomic conflict in which each favors its own transmission, resulting in sex ratio distortion of the progeny when Slx/Slxl1 vs. Sly copy number is unbalanced. They are specifically expressed in male postmeiotic gametes (spermatids) and have opposite effects on gene expression: Sly knockdown leads to the upregulation of hundreds of spermatid-expressed genes, while Slx/Slxl1-deficiency downregulates them. When both Slx/Slxl1 and Sly are knocked-down, sex ratio distortion and gene deregulation are corrected. Slx/Slxl1 and Sly are, therefore, in competition but the molecular mechanism remains unknown. By comparing their chromatin binding profiles and protein partners, we show that SLX/SLXL1 and SLY proteins compete for interaction with H3K4me3-reader SSTY1 (Spermiogenesis-specific-transcript-on-the-Y1) at the promoter of thousands of genes to drive their expression, and that the opposite effect they have on gene expression is mediated by different abilities to recruit SMRT/N-Cor transcriptional complex. Their target genes are predominantly spermatid-specific multicopy genes encoded by the sex chromosomes and the autosomal Speer/Takusan. Many of them have co-amplified with Slx/Slxl1/Sly but also Ssty during muroid rodent evolution. Overall, we identify Ssty as a key element of the X vs. Y intragenomic conflict, which may have influenced gene content and hybrid sterility beyond Mus lineage since Ssty amplification on the Y pre-dated that of Slx/Slxl1/Sly.</p>', 'date' => '2020-07-13', 'pmid' => 'http://www.pubmed.gov/32658962', 'doi' => '10.1093/molbev/msaa175/5870835', 'modified' => '2020-12-18 13:27:51', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 68 => array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ) ), 'Testimonial' => array(), 'Area' => array() ) $country = 'US' $countries_allowed = array( (int) 0 => 'CA', (int) 1 => 'US', (int) 2 => 'IE', (int) 3 => 'GB', (int) 4 => 'DK', (int) 5 => 'NO', (int) 6 => 'SE', (int) 7 => 'FI', (int) 8 => 'NL', (int) 9 => 'BE', (int) 10 => 'LU', (int) 11 => 'FR', (int) 12 => 'DE', (int) 13 => 'CH', (int) 14 => 'AT', (int) 15 => 'ES', (int) 16 => 'IT', (int) 17 => 'PT' ) $outsource = false $other_formats = array() $edit = '' $testimonials = '' $featured_testimonials = '' $related_products = '<li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201140</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-3047" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <form action="/en/carts/add/3047" id="CartAdd/3047Form" method="post" accept-charset="utf-8"><div style="display:none;"><input type="hidden" name="_method" value="POST"/></div><input type="hidden" name="data[Cart][product_id]" value="3047" id="CartProductId"/> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p>Add <input name="data[Cart][quantity]" placeholder="1" value="1" min="1" style="width:60px;display:inline" type="number" id="CartQuantity" required="required"/> <strong> Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico</strong> to my shopping cart.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="checkout" id="checkout" value="checkout" type="submit">Checkout</button> </div> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="keepshop" id="keepshop" type="submit">Keep shopping</button> </div> </div> </div> </div> </form><a class="close-reveal-modal" aria-label="Close">×</a></div><!-- END: ADD TO CART MODAL --><a href="#" id="1-5-ml-tube-holder-dock-for-bioruptor-pico" data-reveal-id="cartModal-3047" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 1.5 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201143</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: QUOTE MODAL --><div id="quoteModal-3048" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h3>Get a quote</h3><p class="lead">You are about to request a quote for <strong>Tube holder for 0.65 ml tubes - Bioruptor<sup>®</sup> Pico</strong>. 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data-reveal-id="cartModal-3049" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 0.2 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack"><img src="/img/product/shearing_technologies/B01200016_tube_holder.jpg" alt="some alt" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01200016</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-1796" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" 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line 118
 How to properly cite this product in your workDiagenode strongly recommends using this: Bioruptor® Pico sonication device (Diagenode Cat# B01080010). Click here to copy to clipboard. Using our products in your publication? Let us know! |
LEO1 Is Required for Efficient Entry into Quiescence, Control of H3K9 Methylation and Gene Expression in Human Fibroblasts |
DeSUMOylation of chromatin-bound proteins limits the rapidtranscriptional reprogramming induced by daunorubicin in acute myeloidleukemias. |
RNA polymerase II CTD is dispensable for transcription and requiredfor termination in human cells. |
Targeting lymphoid-derived IL-17 signaling to delay skin aging. |
Nicotinamide N-methyltransferase sustains a core epigenetic programthat promotes metastatic colonization in breast cancer. |
SOX expression in prostate cancer drives resistance to nuclear hormonereceptor signaling inhibition through the WEE1/CDK1 signaling axis. |
The Effect of Metformin and Carbohydrate-Controlled Diet onDNA Methylation and Gene Expression in the Endometrium of Womenwith Polycystic Ovary Syndrome. |
Chromatin profiling identifies transcriptional readthrough as a conservedmechanism for piRNA biogenesis in mosquitoes. |
Activation of AKT induces EZH2-mediated β-catenin trimethylation incolorectal cancer. |
Detailed molecular and epigenetic characterization of the Pig IPECJ2and Chicken SL-29 cell lines |
Signal-induced enhancer activation requires Ku70 to readtopoisomerase1-DNA covalent complexes. |
Cotranscriptional demethylation induces global loss of H3K4me2 fromactive genes in Arabidopsis |
Epigenetic regulation of plastin 3 expression by the macrosatelliteDXZ4 and the transcriptional regulator CHD4. |
A dataset of definitive endoderm and hepatocyte differentiations fromhuman induced pluripotent stem cells. |
The mineralocorticoid receptor modulates timing and location of genomicbinding by glucocorticoid receptor in response to synthetic glucocorticoidsin keratinocytes. |
Gene Regulatory Interactions at Lamina-Associated Domains |
The aryl hydrocarbon receptor cell intrinsically promotes resident memoryCD8 T cell differentiation and function. |
Impact of Fetal Exposure to Endocrine Disrupting ChemicalMixtures on FOXA3 Gene and Protein Expression in Adult RatTestes. |
Transfer of blocker-based qPCR reactions for DNA methylation analysisinto a microfluidic LoC system using thermal modeling. |
Intranasal administration of Acinetobacter lwoffii in a murine model ofasthma induces IL-6-mediated protection associated with cecal microbiotachanges. |
Trichoderma root colonization triggers epigenetic changes in jasmonic andsalicylic acid pathway-related genes. |
DNA sequence and chromatin modifiers cooperate to confer epigeneticbistability at imprinting control regions. |
Smc5/6 silences episomal transcription by a three-step function. |
Exploration of nuclear body-enhanced sumoylation reveals that PMLrepresses 2-cell features of embryonic stem cells. |
Loss of epigenetic regulation disrupts lineage integrity, inducesaberrant alveogenesis and promotes breast cancer. |
RAD51 protects human cells from transcription-replication conflicts. |
The Arabidopsis APOLO and human UPAT sequence-unrelated longnoncoding RNAs can modulate DNA and histone methylation machineries inplants. |
Prolonged FOS activity disrupts a global myogenic transcriptionalprogram by altering 3D chromatin architecture in primary muscleprogenitor cells. |
Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells. |
Variation in PU.1 binding and chromatin looping at neutrophil enhancersinfluences autoimmune disease susceptibility |
CREBBP/EP300 acetyltransferase inhibition disrupts FOXA1-bound enhancers to inhibit the proliferation of ER+ breast cancer cells. |
Transient regulation of focal adhesion via Tensin3 is required fornascent oligodendrocyte differentiation |
The long noncoding RNA H19 regulates tumor plasticity inneuroendocrine prostate cancer |
Epromoters function as a hub to recruit key transcription factorsrequired for the inflammatory response |
Differential contribution to gene expression prediction of histonemodifications at enhancers or promoters. |
Atg7 deficiency in microglia drives an altered transcriptomic profileassociated with an impaired neuroinflammatory response |
Lasp1 regulates adherens junction dynamics and fibroblast transformationin destructive arthritis |
The lncRNA and the transcription factor WRKY42 target common cell wallEXTENSIN encoding genes to trigger root hair cell elongation. |
Placental uptake and metabolism of 25(OH)Vitamin D determines itsactivity within the fetoplacental unit |
Waves of sumoylation support transcription dynamics during adipocytedifferentiation |
Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes. |
Genetic perturbation of PU.1 binding and chromatin looping at neutrophilenhancers associates with autoimmune disease. |
Fra-1 regulates its target genes via binding to remote enhancers withoutexerting major control on chromatin architecture in triple negative breastcancers. |
Cell-specific alterations inPitx1regulatory landscape activation caused bythe loss of a single enhancer |
Transgenic mice for in vivo epigenome editing with CRISPR-based systems |
Transcriptional programming drives Ibrutinib-resistance evolution in mantlecell lymphoma. |
Coordinated changes in gene expression, H1 variant distribution and genome3D conformation in response to H1 depletion |
REPROGRAMMING CBX8-PRC1 FUNCTION WITH A POSITIVE ALLOSTERICMODULATOR |
Germline activity of the heat shock factor HSF-1 programs theinsulin-receptor daf-2 in C. elegans |
The epigenetic landscape in purified myonuclei from fast and slow muscles |
The glucocorticoid receptor recruits the COMPASS complex to regulateinflammatory transcription at macrophage enhancers. |
A distinct metabolic response characterizes sensitivity to EZH2inhibition in multiple myeloma. |
BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma |
A Tumor Suppressor Enhancer of PTEN in T-cell development and leukemia |
Stronger induction of trained immunity by mucosal BCG or MTBVAC vaccination compared to standard intradermal vaccination. |
Postoperative abdominal sepsis induces selective and persistent changes inCTCF binding within the MHC-II region of human monocytes. |
S-adenosyl-l-homocysteine hydrolase links methionine metabolism to thecircadian clock and chromatin remodeling. |
Genomic profiling of T-cell activation suggests increased sensitivity ofmemory T cells to CD28 costimulation. |
A genetic variant controls interferon-β gene expression in human myeloidcells by preventing C/EBP-β binding on a conserved enhancer. |
BCG Vaccination Induces Long-Term Functional Reprogramming of HumanNeutrophils. |
Macrophage Immune Memory Controls Endometriosis in Mice and Humans. |
UTX/KDM6A suppresses AP-1 and a gliogenesis program during neuraldifferentiation of human pluripotent stem cells. |
Epigenetic regulation of the lineage specificity of primary human dermallymphatic and blood vascular endothelial cells. |
Combined treatment with CBP and BET inhibitors reverses inadvertentactivation of detrimental super enhancer programs in DIPG cells. |
Methylation in pericytes after acute injury promotes chronic kidneydisease. |
Exploring the virulence gene interactome with CRISPR/dCas9 in the humanmalaria parasite. |
Targeted bisulfite sequencing for biomarker discovery. |
Battle of the sex chromosomes: competition between X- and Y-chromosomeencoded proteins for partner interaction and chromatin occupancy drivesmulti-copy gene expression and evolution in muroid rodents. |
BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression |
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Notice (8): Undefined variable: solution_of_interest [APP/View/Products/view.ctp, line 755]Code Context<!-- BEGIN: REQUEST_FORM MODAL --><div id="request_formModal" class="reveal-modal medium" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"><?= $this->element('Forms/simple_form', array('solution_of_interest' => $solution_of_interest, 'header' => $header, 'message' => $message, 'campaign_id' => $campaign_id)) ?>$viewFile = '/home/website-server/www/app/View/Products/view.ctp' $dataForView = array( 'language' => 'en', 'noindex' => 'noindex', 'meta_keywords' => '', 'meta_description' => 'Bioruptor® Pico sonication device', 'meta_title' => 'Bioruptor® Pico sonication device', 'product' => array( 'Product' => array( 'id' => '3046', 'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa fa-arrow-circle-right"></i> <a href="https://www.diagenode.com/pages/chromatin-prep-easyshear-kit-guide">Read more</a></h3> </div> <p> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> </p> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'format' => '1 unit', 'catalog_number' => 'B01080010', 'old_catalog_number' => '', 'sf_code' => 'B01080010-', 'type' => 'ACC', 'search_order' => '00-Machine', 'price_EUR' => '27000', 'price_USD' => '30000', 'price_GBP' => '23500', 'price_JPY' => '4229550', 'price_CNY' => '/', 'price_AUD' => '75000', 'country' => 'ALL', 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'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa 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It allows for reproducible sonication of up to<strong> 12 x 0.65 ml tubes</strong> at a time with a <strong>sample volume of 100 µl</strong>. 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Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>®</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>®</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>®</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div> <div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 µl volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.1 ml Bioruptor® Microtubes (Cat. No. B01200041). <strong>Panel B, 100 µl volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.65 ml Bioruptor® Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 µl volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016). Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37°C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 µl of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div> <div class="small-12 medium-12 large-12 columns"><br /><br /></div> <div class="small-12 medium-12 large-12 columns"> <p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p> </div> <div class="small-12 medium-12 large-12 columns"> <div class="page" title="Page 7"> <table> <tbody> <tr valign="middle"> <td></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>SDS concentration</strong></p> </td> <td style="text-align: center;"> <p>< 0.1%</p> </td> <td style="text-align: center;"> <p>0.2%</p> </td> <td style="text-align: center;"> <p>1%</p> </td> <td style="text-align: center;"> <p>0.5%</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Nuclei isolation</strong></p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>No</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Allows for shearing of... cells/tissue</strong></p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>up to 25 g of tissue</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Corresponding to shearing buffers from</strong></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p> <p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p> </td> </tr> </tbody> </table> <p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor® Pico</span></a></em></p> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'chromatin-shearing', 'meta_keywords' => 'Chromatin shearing,Chromatin Immunoprecipitation,Bioruptor,Sonication,Sonicator', 'meta_description' => 'Diagenode's Bioruptor® is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.', 'meta_title' => 'Chromatin shearing using Bioruptor® sonication device | Diagenode', 'modified' => '2017-11-15 10:14:02', 'created' => '2015-03-05 15:56:30', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3', 'position' => '10', 'parent_id' => null, 'name' => '次世代シーケンシング', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2 style="font-size: 22px;">DNA断片化、ライブラリー調製、自動化：NGSのワンストップショップ</h2> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-12 medium-12 large-12 columns"> <h4>1. 断片化装置を選択してください：150 bp〜75 kbの範囲でDNAを断片化します。</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-pico-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/bioruptor_pico.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/megaruptor2-1-unit"><img src="https://www.diagenode.com/img/product/shearing_technologies/B06010001_megaruptor2.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-one-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/br-one-profil.png" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns">5μlまで断片化：150 bp〜2 kb<br />NGS DNAライブラリー調製およびFFPE核酸抽出に最適で、</td> <td class="small-4 medium-4 large-4 columns">2 kb〜75 kbの範囲をできます。<br />メイトペアライブラリー調製および長いフラグメントDNAシーケンシングに最適で、この軽量デスクトップデバイスで</td> <td class="small-4 medium-4 large-4 columns">20または50μlの断片化が可能です。</td> </tr> </tbody> </table> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-8 medium-8 large-8 columns"> <h4>2. 最適化されたライブラリー調整キットを選択してください。</h4> </th> <th class="small-4 medium-4 large-4 columns"> <h4>3. ライブラリー前処理自動化を選択して、比類のないデータ再現性を実感</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><img src="https://www.diagenode.com/img/product/kits/microPlex_library_preparation.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns"><img src="https://www.diagenode.com/img/product/kits/box_kit.jpg" style="display: block; margin-left: auto; margin-right: auto;" height="173" width="250" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/sx-8g-ip-star-compact-automated-system-1-unit"><img src="https://www.diagenode.com/img/product/automation/B03000002%20_ipstar_compact.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">50pgの低入力：MicroPlex Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">5ng以上：iDeal Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">Achieve great NGS data easily</td> </tr> </tbody> </table> </div> </div> <blockquote> <div class="row"> <div class="small-12 medium-12 large-12 columns"><span class="label" style="margin-bottom: 16px; margin-left: -22px; font-size: 15px;">DiagenodeがNGS研究にぴったりなプロバイダーである理由</span> <p>Diagenodeは15年以上もエピジェネティクス研究に専念、専門としています。 ChIP研究クロマチン用のユニークな断片化システムの開発から始まり、 専門知識を活かし、5μlのせん断体積まで可能で、NGS DNAライブラリーの調製に最適な最先端DNA断片化装置の開発にたどり着きました。 我々は以来、ChIP-seq、Methyl-seq、NGSライブラリー調製用キットを研究開発し、業界をリードする免疫沈降研究と同様に、ライブラリー調製を自動化および完結させる独自の自動化システムを開発にも成功しました。</p> <ul> <li>信頼されるせん断装置</li> <li>様々なインプットからのライブラリ作成キット</li> <li>独自の自動化デバイス</li> </ul> </div> </div> </blockquote> <div class="row"> <div class="small-12 columns"> <ul class="accordion" data-accordion=""> <li class="accordion-navigation"><a href="#panel1a">次世代シーケンシングへの理解とその専門知識</a> <div id="panel1a" class="content"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p><strong>次世代シーケンシング (NGS)</strong> ）は、著しいスケールとハイスループットでシーケンシングを行い、1日に数十億もの塩基生成を可能にします。 NGSのハイスループットは迅速でありながら正確で、再現性のあるデータセットを実現し、さらにシーケンシング費用を削減します。 NGSは、ゲノムシーケンシング、ゲノム再シーケンシング、デノボシーケンシング、トランスクリプトームシーケンシング、その他にDNA-タンパク質相互作用の検出やエピゲノムなどを示します。 指数関数的に増加するシーケンシングデータの需要は、計算分析の障害や解釈、データストレージなどの課題を解決します。</p> <p>アプリケーションおよび出発物質に応じて、数百万から数十億の鋳型DNA分子を大規模に並行してシーケンシングすることが可能です。その為に、異なる化学物質を使用するいくつかの市販のNGSプラットフォームを利用することができます。 NGSプラットフォームの種類によっては、事前準備とライブラリー作成が必要です。</p> <p>NGSにとっても、特にデータ処理と分析に関した大きな課題はあります。第3世代技術はゲノミクス研究にさらに革命を起こすであろうと大きく期待されています。</p> </div> </div> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <p><strong>NGS アプリケーション</strong></p> <ul> <li>全ゲノム配列決定</li> <li>デノボシーケンシング</li> <li>標的配列</li> <li>Exomeシーケンシング</li> <li>トランスクリプトーム配列決定</li> <li>ゲノム配列決定</li> <li>ミトコンドリア配列決定</li> <li>DNA-タンパク質相互作用（ChIP-seq</li> <li>バリアント検出</li> <li>ゲノム仕上げ</li> </ul> </div> <div class="small-6 medium-6 large-6 columns"> <p><strong>研究分野におけるNGS:</strong></p> <ul> <li>腫瘍学</li> <li>リプロダクティブ・ヘルス</li> <li>法医学ゲノミクス</li> <li>アグリゲノミックス</li> <li>複雑な病気</li> <li>微生物ゲノミクス</li> <li>食品・環境ゲノミクス</li> <li>創薬ゲノミクス - パーソナライズド・メディカル</li> </ul> </div> <div class="small-12 medium-12 large-12 columns"> <p><strong>NGSの用語</strong></p> <dl> <dt>リード（読み取り）</dt> <dd>この装置から得られた連続した単一のストレッチ</dd> <dt>断片リード</dt> <dd>フラグメントライブラリからの読み込み。 シーケンシングプラットフォームに応じて、読み取りは通常約100〜300bp。</dd> <dt>断片ペアエンドリード</dt> <dd>断片ライブラリーからDNA断片の各末端2つの読み取り。</dd> <dt>メイトペアリード</dt> <dd>大きなDNA断片（通常は予め定義されたサイズ範囲）の各末端から2つの読み取り。</dd> <dt>カバレッジ（例）</dt> <dd>30×適用範囲とは、参照ゲノム中の各塩基対が平均30回の読み取りを示す。</dd> </dl> </div> </div> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2>NGSプラットフォーム</h2> <h3><a href="http://www.illumina.com" target="_blank">イルミナ</a></h3> <p>イルミナは、クローン的に増幅された鋳型DNA（クラスター）上に位置する、蛍光標識された可逆的鎖ターミネーターヌクレオチドを用いた配列別合成技術を使用。 DNAクラスターは、ガラスフローセルの表面上に固定化され、 ワークフローは、4つのヌクレオチド（それぞれ異なる蛍光色素で標識された）の組み込み、4色イメージング、色素や末端基の切断、取り込み、イメージングなどを繰り返します。フローセルは大規模な並列配列決定を受ける。 この方法により、単一蛍光標識されたヌクレオチドの制御添加によるモノヌクレオチドのエラーを回避する可能性があります。 読み取りの長さは、通常約100〜150 bpです。</p> <h3><a href="http://www.lifetechnologies.com" target="_blank">イオン トレント</a></h3> <p>イオントレントは、半導体技術チップを用いて、合成中にヌクレオチドを取り込む際に放出されたプロトンを検出します。 これは、イオン球粒子と呼ばれるビーズの表面にエマルションPCR（emPCR）を使用し、リンクされた特定のアダプターを用いてDNA断片を増幅します。 各ビーズは1種類のDNA断片で覆われていて、異なるDNA断片を有するビーズは次いで、チップの陽子感知ウェル内に配置されます。 チップには一度に4つのヌクレオチドのうちの1つが浸水し、このプロセスは異なるヌクレオチドで15秒ごとに繰り返されます。 配列決定の間に4つの塩基の各々が1つずつ導入されます、組み込みの場合はプロトンが放出され、電圧信号が取り込みに比例して検出されます。.</p> <h3><a href="http://www.pacificbiosciences.com" target="_blank">パシフィック バイオサイエンス</a></h3> <p>パシフィックバイオサイエンスでは、20kbを超える塩基対の読み取りも、単一分子リアルタイム（SMRT）シーケンシングによる構造および細胞タイプの変化を観察することができます。 このプラットフォームでは、超長鎖二本鎖DNA（dsDNA）断片が、Megaruptor（登録商標）のようなDiagenode装置を用いたランダムシアリングまたは目的の標的領域の増幅によって生成されます。 SMRTbellライブラリーは、ユニバーサルヘアピンアダプターをDNA断片の各末端に連結することによって生成します。 サイズ選択条件による洗浄ステップの後、配列決定プライマーをSMRTbellテンプレートにアニーリングし、鋳型DNAに結合したDNAポリメラーゼを含む配列決定を、蛍光標識ヌクレオチドの存在下で開始。 各塩基が取り込まれると、異なる蛍光のパルスをリアルタイムで検出します。</p> <h3><a href="https://nanoporetech.com" target="_blank">オックスフォード ナノポア</a></h3> <p>Oxford Nanoporeは、単一のDNA分子配列決定に基づく技術を開発します。その技術により生物学的分子、すなわちDNAが一群の電気抵抗性高分子膜として位置するナノスケールの孔（ナノ細孔）またはその近くを通過し、イオン電流が変化します。 この変化に関する情報は、例えば4つのヌクレオチド（AまたはG r CまたはT）ならびに修飾されたヌクレオチドすべてを区別することによって分子情報に訳されます。 シーケンシングミニオンデバイスのフローセルは、数百個のナノポアチャネルのセンサアレイを含みます。 DNAサンプルは、Diagenode社のMegaruptor（登録商標）を用いてランダムシアリングによって生成され得る超長鎖DNAフラグメントが必要です。</p> <h3><a href="http://www.lifetechnologies.com/be/en/home/life-science/sequencing/next-generation-sequencing/solid-next-generation-sequencing.html" target="_blank">SOLiD</a></h3> <p>SOLiDは、ユニークな化学作用により、何千という個々のDNA分子の同時配列決定を可能にします。 それは、アダプター対ライブラリーのフラグメントが適切で、せん断されたゲノムDNAへのアダプターのライゲーションによるライブラリー作製から始まります。 次のステップでは、エマルジョンPCR（emPCR）を実施して、ビーズの表面上の個々の鋳型DNA分子をクローン的に増幅。 emPCRでは、個々の鋳型DNAをPCR試薬と混合し、水中油型エマルジョン内の疎水性シェルで囲まれた水性液滴内のプライマーコートビーズを、配列決定のためにロードするスライドガラスの表面にランダムに付着。 この技術は、シークエンシングプライマーへのライゲーションで競合する4つの蛍光標識されたジ塩基プローブのセットを使用します。</p> <h3><a href="http://454.com/products/technology.asp" target="_blank">454</a></h3> <p>454は、大規模並列パイロシーケンシングを利用しています。 始めに全ゲノムDNAまたは標的遺伝子断片の300〜800bp断片のライブラリー調製します。 次に、DNAフラグメントへのアダプターの付着および単一のDNA鎖の分離。 その後アダプターに連結されたDNAフラグメントをエマルジョンベースのクローン増幅（emPCR）で処理し、DNAライブラリーフラグメントをミクロンサイズのビーズ上に配置します。 各DNA結合ビーズを光ファイバーチップ上のウェルに入れ、器具に挿入します。 4つのDNAヌクレオチドは、配列決定操作中に固定された順序で連続して加えられ、並行して配列決定されます。</p> </div> </div> </div> </li> </ul> </div> </div>', 'in_footer' => true, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'next-generation-sequencing', 'meta_keywords' => 'Next-generation sequencing,NGS,Whole genome sequencing,NGS platforms,DNA/RNA shearing', 'meta_description' => 'Diagenode offers kits and DNA/RNA shearing technology prior to next-generation sequencing, many Next-generation sequencing platforms require preparation of the DNA.', 'meta_title' => 'Next-generation sequencing (NGS) Applications and Methods | Diagenode', 'modified' => '2018-07-26 05:24:29', 'created' => '2015-04-01 22:47:04', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '13', 'position' => '10', 'parent_id' => '3', 'name' => 'DNA/RNA shearing', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns">In recent years, advances in Next-Generation Sequencing (NGS) have revolutionized genomics and biology. This growth has fueled demands on upstream techniques for optimal sample preparation and genomic library construction. One of the most critical aspects of optimal library preparation is the quality of the DNA to be sequenced. The DNA must first be effectively and consistently sheared into the appropriate fragment size (depending on the sequencing platform) to enable sensitive and reliable NGS results. The <strong>Bioruptor</strong><sup>®</sup> <strong>Pico</strong> and the <strong>Megaruptor</strong><sup>®</sup> provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows. Follow our guidelines and find the good parameters for your expected DNA size: <a href="https://pybrevet.typeform.com/to/o8cQfM">DNA shearing with the Bioruptor<sup>®</sup></a>.</div> </div> <p></p> <div class="row"> <div class="small-7 medium-7 large-7 columns text-center"><img src="https://www.diagenode.com/img/applications/true-flexibility-with-br-ngs.jpg" /></div> <div class="small-5 medium-5 large-5 columns"><small><strong>Programmable DNA size distribution and high reproducibility with Bioruptor<sup>®</sup> Pico using 0.65 (panel A) or 0.1 ml (panel B) microtubes</strong>. <b>Panel A:</b> 200 bp after 13 cycles (13 sec ON/OFF) using 100 µl volume. Average size: 204; CV%:1.89%). <b>Panel B:</b> 200 bp after 20 cycles (30 sec ON/OFF) using 10 µl volume. (Average size: 215 bp; CV%: 6.6%). <b>Panel A & B:</b> peak electropherogram view. <b>Panel C & D:</b> virtual gel view.</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-10 medium-10 large-10 columns text-center end small-offset-1"><img src="https://www.diagenode.com/img/applications/megaruptor-short-frag.jpg" /></div> <div class="small-12 medium-12 large-12 columns"><small><strong> Reproducible and narrow DNA size distribution with Megaruptor® using short fragment size Hydropores Validation using two different DNA sources and two different methods of analysis. A:</strong> Shearing of lambda phage genomic DNA (20 ng/μl; 150 μl/sample) sheared at different speed settings and analyzed on 1% agarose gel. <strong>B:</strong> Bioanalyzer profiles of human genomic DNA (20 ng/μl; 150 μl/sample) sheared at different software settings of 2 and 5 kb. Three independent experiments were run for each setting. (Agilent DNA 12000 kit was used for separation and fragment sizing).</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-4 medium-4 large-4 columns text-center"><img src="https://www.diagenode.com/img/applications/megaruptor-long-frag.jpg" /></div> <div class="small-8 medium-8 large-8 columns"><small><strong> Demonstrated shearing to fragment sizes between 15 kb and 75 kb with Megaruptor® using long fragment size Hydropores. </strong>Image shows DNA size distribution of human genomic DNA sheared with long fragment Hydropores. DNA was analyzed by pulsed field gel electrophoresis (PFGE) in 1% agarose gel and a mean size of smears was estimated using Image Lab 4.1 software.<br /> * indicates unsheared DNA </small></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'dna-rna-shearing', 'meta_keywords' => 'DNA/RNA shearing,Bioruptor® Pico,Megaruptor®,Next-Generation Sequencing ', 'meta_description' => 'Bioruptor® Pico and the Megaruptor® provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows.', 'meta_title' => 'DNA shearing & RNA shearing for Next-Generation Sequencing (NGS) | Diagenode', 'modified' => '2017-12-08 14:44:11', 'created' => '2014-10-29 12:45:41', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '17', 'position' => '10', 'parent_id' => '4', 'name' => 'Protein extraction', 'description' => '<div class="row"> <div class="large-12 columns">Various biochemical and analytical techniques require the extraction of protein from tissues or mammalian, yeast and bacterial cells. Obtaining high quality and yields of proteins is important for further downstream protein characterization such as in PAGE, western blotting, mass spectrometry or protein purification. The efficient disruption and homogenization of tissues and cultured cells obtained in just one step using <strong>Diagenode's Bioruptor</strong><sup>®</sup> deliver high quality protein.</div> </div> <p></p> <div class="row"> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_standard_plus.png" /> <p><small>Western blot analysis of GAPDH and HSP90 proteins in tissues (various mouse tissues) and cultured cell extracts (HeLA).</small></p> </div> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_pico.png" /> <p><small>Western blot analysis of GAPDH and ß-tubulin proteins in tissues (mouse liver) and cultured cell extracts (HeLA).</small></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'protein-extraction', 'meta_keywords' => 'Protein extraction,Bioruptor,Sonication,Protein Analysis', 'meta_description' => 'Diagenode provides efficient disruption and homogenization of tissues and cultured cells obtained in just one step using Bioruptor® deliver high quality protein.', 'meta_title' => 'Protein extraction using Bioruptor® Sonication device | Diagenode', 'modified' => '2017-10-16 14:39:42', 'created' => '2014-07-02 04:41:03', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '6', 'position' => '10', 'parent_id' => '1', 'name' => 'メチル化DNA結合タンパク質', 'description' => '<div class="row"> <div class="large-12 columns">MBD方法は、メチル化DNAに対するH6-GST-MBD融合タンパク質の非常に高い親和性に基づいています。 このタンパク質は、N末端His6タグを含むグルタチオン-S-トランスフェラーゼ（GST）とのC末端融合物として、ヒトMeCP2のメチル結合ドメイン（MBD）を含有します。 このH6-GST-MBD融合タンパク質を用いて、メチル化CpGを含むDNAを特異的に単離する事が可能です。<br /><br />DiagenodeのMethylCap®キットは、二本鎖DNAの高濃縮と、メチル化CpG密度の関数における微分分画を可能にします。 分画はサンプルの複雑さを軽減し、次世代のシーケンシングを容易にします。 MethylCapアッセイに先立ち、DNAを最初に抽出し、Picoruptorソニケーターを用いて断片化します。<br /> <h3>概要</h3> <p class="text-center"><br /><img src="https://www.diagenode.com/img/applications/methyl_binding_domain_overview.jpg" /></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'methylbinding-domain-protein', 'meta_keywords' => 'Epigenetic,Methylbinding Domain Protein,MBD,DNA methylation,DNA replication,MethylCap,MethylCap assay,', 'meta_description' => 'Methylbinding Domain Protein(MBD) approach is based on the very high affinity of a H6-GST-MBD fusion protein for methylated DNA. This protein consists of the methyl binding domain (MBD) of human MeCP2, as a C-terminal fusion with Glutathione-S-transferase', 'meta_title' => 'Epigenetic Methylbinding Domain Protein(MBD) - DNA methylation | Diagenode', 'modified' => '2019-03-22 12:32:12', 'created' => '2015-06-02 17:05:42', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '9', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-seq', 'description' => '<div class="row"> <div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div> <div class="large-12 columns"></div> <h5 class="large-12 columns"><strong></strong></h5> <h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div> <div class="large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by sonication to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with <strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: Reverse cross-links, elute, and purify </li> <li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify IP'd material</li> <li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chromatin-immunoprecipitation-sequencing', 'meta_keywords' => 'Chromatin Immunoprecipitation Sequencing,ChIP-Seq,ChIP-seq grade antibodies,DNA purification,qPCR,Shearing of chromatin', 'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing', 'meta_title' => 'Chromatin Immunoprecipitation - ChIP-seq Kits - Dna methylation | Diagenode', 'modified' => '2017-11-14 09:57:16', 'created' => '2015-04-12 18:08:46', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '11', 'position' => '10', 'parent_id' => '3', 'name' => 'FFPE DNA extraction', 'description' => '<div class="row"> <div class="large-12 columns">Diagenode's high yields FFPE DNA extraction using Bioruptor<sup><span>®</span></sup> is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no toxic reagents, digest tissues, and purify DNA with high yields and low sample degradation. The DNA can then be analyzed by traditional methods or can be sheared with the Bioruptor<sup>®</sup> Pico ultrasonicator for downstream NGS library prep using the MicroPlex Library Preparation Kit.</div> <div class="small-12 medium-12 large-12 columns text-center"><img src="https://www.diagenode.com/img/applications/ffpe_workflow.png" /></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'ffpe-dna-extraction', 'meta_keywords' => 'FFPE DNA extraction,Next-Gen Sequencing,Bioruptor® ultrasonicator', 'meta_description' => 'Diagenode's high yields FFPE DNA extraction using Bioruptor is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no tox', 'meta_title' => 'FFPE DNA extraction using Bioruptor® ultrasonicator | Diagenode', 'modified' => '2017-10-16 14:34:57', 'created' => '2014-10-01 01:24:40', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '10', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-qPCR', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns text-justify"> <p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p> <p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p> </div> <div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div> <div class="small-12 medium-12 large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li> <li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chip-qpcr', 'meta_keywords' => 'Chromatin immunoprecipitation,ChIP Quantitative PCR,polymerase chain reaction (PCR)', 'meta_description' => 'Diagenode's ChIP qPCR kits can be used to quantify enriched DNA after chromatin immunoprecipitation. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of', 'meta_title' => 'ChIP Quantitative PCR (ChIP-qPCR) | Diagenode', 'modified' => '2018-01-09 16:46:56', 'created' => '2014-12-11 00:22:08', 'ProductsApplication' => array( [maximum depth reached] ) ) ), 'Category' => array( (int) 0 => array( 'id' => '6', 'position' => '1', 'parent_id' => '1', 'name' => 'Bioruptor<sup>®</sup>', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"><br /> <p><span>Diagenode focuses on state-of-the-art preparation of high quality biological and chemical samples by developing the industry’s most advanced water bath sonicators and hydrodynamic devices. Our instruments are ideal for a number of applications in various fields of studies including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</span></p> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor/TAB-BR-comparaison.pdf" target="_blank"><img src="https://www.diagenode.com/img/bouton-comparaison.png" /></a></p> </div> <!-- <center> <div class="small-12 medium-4 large-4 columns"> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img 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crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script>// <![CDATA[ (function (d) { var js, id = "genially-embed-js", ref = d.getElementsByTagName("script")[0]; if (d.getElementById(id)) { return; } js = d.createElement("script"); js.id = id; js.async = true; js.src = "https://view.genial.ly/static/embed/embed.js"; ref.parentNode.insertBefore(js, ref); }(document)); // ]]></script> </div> </div>--> <p><span> <br /></span></p> <div class="spacer"></div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">Reproductibility is our priority</h2> </div> </div> <div><img src="https://www.diagenode.com/img/shearing/reproductibility.png" alt="reproductibility" /> <p class="bottom_note"></p> </div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">An affordable instrument for wide range of applications</h2> </div> </div> <p style="text-align: center;">Designed for any researchers, the Bioruptor gives the user the right level of flexibility.</p> <table style="width: 972px;"> <tbody> <tr style="height: 56px;"> <th style="width: 380px; height: 56px;"></th> <th class="text-center" style="width: 126px; height: 56px;">Bioruptor</th> <th class="text-center" style="width: 141px; height: 56px;">Cup Horn Sonicators</th> <th class="text-center" style="width: 156px; height: 56px;">Focused <br />ultra-sonicators</th> <th class="text-center" style="width: 155px; height: 56px;">Multi Sample Sonicator</th> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Instrument pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Consumables pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Range of applications</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Scalable and sample volume flexibility</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Throughput</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> </tbody> </table> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;"></h2> <h2 style="text-align: center;">Bioruptor ultrasonication for best results in:</h2> <p><b><span>✓ Chromatin shearing</span><span> </span><span style="font-weight: 400;">- Industry leader in accurate and tight fragment ranges</span></b></p> <p><b><span>✓ DNA shearing</span><span> </span><span style="font-weight: 400;">- Excellent results for optimal fragment lengths in NGS library prep</span></b></p> <p><b><span>✓<span> </span></span>Protein aggregation studies </b><span style="font-weight: 400;">- Standardizing seeding with the robust Bioruptor.<br /></span><i><span style="font-weight: 400;">Read the app note by Dr. Kelvin Luk at the University of Pennsylvania </span></i><a href="https://www.diagenode.com/en/documents/standardizing-seeding-experiments-for-the-understanding-of-parkinson-disease" style="color: #13b29c;"><i><span style="font-weight: 400;">“Standardizing seeding experiments using the Bioruptor® for the understanding of the neuronal alpha-synuclein pathology”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>3D genome analysis with Hi-C</b><span style="font-weight: 400;"> - Preparing chromatin libraries with high-quality sonication.<br /></span><i><span style="font-weight: 400;">Read the app note, “</span></i><a href="https://www.diagenode.com/en/documents/applicationnote-arima-low-input" style="color: #13b29c;"><i><span style="font-weight: 400;">Unlock Low-Input 3D Genome Analysis with the Arima-HiC Kit”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>Mass spectrometry</b> <b>and increasing protein identification</b><span style="font-weight: 400;">- Sample preparation using Preomics iST and Bioruptor sonication.<br /></span><i><span style="font-weight: 400;">Read the app note “</span></i><a href="https://www.diagenode.com/en/documents/wp-ist-adaptators" style="color: #13b29c;"><i><span style="font-weight: 400;">Increase your iST ultrasonication throughput with the new Bioruptor® Pico cartridge holder”</span></i></a></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>Cell lysis, liposome prep, protein extraction, RNA extraction and more</b></span></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>CUT&RUN –Sonication of input DNA (for enrichment comparison) for NGS</b></span></p> </div> </div> <p><a href="https://www.diagenode.com/en/categories/bioruptor-maintenance"><img src="https://www.diagenode.com/img/banners/maintenance-banner-br.png" /></a></p> <p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" 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When studying samples that are difficult to obtain or grow, low input solutions can help you understand genome structure across a new range of low input samples. In addition, the Diagenode Bioruptor Pico assures that chromatin is sheared to optimal fragment lengths.</span></p>', 'image_id' => '247', 'type' => 'Application Note', 'url' => 'files/application_notes/ApplicationNote-Arima-Low-Input.pdf', 'slug' => 'applicationnote-arima-low-input', 'meta_keywords' => 'application note arima low input', 'meta_description' => 'application note arima low input', 'modified' => '2021-02-09 09:55:59', 'created' => '2021-02-09 09:55:59', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1074', 'name' => 'Datasheet of Bioruptor tubes', 'description' => '<p>Datasheet of Diagenode tubes for Bioruptor Pico and Bioruptor Plus.</p>', 'image_id' => null, 'type' => 'Datasheet', 'url' => 'files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf', 'slug' => 'tds-bioruptor-tubes', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2022-02-23 12:21:44', 'created' => '2020-03-23 10:41:46', 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'modified' => '2020-01-10 10:53:08', 'created' => '2020-01-10 10:53:08', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '1805', 'name' => 'product/shearing_technologies/B01080000-3.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:46', 'created' => '2020-01-10 10:53:46', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1806', 'name' => 'product/shearing_technologies/B01080000-4.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:56', 'created' => '2020-01-10 10:53:56', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1807', 'name' => 'product/shearing_technologies/B01080000-5.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:54:06', 'created' => '2020-01-10 10:54:06', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => '2018-02-14 15:41:46', 'ProductsImage' => array( [maximum depth reached] ) ) ), 'Promotion' => array(), 'Protocol' => array( (int) 0 => array( 'id' => '73', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:16:00', 'created' => '0000-00-00 00:00:00', 'ProductsProtocol' => array( [maximum depth reached] ) ) ), 'Publication' => array( (int) 0 => array( 'id' => '4881', 'name' => 'LEO1 Is Required for Efficient Entry into Quiescence, Control of H3K9 Methylation and Gene Expression in Human Fibroblasts', 'authors' => 'Laurent M. et al.', 'description' => '<p><span>(1) Background: The LEO1 (Left open reading frame 1) protein is a conserved subunit of the PAF1C complex (RNA polymerase II-associated factor 1 complex). PAF1C has well-established mechanistic functions in elongation of transcription and RNA processing. We previously showed, in fission yeast, that LEO1 controls histone H3K9 methylation levels by affecting the turnover of histone H3 in chromatin, and that it is essential for the proper regulation of gene expression during cellular quiescence. Human fibroblasts enter a reversible quiescence state upon serum deprivation in the growth media. Here we investigate the function of LEO1 in human fibroblasts. (2) Methods: We knocked out the </span><span class="html-italic">LEO1</span><span><span> </span>gene using CRISPR/Cas9 methodology in human fibroblasts and verified that the LEO1 protein was undetectable by Western blot. We characterized the phenotype of the<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout cells with FACS analysis and cell growth assays. We used RNA-sequencing using spike-in controls to measure gene expression and spike-in controlled ChIP-sequencing experiments to measure the histone modification H3K9me2 genome-wide. (3) Results: Gene expression levels are altered in quiescent cells, however factors controlling chromatin and gene expression changes in quiescent human cells are largely unknown. The<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout fibroblasts are viable but have reduced metabolic activity compared to wild-type cells.<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells showed a slower entry into quiescence and a different morphology compared to wild-type cells. Gene expression was generally reduced in quiescent wild-type cells. The downregulated genes included genes involved in cell proliferation. A small number of genes were upregulated in quiescent wild-type cells including several genes involved in ERK1/ERK2 and Wnt signaling. In quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells, many genes were mis-regulated compared to wild-type cells. This included genes involved in Calcium ion transport and cell morphogenesis. Finally, spike-in controlled ChIP-sequencing experiments demonstrated that the histone modification H3K9me2 levels are globally increased in quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells. (4) Conclusions: Thus, LEO1 is important for proper entry into cellular quiescence, control of H3K9me2 levels, and gene expression in human fibroblasts.</span></p>', 'date' => '2023-11-17', 'pmid' => 'https://www.mdpi.com/2218-273X/13/11/1662', 'doi' => 'https://doi.org/10.3390/biom13111662', 'modified' => '2023-11-21 12:01:53', 'created' => '2023-11-21 12:01:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '4845', 'name' => 'DeSUMOylation of chromatin-bound proteins limits the rapidtranscriptional reprogramming induced by daunorubicin in acute myeloidleukemias.', 'authors' => 'Boulanger M. et al.', 'description' => '<p>Genotoxicants have been used for decades as front-line therapies against cancer on the basis of their DNA-damaging actions. However, some of their non-DNA-damaging effects are also instrumental for killing dividing cells. We report here that the anthracycline Daunorubicin (DNR), one of the main drugs used to treat Acute Myeloid Leukemia (AML), induces rapid (3 h) and broad transcriptional changes in AML cells. The regulated genes are particularly enriched in genes controlling cell proliferation and death, as well as inflammation and immunity. These transcriptional changes are preceded by DNR-dependent deSUMOylation of chromatin proteins, in particular at active promoters and enhancers. Surprisingly, inhibition of SUMOylation with ML-792 (SUMO E1 inhibitor), dampens DNR-induced transcriptional reprogramming. Quantitative proteomics shows that the proteins deSUMOylated in response to DNR are mostly transcription factors, transcriptional co-regulators and chromatin organizers. Among them, the CCCTC-binding factor CTCF is highly enriched at SUMO-binding sites found in cis-regulatory regions. This is notably the case at the promoter of the DNR-induced NFKB2 gene. DNR leads to a reconfiguration of chromatin loops engaging CTCF- and SUMO-bound NFKB2 promoter with a distal cis-regulatory region and inhibition of SUMOylation with ML-792 prevents these changes.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37462077', 'doi' => '10.1093/nar/gkad581', 'modified' => '2023-08-01 14:16:43', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '4846', 'name' => 'RNA polymerase II CTD is dispensable for transcription and requiredfor termination in human cells.', 'authors' => 'Yahia Y. et al.', 'description' => '<p>The largest subunit of RNA polymerase (Pol) II harbors an evolutionarily conserved C-terminal domain (CTD), composed of heptapeptide repeats, central to the transcriptional process. Here, we analyze the transcriptional phenotypes of a CTD-Δ5 mutant that carries a large CTD truncation in human cells. Our data show that this mutant can transcribe genes in living cells but displays a pervasive phenotype with impaired termination, similar to but more severe than previously characterized mutations of CTD tyrosine residues. The CTD-Δ5 mutant does not interact with the Mediator and Integrator complexes involved in the activation of transcription and processing of RNAs. Examination of long-distance interactions and CTCF-binding patterns in CTD-Δ5 mutant cells reveals no changes in TAD domains or borders. Our data demonstrate that the CTD is largely dispensable for the act of transcription in living cells. We propose a model in which CTD-depleted Pol II has a lower entry rate onto DNA but becomes pervasive once engaged in transcription, resulting in a defect in termination.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37424514', 'doi' => '10.15252/embr.202256150', 'modified' => '2023-08-01 14:17:54', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '4793', 'name' => 'Targeting lymphoid-derived IL-17 signaling to delay skin aging.', 'authors' => 'Paloma S. et al.', 'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, γδ T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-κB in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218', 'doi' => '10.1038/s43587-023-00431-z', 'modified' => '2023-06-14 15:56:56', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '4796', 'name' => 'Nicotinamide N-methyltransferase sustains a core epigenetic programthat promotes metastatic colonization in breast cancer.', 'authors' => 'Couto J.P. et al.', 'description' => '<p><span>Metastatic colonization of distant organs accounts for over 90% of deaths related to solid cancers, yet the molecular determinants of metastasis remain poorly understood. Here, we unveil a mechanism of colonization in the aggressive basal-like subtype of breast cancer that is driven by the NAD</span><sup>+</sup><span><span> </span>metabolic enzyme nicotinamide N-methyltransferase (NNMT). We demonstrate that NNMT imprints a basal genetic program into cancer cells, enhancing their plasticity. In line, NNMT expression is associated with poor clinical outcomes in patients with breast cancer. Accordingly, ablation of NNMT dramatically suppresses metastasis formation in pre-clinical mouse models. Mechanistically, NNMT depletion results in a methyl overflow that increases histone H3K9 trimethylation (H3K9me3) and DNA methylation at the promoters of PR/SET Domain-5 (PRDM5) and extracellular matrix-related genes. PRDM5 emerged in this study as a pro-metastatic gene acting via induction of cancer-cell intrinsic transcription of collagens. Depletion of PRDM5 in tumor cells decreases COL1A1 deposition and impairs metastatic colonization of the lungs. These findings reveal a critical activity of the NNMT-PRDM5-COL1A1 axis for cancer cell plasticity and metastasis in basal-like breast cancer.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37259596', 'doi' => '10.15252/embj.2022112559', 'modified' => '2023-06-15 08:35:19', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '4812', 'name' => 'SOX expression in prostate cancer drives resistance to nuclear hormonereceptor signaling inhibition through the WEE1/CDK1 signaling axis.', 'authors' => 'Williams A. et al.', 'description' => '<p><span>The development of androgen receptor signaling inhibitor (ARSI) drug resistance in prostate cancer (PC) remains therapeutically challenging. Our group has described the role of sex determining region Y-box 2 (SOX2) overexpression in ARSI-resistant PC. Continuing this work, we report that NR3C1, the gene encoding glucocorticoid receptor (GR), is a novel SOX2 target in PC, positively regulating its expression. Similar to ARSI treatment, SOX2-positive PC cells are insensitive to GR signaling inhibition using a GR modulating therapy. To understand SOX2-mediated nuclear hormone receptor signaling inhibitor (NHRSI) insensitivity, we performed RNA-seq in SOX2-positive and -negative PC cells following NHRSI treatment. RNA-seq prioritized differentially regulated genes mediating the cell cycle, including G2 checkpoint WEE1 Kinase (WEE1) and cyclin-dependent kinase 1 (CDK1). Additionally, WEE1 and CDK1 were differentially expressed in PC patient tumors dichotomized by high vs low SOX2 gene expression. Importantly, pharmacological targeting of WEE1 (WEE1i) in combination with an ARSI or GR modulator re-sensitizes SOX2-positive PC cells to nuclear hormone receptor signaling inhibition in vitro, and WEE1i combined with ARSI significantly slowed tumor growth in vivo. Collectively, our data suggest SOX2 predicts NHRSI resistance, and simultaneously indicates the addition of WEE1i to improve therapeutic efficacy of NHRSIs in SOX2-positive PC.</span></p>', 'date' => '2023-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37169162', 'doi' => '10.1016/j.canlet.2023.216209', 'modified' => '2023-06-15 08:58:59', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '4787', 'name' => 'The Effect of Metformin and Carbohydrate-Controlled Diet onDNA Methylation and Gene Expression in the Endometrium of Womenwith Polycystic Ovary Syndrome.', 'authors' => 'Garcia-Gomez E. et al.', 'description' => '<p>Polycystic ovary syndrome (PCOS) is an endocrine disease associated with infertility and metabolic disorders in reproductive-aged women. In this study, we evaluated the expression of eight genes related to endometrial function and their DNA methylation levels in the endometrium of PCOS patients and women without the disease (control group). In addition, eight of the PCOS patients underwent intervention with metformin (1500 mg/day) and a carbohydrate-controlled diet (type and quantity) for three months. Clinical and metabolic parameters were determined, and RT-qPCR and MeDIP-qPCR were used to evaluate gene expression and DNA methylation levels, respectively. Decreased expression levels of , , and genes and increased DNA methylation levels of the promoter were found in the endometrium of PCOS patients compared to controls. After metformin and nutritional intervention, some metabolic and clinical variables improved in PCOS patients. This intervention was associated with increased expression of , , and genes and reduced DNA methylation levels of the promoter in the endometrium of PCOS women. Our preliminary findings suggest that metformin and a carbohydrate-controlled diet improve endometrial function in PCOS patients, partly by modulating DNA methylation of the gene promoter and the expression of genes implicated in endometrial receptivity and insulin signaling.</p>', 'date' => '2023-04-01', 'pmid' => 'https://doi.org/10.3390%2Fijms24076857', 'doi' => '10.3390/ijms24076857', 'modified' => '2023-06-12 08:58:33', 'created' => '2023-05-05 12:34:24', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '4763', 'name' => 'Chromatin profiling identifies transcriptional readthrough as a conservedmechanism for piRNA biogenesis in mosquitoes.', 'authors' => 'Qu J. et al.', 'description' => '<p>The piRNA pathway in mosquitoes differs substantially from other model organisms, with an expanded PIWI gene family and functions in antiviral defense. Here, we define core piRNA clusters as genomic loci that show ubiquitous piRNA expression in both somatic and germline tissues. These core piRNA clusters are enriched for non-retroviral endogenous viral elements (nrEVEs) in antisense orientation and depend on key biogenesis factors, Veneno, Tejas, Yb, and Shutdown. Combined transcriptome and chromatin state analyses identify transcriptional readthrough as a conserved mechanism for cluster-derived piRNA biogenesis in the vector mosquitoes Aedes aegypti, Aedes albopictus, Culex quinquefasciatus, and Anopheles gambiae. Comparative analyses between the two Aedes species suggest that piRNA clusters function as traps for nrEVEs, allowing adaptation to environmental challenges such as virus infection. Our systematic transcriptome and chromatin state analyses lay the foundation for studies of gene regulation, genome evolution, and piRNA function in these important vector species.</p>', 'date' => '2023-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36930642', 'doi' => '10.1016/j.celrep.2023.112257', 'modified' => '2023-04-17 09:12:37', 'created' => '2023-04-14 13:41:22', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 8 => array( 'id' => '4720', 'name' => 'Activation of AKT induces EZH2-mediated β-catenin trimethylation incolorectal cancer.', 'authors' => 'Ghobashi A. H. et al.', 'description' => '<p>Colorectal cancer (CRC) develops in part through the deregulation of different signaling pathways, including activation of the WNT/β-catenin and PI3K/AKT pathways. Enhancer of zeste homolog 2 (EZH2) is a lysine methyltransferase that is involved in regulating stem cell development and differentiation and is overexpressed in CRC. However, depending on the study EZH2 has been found to be both positively and negatively correlated with the survival of CRC patients suggesting that EZH2's role in CRC may be context specific. In this study, we explored how PI3K/AKT activation alters EZH2's role in CRC. We found that activation of AKT by PTEN knockdown or by hydrogen peroxide treatment induced EZH2 phosphorylation at serine 21. Phosphorylation of EZH2 resulted in EZH2-mediated methylation of β-catenin and an associated increased interaction between β-catenin, TCF1, and RNA polymerase II. AKT activation increased β-catenin's enrichment across the genome and EZH2 inhibition reduced this enrichment by reducing the methylation of β-catenin. Furthermore, PTEN knockdown increased the expression of epithelial-mesenchymal transition (EMT)-related genes, and somewhat unexpectedly EZH2 inhibition further increased the expression of these genes. Consistent with these findings, EZH2 inhibition enhanced the migratory phenotype of PTEN knockdown cells. Overall, we demonstrated that EZH2 modulates AKT-induced changes in gene expression through the AKT/EZH2/ β-catenin axis in CRC with active PI3K/AKT signaling. Therefore, it is important to consider the use of EZH2 inhibitors in CRC with caution as these inhibitors will inhibit EZH2-mediated methylation of histone and non-histone targets such as β-catenin, which can have tumor-promoting effects.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1101%2F2023.01.31.526429', 'doi' => '10.1101/2023.01.31.526429', 'modified' => '2023-03-28 09:13:16', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 9 => array( 'id' => '4667', 'name' => 'Detailed molecular and epigenetic characterization of the Pig IPECJ2and Chicken SL-29 cell lines', 'authors' => 'de Vos J. et al.', 'description' => '<p>The pig IPECJ2 and chicken SL-29 cell lines are of interest because of their untransformed nature and wide use in functional studies. Molecular characterization of these cell lines is important to gain insight into possible molecular aberrations. The aims of this paper are providing a molecular and epigenetic characterization of the IPEC-J2 and SL-29 cell lines and providing a cell-line reference for the FAANG community, and future biomedical research. Whole genome sequencing , gene expression, DNA methylation , chromatin accessibility and ChIP-seq of four histone marks (H3K4me1, H3K4me3, H3K27ac, H3K27me3) and an insulator (CTCF) are used to achieve these aims. Heteroploidy (aneuploidy) of various chromosomes was observed from whole genome sequencing analysis in both cell lines. Furthermore, higher gene expression for genes located on chromosomes with aneuploidy in comparison to diploid chromosomes was observed. Regulatory complexity of gene expression, DNA methylation and chromatin accessibility was investigated through an integrative approach.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.isci.2023.106252', 'doi' => '10.1016/j.isci.2023.106252', 'modified' => '2023-04-07 16:52:26', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 10 => array( 'id' => '4673', 'name' => 'Signal-induced enhancer activation requires Ku70 to readtopoisomerase1-DNA covalent complexes.', 'authors' => 'Tan Y. et al.', 'description' => '<p>Enhancer activation serves as the main mechanism regulating signal-dependent transcriptional programs, ensuring cellular plasticity, yet central questions persist regarding their mechanism of activation. Here, by successfully mapping topoisomerase I-DNA covalent complexes genome-wide, we find that most, if not all, acutely activated enhancers, including those induced by 17β-estradiol, dihydrotestosterone, tumor necrosis factor alpha and neuronal depolarization, are hotspots for topoisomerase I-DNA covalent complexes, functioning as epigenomic signatures read by the classic DNA damage sensor protein, Ku70. Ku70 in turn nucleates a heterochromatin protein 1 gamma (HP1γ)-mediator subunit Med26 complex to facilitate acute, but not chronic, transcriptional activation programs. Together, our data uncover a broad, unappreciated transcriptional code, required for most, if not all, acute signal-dependent enhancer activation events in both mitotic and postmitotic cells.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36747093', 'doi' => '10.1038/s41594-022-00883-8', 'modified' => '2023-04-14 09:24:10', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 11 => array( 'id' => '4668', 'name' => 'Cotranscriptional demethylation induces global loss of H3K4me2 fromactive genes in Arabidopsis', 'authors' => 'Mori S. et al.', 'description' => '<p>Based on studies of animals and yeasts, methylation of histone H3 lysine 4 (H3K4me1/2/3, for mono-, di-, and tri-methylation, respectively) is regarded as the key epigenetic modification of transcriptionally active genes. In plants, however, H3K4me2 correlates negatively with transcription, and the regulatory mechanisms of this counterintuitive H3K4me2 distribution in plants remain largely unexplored. A previous genetic screen for factors regulating plant regeneration identified Arabidopsis LYSINE-SPECIFIC DEMETHYLASE 1-LIKE 3 (LDL3), which is a major H3K4me2 demethylase. Here, we show that LDL3-mediated H3K4me2 demethylation depends on the transcription elongation factor Paf1C and phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII). In addition, LDL3 binds to phosphorylated RNAPII. These results suggest that LDL3 is recruited to transcribed genes by binding to elongating RNAPII and demethylates H3K4me2 cotranscriptionally. Importantly, the negative correlation between H3K4me2 and transcription is disrupted in the ldl3 mutant, demonstrating the genome-wide impacts of the transcription-driven LDL3 pathway to control H3K4me2 in plants. Our findings implicate H3K4me2 in plants as chromatin memory for transcriptionally repressive states, which ensures robust gene control.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.02.17.528985v1', 'doi' => '10.1101/2023.02.17.528985', 'modified' => '2023-04-14 09:31:55', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 12 => array( 'id' => '4670', 'name' => 'Epigenetic regulation of plastin 3 expression by the macrosatelliteDXZ4 and the transcriptional regulator CHD4.', 'authors' => 'Strathmann E. A. et al.', 'description' => '<p>Dysregulated Plastin 3 (PLS3) levels associate with a wide range of skeletal and neuromuscular disorders and the most common types of solid and hematopoietic cancer. Most importantly, PLS3 overexpression protects against spinal muscular atrophy. Despite its crucial role in F-actin dynamics in healthy cells and its involvement in many diseases, the mechanisms that regulate PLS3 expression are unknown. Interestingly, PLS3 is an X-linked gene and all asymptomatic SMN1-deleted individuals in SMA-discordant families who exhibit PLS3 upregulation are female, suggesting that PLS3 may escape X chromosome inactivation. To elucidate mechanisms contributing to PLS3 regulation, we performed a multi-omics analysis in two SMA-discordant families using lymphoblastoid cell lines and iPSC-derived spinal motor neurons originated from fibroblasts. We show that PLS3 tissue-specifically escapes X-inactivation. PLS3 is located ∼500 kb proximal to the DXZ4 macrosatellite, which is essential for X chromosome inactivation. By applying molecular combing in a total of 25 lymphoblastoid cell lines (asymptomatic individuals, individuals with SMA, control subjects) with variable PLS3 expression, we found a significant correlation between the copy number of DXZ4 monomers and PLS3 levels. Additionally, we identified chromodomain helicase DNA binding protein 4 (CHD4) as an epigenetic transcriptional regulator of PLS3 and validated co-regulation of the two genes by siRNA-mediated knock-down and overexpression of CHD4. We show that CHD4 binds the PLS3 promoter by performing chromatin immunoprecipitation and that CHD4/NuRD activates the transcription of PLS3 by dual-luciferase promoter assays. Thus, we provide evidence for a multilevel epigenetic regulation of PLS3 that may help to understand the protective or disease-associated PLS3 dysregulation.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.ajhg.2023.02.004', 'doi' => '10.1016/j.ajhg.2023.02.004', 'modified' => '2023-04-14 09:36:04', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 13 => array( 'id' => '4672', 'name' => 'A dataset of definitive endoderm and hepatocyte differentiations fromhuman induced pluripotent stem cells.', 'authors' => 'Tanaka Y. et al.', 'description' => '<p>Hepatocytes are a major parenchymal cell type in the liver and play an essential role in liver function. Hepatocyte-like cells can be differentiated in vitro from induced pluripotent stem cells (iPSCs) via definitive endoderm (DE)-like cells and hepatoblast-like cells. Here, we explored the in vitro differentiation time-course of hepatocyte-like cells. We performed methylome and transcriptome analyses for hepatocyte-like cell differentiation. We also analyzed DE-like cell differentiation by methylome, transcriptome, chromatin accessibility, and GATA6 binding profiles, using finer time-course samples. In this manuscript, we provide a detailed description of the dataset and the technical validations. Our data may be valuable for the analysis of the molecular mechanisms underlying hepatocyte and DE differentiations.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36788249', 'doi' => '10.1038/s41597-023-02001-9', 'modified' => '2023-04-14 09:41:29', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 14 => array( 'id' => '4643', 'name' => 'The mineralocorticoid receptor modulates timing and location of genomicbinding by glucocorticoid receptor in response to synthetic glucocorticoidsin keratinocytes.', 'authors' => 'Carceller-Zazo E. et al.', 'description' => '<p>Glucocorticoids (GCs) exert potent antiproliferative and anti-inflammatory properties, explaining their therapeutic efficacy for skin diseases. GCs act by binding to the GC receptor (GR) and the mineralocorticoid receptor (MR), co-expressed in classical and non-classical targets including keratinocytes. Using knockout mice, we previously demonstrated that GR and MR exert essential nonoverlapping functions in skin homeostasis. These closely related receptors may homo- or heterodimerize to regulate transcription, and theoretically bind identical GC-response elements (GRE). We assessed the contribution of MR to GR genomic binding and the transcriptional response to the synthetic GC dexamethasone (Dex) using control (CO) and MR knockout (MR ) keratinocytes. GR chromatin immunoprecipitation (ChIP)-seq identified peaks common and unique to both genotypes upon Dex treatment (1 h). GREs, AP-1, TEAD, and p53 motifs were enriched in CO and MR peaks. However, GR genomic binding was 35\% reduced in MR , with significantly decreased GRE enrichment, and reduced nuclear GR. Surface plasmon resonance determined steady state affinity constants, suggesting preferred dimer formation as MR-MR > GR-MR ~ GR-GR; however, kinetic studies demonstrated that GR-containing dimers had the longest lifetimes. Despite GR-binding differences, RNA-seq identified largely similar subsets of differentially expressed genes in both genotypes upon Dex treatment (3 h). However, time-course experiments showed gene-dependent differences in the magnitude of expression, which correlated with earlier and more pronounced GR binding to GRE sites unique to CO including near Nr3c1. Our data show that endogenous MR has an impact on the kinetics and differential genomic binding of GR, affecting the time-course, specificity, and magnitude of GC transcriptional responses in keratinocytes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36527388', 'doi' => '10.1096/fj.202201199RR', 'modified' => '2023-03-28 08:55:08', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 15 => array( 'id' => '4605', 'name' => 'Gene Regulatory Interactions at Lamina-Associated Domains', 'authors' => 'Madsen-Østerbye J. et al.', 'description' => '<p>The nuclear lamina provides a repressive chromatin environment at the nuclear periphery. However, whereas most genes in lamina-associated domains (LADs) are inactive, over ten percent reside in local euchromatic contexts and are expressed. How these genes are regulated and whether they are able to interact with regulatory elements remain unclear. Here, we integrate publicly available enhancer-capture Hi-C data with our own chromatin state and transcriptomic datasets to show that inferred enhancers of active genes in LADs are able to form connections with other enhancers within LADs and outside LADs. Fluorescence in situ hybridization analyses show proximity changes between differentially expressed genes in LADs and distant enhancers upon the induction of adipogenic differentiation. We also provide evidence of involvement of lamin A/C, but not lamin B1, in repressing genes at the border of an in-LAD active region within a topological domain. Our data favor a model where the spatial topology of chromatin at the nuclear lamina is compatible with gene expression in this dynamic nuclear compartment.</p>', 'date' => '2023-01-01', 'pmid' => 'https://doi.org/10.3390%2Fgenes14020334', 'doi' => '10.3390/genes14020334', 'modified' => '2023-04-04 08:57:32', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 16 => array( 'id' => '4578', 'name' => 'The aryl hydrocarbon receptor cell intrinsically promotes resident memoryCD8 T cell differentiation and function.', 'authors' => 'Dean J. W. et al.', 'description' => '<p>The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4 T cells; however, its cell-intrinsic role in CD8 T cells remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8 T cell (T) differentiation and function. Genetic ablation of Ahr in mouse CD8 T cells leads to increased CD127KLRG1 short-lived effector cells and CD44CD62L T central memory cells but reduced granzyme-B-producing CD69CD103 T cells. Genome-wide analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8 T cell population, revealed by single-cell RNA-seq, is diminished upon Ahr deletion, compromising anti-tumor immunity. Human intestinal intraepithelial CD8 T cells also highly express AHR that regulates in vitro T differentiation and granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8 T cell immunity.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36640340', 'doi' => '10.1016/j.celrep.2022.111963', 'modified' => '2023-04-11 10:14:26', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 17 => array( 'id' => '4577', 'name' => 'Impact of Fetal Exposure to Endocrine Disrupting ChemicalMixtures on FOXA3 Gene and Protein Expression in Adult RatTestes.', 'authors' => 'Walker C. et al.', 'description' => '<p>Perinatal exposure to endocrine disrupting chemicals (EDCs) has been shown to affect male reproductive functions. However, the effects on male reproduction of exposure to EDC mixtures at doses relevant to humans have not been fully characterized. In previous studies, we found that in utero exposure to mixtures of the plasticizer di(2-ethylhexyl) phthalate (DEHP) and the soy-based phytoestrogen genistein (Gen) induced abnormal testis development in rats. In the present study, we investigated the molecular basis of these effects in adult testes from the offspring of pregnant SD rats gavaged with corn oil or Gen + DEHP mixtures at 0.1 or 10 mg/kg/day. Testicular transcriptomes were determined by microarray and RNA-seq analyses. A protein analysis was performed on paraffin and frozen testis sections, mainly by immunofluorescence. The transcription factor forkhead box protein 3 (FOXA3), a key regulator of Leydig cell function, was identified as the most significantly downregulated gene in testes from rats exposed in utero to Gen + DEHP mixtures. FOXA3 protein levels were decreased in testicular interstitium at a dose previously found to reduce testosterone levels, suggesting a primary effect of fetal exposure to Gen + DEHP on adult Leydig cells, rather than on spermatids and Sertoli cells, also expressing FOXA3. Thus, FOXA3 downregulation in adult testes following fetal exposure to Gen + DEHP may contribute to adverse male reproductive outcomes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36674726', 'doi' => '10.3390/ijms24021211', 'modified' => '2023-04-11 10:18:58', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 18 => array( 'id' => '4721', 'name' => 'Transfer of blocker-based qPCR reactions for DNA methylation analysisinto a microfluidic LoC system using thermal modeling.', 'authors' => 'Kärcher J.et al.', 'description' => '<p>Changes in the DNA methylation landscape are associated with many diseases like cancer. Therefore, DNA methylation analysis is of great interest for molecular diagnostics and can be applied, e.g., for minimally invasive diagnostics in liquid biopsy samples like blood plasma. Sensitive detection of local methylation, which occurs in various cancer types, can be achieved with quantitative HeavyMethyl-PCR using oligonucleotides that block the amplification of unmethylated DNA. A transfer of these quantitative PCRs (qPCRs) into point-of-care (PoC) devices like microfluidic Lab-on-Chip (LoC) cartridges can be challenging as LoC systems show significantly different thermal properties than qPCR cyclers. We demonstrate how an adequate thermal model of the specific LoC system can help us to identify a suitable thermal profile, even for complex HeavyMethyl qPCRs, with reduced experimental effort. Using a simulation-based approach, we demonstrate a proof-of-principle for the successful LoC transfer of colorectal /-qPCR from Epi Procolon® colorectal carcinoma test, by avoidance of oligonucleotide interactions.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36506005', 'doi' => '10.1063/5.0108374', 'modified' => '2023-03-28 09:15:30', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 19 => array( 'id' => '4575', 'name' => 'Intranasal administration of Acinetobacter lwoffii in a murine model ofasthma induces IL-6-mediated protection associated with cecal microbiotachanges.', 'authors' => 'Alashkar A. B. et al.', 'description' => '<p>BACKGROUND: Early-life exposure to certain environmental bacteria including Acinetobacter lwoffii (AL) has been implicated in protection from chronic inflammatory diseases including asthma later in life. However, the underlying mechanisms at the immune-microbe interface remain largely unknown. METHODS: The effects of repeated intranasal AL exposure on local and systemic innate immune responses were investigated in wild-type and Il6 , Il10 , and Il17 mice exposed to ovalbumin-induced allergic airway inflammation. Those investigations were expanded by microbiome analyses. To assess for AL-associated changes in gene expression, the picture arising from animal data was supplemented by in vitro experiments of macrophage and T-cell responses, yielding expression and epigenetic data. RESULTS: The asthma preventive effect of AL was confirmed in the lung. Repeated intranasal AL administration triggered a proinflammatory immune response particularly characterized by elevated levels of IL-6, and consequently, IL-6 induced IL-10 production in CD4 T-cells. Both IL-6 and IL-10, but not IL-17, were required for asthma protection. AL had a profound impact on the gene regulatory landscape of CD4 T-cells which could be largely recapitulated by recombinant IL-6. AL administration also induced marked changes in the gastrointestinal microbiome but not in the lung microbiome. By comparing the effects on the microbiota according to mouse genotype and AL-treatment status, we have identified microbial taxa that were associated with either disease protection or activity. CONCLUSION: These experiments provide a novel mechanism of Acinetobacter lwoffii-induced asthma protection operating through IL-6-mediated epigenetic activation of IL-10 production and with associated effects on the intestinal microbiome.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36458896', 'doi' => '10.1111/all.15606', 'modified' => '2023-04-11 10:23:07', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 20 => array( 'id' => '4574', 'name' => 'Trichoderma root colonization triggers epigenetic changes in jasmonic andsalicylic acid pathway-related genes.', 'authors' => 'Agostini R. B. et al.', 'description' => '<p>Beneficial interactions between plant-roots and Trichoderma spp. lead to a local and systemic enhancement of the plant immune system through a mechanism known as priming of defenses. In recent reports, we outlined a repertoire of genes and proteins differentially regulated in distant tissues of maize plants previously inoculated with Trichoderma atroviride. To further investigate the mechanisms involved in the systemic activation of plant responses, we continued evaluating the regulatory aspects of a selected group of genes when priming is triggered in maize plants. We conducted a time-course expression experiment from the beginning of the interaction between T. atroviride and maize roots, along plant vegetative growth and during Colletotrichum graminicola leaf infection. In addition to gene expression studies, the levels of jasmonic and salicylic acid were determined in the same samples for a comprehensive understanding of the gene expression results. Lastly, chromatin structure and modification assays were designed to evaluate the role of epigenetic marks during the long-lasting activation of the primed state of maize plants. The overall analysis of the results allowed us to shed some light on the interplay between the phytohormones and epigenetic regulatory events in the systemic and long-lasting regulation of maize plant defenses after Trichoderma inoculation.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36575905', 'doi' => '10.1093/jxb/erac518', 'modified' => '2023-04-14 09:08:14', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 21 => array( 'id' => '4474', 'name' => 'DNA sequence and chromatin modifiers cooperate to confer epigeneticbistability at imprinting control regions.', 'authors' => 'Butz S. et al.', 'description' => '<p>Genomic imprinting is regulated by parental-specific DNA methylation of imprinting control regions (ICRs). Despite an identical DNA sequence, ICRs can exist in two distinct epigenetic states that are memorized throughout unlimited cell divisions and reset during germline formation. Here, we systematically study the genetic and epigenetic determinants of this epigenetic bistability. By iterative integration of ICRs and related DNA sequences to an ectopic location in the mouse genome, we first identify the DNA sequence features required for maintenance of epigenetic states in embryonic stem cells. The autonomous regulatory properties of ICRs further enabled us to create DNA-methylation-sensitive reporters and to screen for key components involved in regulating their epigenetic memory. Besides DNMT1, UHRF1 and ZFP57, we identify factors that prevent switching from methylated to unmethylated states and show that two of these candidates, ATF7IP and ZMYM2, are important for the stability of DNA and H3K9 methylation at ICRs in embryonic stem cells.</p>', 'date' => '2022-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36333500', 'doi' => '10.1038/s41588-022-01210-z', 'modified' => '2022-11-18 12:20:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 22 => array( 'id' => '4493', 'name' => 'Smc5/6 silences episomal transcription by a three-step function.', 'authors' => 'Abdul F. et al.', 'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36097294', 'doi' => '10.1038/s41594-022-00829-0', 'modified' => '2022-11-18 12:41:42', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 23 => array( 'id' => '4495', 'name' => 'Exploration of nuclear body-enhanced sumoylation reveals that PMLrepresses 2-cell features of embryonic stem cells.', 'authors' => 'Tessier S. et al.', 'description' => '<p>Membrane-less organelles are condensates formed by phase separation whose functions often remain enigmatic. Upon oxidative stress, PML scaffolds Nuclear Bodies (NBs) to regulate senescence or metabolic adaptation. PML NBs recruit many partner proteins, but the actual biochemical mechanism underlying their pleiotropic functions remains elusive. Similarly, PML role in embryonic stem cell (ESC) and retro-element biology is unsettled. Here we demonstrate that PML is essential for oxidative stress-driven partner SUMO2/3 conjugation in mouse ESCs (mESCs) or leukemia, a process often followed by their poly-ubiquitination and degradation. Functionally, PML is required for stress responses in mESCs. Differential proteomics unravel the KAP1 complex as a PML NB-dependent SUMO2-target in arsenic-treated APL mice or mESCs. PML-driven KAP1 sumoylation enables activation of this key epigenetic repressor implicated in retro-element silencing. Accordingly, Pml mESCs re-express transposable elements and display 2-Cell-Like features, the latter enforced by PML-controlled SUMO2-conjugation of DPPA2. Thus, PML orchestrates mESC state by coordinating SUMO2-conjugation of different transcriptional regulators, raising new hypotheses about PML roles in cancer.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36175410', 'doi' => '10.1038/s41467-022-33147-6', 'modified' => '2022-11-21 10:21:48', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 24 => array( 'id' => '4502', 'name' => 'Loss of epigenetic regulation disrupts lineage integrity, inducesaberrant alveogenesis and promotes breast cancer.', 'authors' => 'Langille E. et al.', 'description' => '<p>Systematically investigating the scores of genes mutated in cancer and discerning disease drivers from inconsequential bystanders is a prerequisite for Precision Medicine but remains challenging. Here, we developed a somatic CRISPR/Cas9 mutagenesis screen to study 215 recurrent 'long-tail' breast cancer genes, which revealed epigenetic regulation as a major tumor suppressive mechanism. We report that components of the BAP1 and the COMPASS-like complexes, including KMT2C/D, KDM6A, BAP1 and ASXL1/2 ("EpiDrivers"), cooperate with PIK3CAH1047R to transform mouse and human breast epithelial cells. Mechanistically, we find that activation of PIK3CAH1047R and concomitant EpiDriver loss triggered an alveolar-like lineage conversion of basal mammary epithelial cells and accelerated formation of luminal-like tumors, suggesting a basal origin for luminal tumors. EpiDrivers mutations are found in ~39\% of human breast cancers and ~50\% of ductal-carcinoma-in-situ express casein suggesting that lineage infidelity and alveogenic mimicry may significantly contribute to early steps of breast cancer etiology.</p>', 'date' => '2022-09-01', 'pmid' => 'https://aacrjournals.org/cancerdiscovery/article-abstract/doi/10.1158/2159-8290.CD-21-0865/709222/Loss-of-epigenetic-regulation-disrupts-lineage?redirectedFrom=fulltext', 'doi' => '10.1158/2159-8290.CD-21-0865', 'modified' => '2022-11-21 10:34:24', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 25 => array( 'id' => '4449', 'name' => 'RAD51 protects human cells from transcription-replication conflicts.', 'authors' => 'Bhowmick R. et al.', 'description' => '<p>Oncogene activation during tumorigenesis promotes DNA replication stress (RS), which subsequently drives the formation of cancer-associated chromosomal rearrangements. Many episodes of physiological RS likely arise due to conflicts between the DNA replication and transcription machineries operating simultaneously at the same loci. One role of the RAD51 recombinase in human cells is to protect replication forks undergoing RS. Here, we have identified a key role for RAD51 in preventing transcription-replication conflicts (TRCs) from triggering replication fork breakage. The genomic regions most affected by RAD51 deficiency are characterized by being replicated and transcribed in early S-phase and show significant overlap with loci prone to cancer-associated amplification. Consistent with a role for RAD51 in protecting against transcription-replication conflicts, many of the adverse effects of RAD51 depletion are ameliorated by inhibiting early S-phase transcription. We propose a model whereby RAD51 suppresses fork breakage and subsequent inadvertent amplification of genomic loci prone to experiencing TRCs.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36002000', 'doi' => '10.1016/j.molcel.2022.07.010', 'modified' => '2022-10-14 16:44:54', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 26 => array( 'id' => '4511', 'name' => 'The Arabidopsis APOLO and human UPAT sequence-unrelated longnoncoding RNAs can modulate DNA and histone methylation machineries inplants.', 'authors' => 'Fonouni-Farde C. et al.', 'description' => '<p>BACKGROUND: RNA-DNA hybrid (R-loop)-associated long noncoding RNAs (lncRNAs), including the Arabidopsis lncRNA AUXIN-REGULATED PROMOTER LOOP (APOLO), are emerging as important regulators of three-dimensional chromatin conformation and gene transcriptional activity. RESULTS: Here, we show that in addition to the PRC1-component LIKE HETEROCHROMATIN PROTEIN 1 (LHP1), APOLO interacts with the methylcytosine-binding protein VARIANT IN METHYLATION 1 (VIM1), a conserved homolog of the mammalian DNA methylation regulator UBIQUITIN-LIKE CONTAINING PHD AND RING FINGER DOMAINS 1 (UHRF1). The APOLO-VIM1-LHP1 complex directly regulates the transcription of the auxin biosynthesis gene YUCCA2 by dynamically determining DNA methylation and H3K27me3 deposition over its promoter during the plant thermomorphogenic response. Strikingly, we demonstrate that the lncRNA UHRF1 Protein Associated Transcript (UPAT), a direct interactor of UHRF1 in humans, can be recognized by VIM1 and LHP1 in plant cells, despite the lack of sequence homology between UPAT and APOLO. In addition, we show that increased levels of APOLO or UPAT hamper VIM1 and LHP1 binding to YUCCA2 promoter and globally alter the Arabidopsis transcriptome in a similar manner. CONCLUSIONS: Collectively, our results uncover a new mechanism in which a plant lncRNA coordinates Polycomb action and DNA methylation through the interaction with VIM1, and indicates that evolutionary unrelated lncRNAs with potentially conserved structures may exert similar functions by interacting with homolog partners.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36038910', 'doi' => '10.1186/s13059-022-02750-7', 'modified' => '2022-11-21 10:43:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 27 => array( 'id' => '4552', 'name' => 'Prolonged FOS activity disrupts a global myogenic transcriptionalprogram by altering 3D chromatin architecture in primary muscleprogenitor cells.', 'authors' => 'Barutcu A Rasim et al.', 'description' => '<p>BACKGROUND: The AP-1 transcription factor, FBJ osteosarcoma oncogene (FOS), is induced in adult muscle satellite cells (SCs) within hours following muscle damage and is required for effective stem cell activation and muscle repair. However, why FOS is rapidly downregulated before SCs enter cell cycle as progenitor cells (i.e., transiently expressed) remains unclear. Further, whether boosting FOS levels in the proliferating progeny of SCs can enhance their myogenic properties needs further evaluation. METHODS: We established an inducible, FOS expression system to evaluate the impact of persistent FOS activity in muscle progenitor cells ex vivo. We performed various assays to measure cellular proliferation and differentiation, as well as uncover changes in RNA levels and three-dimensional (3D) chromatin interactions. RESULTS: Persistent FOS activity in primary muscle progenitor cells severely antagonizes their ability to differentiate and form myotubes within the first 2 weeks in culture. RNA-seq analysis revealed that ectopic FOS activity in muscle progenitor cells suppressed a global pro-myogenic transcriptional program, while activating a stress-induced, mitogen-activated protein kinase (MAPK) transcriptional signature. Additionally, we observed various FOS-dependent, chromosomal re-organization events in A/B compartments, topologically associated domains (TADs), and genomic loops near FOS-regulated genes. CONCLUSIONS: Our results suggest that elevated FOS activity in recently activated muscle progenitor cells perturbs cellular differentiation by altering the 3D chromosome organization near critical pro-myogenic genes. This work highlights the crucial importance of tightly controlling FOS expression in the muscle lineage and suggests that in states of chronic stress or disease, persistent FOS activity in muscle precursor cells may disrupt the muscle-forming process.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35971133', 'doi' => '10.1186/s13395-022-00303-x', 'modified' => '2022-11-24 10:11:55', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 28 => array( 'id' => '4452', 'name' => 'Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.', 'authors' => 'Schomann T. et al.', 'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>', 'date' => '2022-07-01', 'pmid' => 'https://doi.org/10.3390%2Fbiom12081048', 'doi' => '10.3390/biom12081048', 'modified' => '2022-10-21 09:33:25', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 29 => array( 'id' => '4446', 'name' => 'Variation in PU.1 binding and chromatin looping at neutrophil enhancersinfluences autoimmune disease susceptibility', 'authors' => 'Watt S. et al. ', 'description' => '<p>Neutrophils play fundamental roles in innate inflammatory response, shape adaptive immunity1, and have been identified as a potentially causal cell type underpinning genetic associations with immune system traits and diseases2,3 The majority of these variants are non-coding and the underlying mechanisms are not fully understood. Here, we profiled the binding of one of the principal myeloid transcriptional regulators, PU.1, in primary neutrophils across nearly a hundred volunteers, and elucidate the coordinated genetic effects of PU.1 binding variation, local chromatin state, promoter-enhancer interactions and gene expression. We show that PU.1 binding and the associated chain of molecular changes underlie genetically-driven differences in cell count and autoimmune disease susceptibility. Our results advance interpretation for genetic loci associated with neutrophil biology and immune disease.</p>', 'date' => '2022-05-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/620260v1.abstract', 'doi' => '10.1101/620260', 'modified' => '2022-10-14 16:39:03', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 30 => array( 'id' => '4217', 'name' => 'CREBBP/EP300 acetyltransferase inhibition disrupts FOXA1-bound enhancers to inhibit the proliferation of ER+ breast cancer cells.', 'authors' => 'Bommi-Reddy A. et al.', 'description' => '<p><span>Therapeutic targeting of the estrogen receptor (ER) is a clinically validated approach for estrogen receptor positive breast cancer (ER+ BC), but sustained response is limited by acquired resistance. Targeting the transcriptional coactivators required for estrogen receptor activity represents an alternative approach that is not subject to the same limitations as targeting estrogen receptor itself. In this report we demonstrate that the acetyltransferase activity of coactivator paralogs CREBBP/EP300 represents a promising therapeutic target in ER+ BC. Using the potent and selective inhibitor CPI-1612, we show that CREBBP/EP300 acetyltransferase inhibition potently suppresses in vitro and in vivo growth of breast cancer cell line models and acts in a manner orthogonal to directly targeting ER. CREBBP/EP300 acetyltransferase inhibition suppresses ER-dependent transcription by targeting lineage-specific enhancers defined by the pioneer transcription factor FOXA1. These results validate CREBBP/EP300 acetyltransferase activity as a viable target for clinical development in ER+ breast cancer.</span></p>', 'date' => '2022-03-30', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/35353838/', 'doi' => '10.1371/journal.pone.0262378', 'modified' => '2022-04-12 10:56:54', 'created' => '2022-04-12 10:56:54', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 31 => array( 'id' => '4407', 'name' => 'Transient regulation of focal adhesion via Tensin3 is required fornascent oligodendrocyte differentiation', 'authors' => 'Merour E. et al.', 'description' => '<p>The differentiation of oligodendroglia from oligodendrocyte precursor cells (OPCs) to complex and extensive myelinating oligodendrocytes (OLs) is a multistep process that involves largescale morphological changes with significant strain on the cytoskeleton. While key chromatin and transcriptional regulators of differentiation have been identified, their target genes responsible for the morphological changes occurring during OL myelination are still largely unknown. Here, we show that the regulator of focal adhesion, Tensin3 (Tns3), is a direct target gene of Olig2, Chd7, and Chd8, transcriptional regulators of OL differentiation. Tns3 is transiently upregulated and localized to cell processes of immature OLs, together with integrin-β1, a key mediator of survival at this transient stage. Constitutive Tns3 loss-of-function leads to reduced viability in mouse and humans, with surviving knockout mice still expressing Tns3 in oligodendroglia. Acute deletion of Tns3 in vivo, either in postnatal neural stem cells (NSCs) or in OPCs, leads to a two-fold reduction in OL numbers. We find that the transient upregulation of Tns3 is required to protect differentiating OPCs and immature OLs from cell death by preventing the upregulation of p53, a key regulator of apoptosis. Altogether, our findings reveal a specific time window during which transcriptional upregulation of Tns3 in immature OLs is required for OL differentiation likely by mediating integrin-β1 survival signaling to the actin cytoskeleton as OL undergo the large morphological changes required for their terminal differentiation.</p>', 'date' => '2022-02-01', 'pmid' => 'https://doi.org/10.1101%2F2022.02.25.481980', 'doi' => '10.1101/2022.02.25.481980', 'modified' => '2022-08-11 15:05:41', 'created' => '2022-08-11 12:14:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 32 => array( 'id' => '4238', 'name' => 'The long noncoding RNA H19 regulates tumor plasticity inneuroendocrine prostate cancer', 'authors' => 'Singh N. et al.', 'description' => '<p>Neuroendocrine (NE) prostate cancer (NEPC) is a lethal subtype of castration-resistant prostate cancer (PCa) arising either de novo or from transdifferentiated prostate adenocarcinoma following androgen deprivation therapy (ADT). Extensive computational analysis has identified a high degree of association between the long noncoding RNA (lncRNA) H19 and NEPC, with the longest isoform highly expressed in NEPC. H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown). It contributes to treatment resistance, with the knockdown of H19 re-sensitizing PCa to ADT. It is also essential for the proliferation and invasion of NEPC. H19 levels are negatively regulated by androgen signaling via androgen receptor (AR). When androgen is absent SOX2 levels increase, driving H19 transcription and facilitating transdifferentiation. H19 facilitates the PRC2 complex in regulating methylation changes at H3K27me3/H3K4me3 histone sites of AR-driven and NEPC-related genes. Additionally, this lncRNA induces alterations in genome-wide DNA methylation on CpG sites, further regulating genes associated with the NEPC phenotype. Our clinical data identify H19 as a candidate diagnostic marker and predictive marker of NEPC with elevated H19 levels associated with an increased probability of biochemical recurrence and metastatic disease in patients receiving ADT. Here we report H19 as an early upstream regulator of cell fate, plasticity, and treatment resistance in NEPC that can reverse/transform cells to a treatable form of PCa once therapeutically deactivated.</p>', 'date' => '2021-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34934057', 'doi' => '10.1038/s41467-021-26901-9', 'modified' => '2022-05-19 17:06:50', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 33 => array( 'id' => '4239', 'name' => 'Epromoters function as a hub to recruit key transcription factorsrequired for the inflammatory response', 'authors' => 'Santiago-Algarra D. et al. ', 'description' => '<p>Gene expression is controlled by the involvement of gene-proximal (promoters) and distal (enhancers) regulatory elements. Our previous results demonstrated that a subset of gene promoters, termed Epromoters, work as bona fide enhancers and regulate distal gene expression. Here, we hypothesized that Epromoters play a key role in the coordination of rapid gene induction during the inflammatory response. Using a high-throughput reporter assay we explored the function of Epromoters in response to type I interferon. We find that clusters of IFNa-induced genes are frequently associated with Epromoters and that these regulatory elements preferentially recruit the STAT1/2 and IRF transcription factors and distally regulate the activation of interferon-response genes. Consistently, we identified and validated the involvement of Epromoter-containing clusters in the regulation of LPS-stimulated macrophages. Our findings suggest that Epromoters function as a local hub recruiting the key TFs required for coordinated regulation of gene clusters during the inflammatory response.</p>', 'date' => '2021-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34795220', 'doi' => '10.1038/s41467-021-26861-0', 'modified' => '2022-05-19 17:10:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 34 => array( 'id' => '4231', 'name' => 'Differential contribution to gene expression prediction of histonemodifications at enhancers or promoters.', 'authors' => 'González-Ramírez M. et al.', 'description' => '<p>The ChIP-seq signal of histone modifications at promoters is a good predictor of gene expression in different cellular contexts, but whether this is also true at enhancers is not clear. To address this issue, we develop quantitative models to characterize the relationship of gene expression with histone modifications at enhancers or promoters. We use embryonic stem cells (ESCs), which contain a full spectrum of active and repressed (poised) enhancers, to train predictive models. As many poised enhancers in ESCs switch towards an active state during differentiation, predictive models can also be trained on poised enhancers throughout differentiation and in development. Remarkably, we determine that histone modifications at enhancers, as well as promoters, are predictive of gene expression in ESCs and throughout differentiation and development. Importantly, we demonstrate that their contribution to the predictive models varies depending on their location in enhancers or promoters. Moreover, we use a local regression (LOESS) to normalize sequencing data from different sources, which allows us to apply predictive models trained in a specific cellular context to a different one. We conclude that the relationship between gene expression and histone modifications at enhancers is universal and different from promoters. Our study provides new insight into how histone modifications relate to gene expression based on their location in enhancers or promoters.</p>', 'date' => '2021-09-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473698/', 'doi' => '10.1371/journal.pcbi.1009368', 'modified' => '2022-05-19 16:50:59', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 35 => array( 'id' => '4315', 'name' => 'Atg7 deficiency in microglia drives an altered transcriptomic profileassociated with an impaired neuroinflammatory response', 'authors' => 'Friess L. et al.', 'description' => '<p>Microglia, resident immunocompetent cells of the central nervous system, can display a range of reaction states and thereby exhibit distinct biological functions across development, adulthood and under disease conditions. Distinct gene expression profiles are reported to define each of these microglial reaction states. Hence, the identification of modulators of selective microglial transcriptomic signature, which have the potential to regulate unique microglial function has gained interest. Here, we report the identification of ATG7 (Autophagy-related 7) as a selective modulator of an NF-κB-dependent transcriptional program controlling the pro-inflammatory response of microglia. We also uncover that microglial Atg7-deficiency was associated with reduced microglia-mediated neurotoxicity, and thus a loss of biological function associated with the pro-inflammatory microglial reactive state. Further, we show that Atg7-deficiency in microglia did not impact on their ability to respond to alternative stimulus, such as one driving them towards an anti-inflammatory/tumor supportive phenotype. The identification of distinct regulators, such as Atg7, controlling specific microglial transcriptional programs could lead to developing novel therapeutic strategies aiming to manipulate selected microglial phenotypes, instead of the whole microglial population with is associated with several pitfalls. Supplementary Information The online version contains supplementary material available at 10.1186/s13041-021-00794-7.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34082793', 'doi' => '10.1186/s13041-021-00794-7', 'modified' => '2022-08-02 16:47:13', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 36 => array( 'id' => '4349', 'name' => 'Lasp1 regulates adherens junction dynamics and fibroblast transformationin destructive arthritis', 'authors' => 'Beckmann D. et al.', 'description' => '<p>The LIM and SH3 domain protein 1 (Lasp1) was originally cloned from metastatic breast cancer and characterised as an adaptor molecule associated with tumourigenesis and cancer cell invasion. However, the regulation of Lasp1 and its function in the aggressive transformation of cells is unclear. Here we use integrative epigenomic profiling of invasive fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA) and from mouse models of the disease, to identify Lasp1 as an epigenomically co-modified region in chronic inflammatory arthritis and a functionally important binding partner of the Cadherin-11/β-Catenin complex in zipper-like cell-to-cell contacts. In vitro, loss or blocking of Lasp1 alters pathological tissue formation, migratory behaviour and platelet-derived growth factor response of arthritic FLS. In arthritic human TNF transgenic mice, deletion of Lasp1 reduces arthritic joint destruction. Therefore, we show a function of Lasp1 in cellular junction formation and inflammatory tissue remodelling and identify Lasp1 as a potential target for treating inflammatory joint disorders associated with aggressive cellular transformation.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34131132', 'doi' => '10.1038/s41467-021-23706-8', 'modified' => '2022-08-03 17:02:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 37 => array( 'id' => '4136', 'name' => 'The lncRNA and the transcription factor WRKY42 target common cell wallEXTENSIN encoding genes to trigger root hair cell elongation.', 'authors' => 'Pacheco, J. M. et al.', 'description' => '<p>Plant long noncoding RNAs (lncRNAs) are key chromatin dynamics regulators, directing the transcriptional programs driving a wide variety of developmental outputs. Recently, we uncovered how the lncRNA () directly recognizes the locus encoding the root hair (RH) master regulator () modulating its transcriptional activation and leading to low temperature-induced RH elongation. We further demonstrated that interacts with the transcription factor WRKY42 in a novel ribonucleoprotein complex shaping epigenetic environment and integrating signals governing RH growth and development. In this work, we expand this model showing that is able to bind and positively control the expression of several cell wall EXTENSIN (EXT) encoding genes, including , a key regulator for RH growth. Interestingly, emerged as a novel common target of and WRKY42. Furthermore, we showed that the ROS homeostasis-related gene is deregulated upon overexpression, likely through the RHD6-RSL4 pathway, and that is required for low temperature-dependent enhancement of RH growth. Collectively, our results uncover an intricate regulatory network involving the /WRKY42 hub in the control of master and effector genes during RH development.</p>', 'date' => '2021-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33944666', 'doi' => '10.1080/15592324.2021.1920191', 'modified' => '2021-12-13 09:06:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 38 => array( 'id' => '4143', 'name' => 'Placental uptake and metabolism of 25(OH)Vitamin D determines itsactivity within the fetoplacental unit', 'authors' => 'Ashley, B. et al.', 'description' => '<p>Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes, but the underlying mechanisms have not been elucidated. Using physiological human placental perfusion approaches and intact villous explants we demonstrate a role for the placenta in regulating the relationships between maternal 25(OH)D concentrations and fetal physiology. Here, we demonstrate active placental uptake of 25(OH)D3 by endocytosis and placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the fetal and maternal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than solely the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer, including transcriptional activation and inflammatory responses. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta; with widespread effects on the placenta itself. These data show complex and synergistic interplay between vitamin D and the placenta, and inform possible interventions to optimise placental function to better support fetal growth and the maternal adaptations to pregnancy.</p>', 'date' => '2021-05-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.01.431439', 'doi' => '10.1101/2021.03.01.431439', 'modified' => '2021-12-13 09:29:25', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 39 => array( 'id' => '4147', 'name' => 'Waves of sumoylation support transcription dynamics during adipocytedifferentiation', 'authors' => 'Zhao, X. et al.', 'description' => '<p>Tight control of gene expression networks required for adipose tissue formation and plasticity is essential for adaptation to energy needs and environmental cues. However, little is known about the mechanisms that orchestrate the dramatic transcriptional changes leading to adipocyte differentiation. We investigated the regulation of nascent transcription by the sumoylation pathway during adipocyte differentiation using SLAMseq and ChIPseq. We discovered that the sumoylation pathway has a dual function in differentiation; it supports the initial downregulation of pre-adipocyte-specific genes, while it promotes the establishment of the mature adipocyte transcriptional program. By characterizing sumoylome dynamics in differentiating adipocytes by mass spectrometry, we found that sumoylation of specific transcription factors like Pparγ/RXR and their co-factors is associated with the transcription of adipogenic genes. Our data demonstrate that the sumoylation pathway coordinates the rewiring of transcriptional networks required for formation of functional adipocytes. This study also provides an in-depth resource of gene transcription dynamics, SUMO-regulated genes and sumoylation sites during adipogenesis.</p>', 'date' => '2021-04-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.20.432084', 'doi' => '10.1101/2021.02.20.432084', 'modified' => '2021-12-14 09:23:28', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 40 => array( 'id' => '4171', 'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.', 'authors' => 'Ryan, Genevieve E. et al.', 'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse LβT2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733', 'doi' => '10.1016/j.mce.2021.111286', 'modified' => '2021-12-21 15:57:35', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 41 => array( 'id' => '4181', 'name' => 'Genetic perturbation of PU.1 binding and chromatin looping at neutrophilenhancers associates with autoimmune disease.', 'authors' => 'Watt, Stephen et al.', 'description' => '<p>Neutrophils play fundamental roles in innate immune response, shape adaptive immunity, and are a potentially causal cell type underpinning genetic associations with immune system traits and diseases. Here, we profile the binding of myeloid master regulator PU.1 in primary neutrophils across nearly a hundred volunteers. We show that variants associated with differential PU.1 binding underlie genetically-driven differences in cell count and susceptibility to autoimmune and inflammatory diseases. We integrate these results with other multi-individual genomic readouts, revealing coordinated effects of PU.1 binding variants on the local chromatin state, enhancer-promoter contacts and downstream gene expression, and providing a functional interpretation for 27 genes underlying immune traits. Collectively, these results demonstrate the functional role of PU.1 and its target enhancers in neutrophil transcriptional control and immune disease susceptibility.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863903', 'doi' => '10.1038/s41467-021-22548-8', 'modified' => '2021-12-21 16:50:30', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 42 => array( 'id' => '4126', 'name' => 'Fra-1 regulates its target genes via binding to remote enhancers withoutexerting major control on chromatin architecture in triple negative breastcancers.', 'authors' => 'Bejjani, Fabienne and Tolza, Claire and Boulanger, Mathias and Downes,Damien and Romero, Raphaël and Maqbool, Muhammad Ahmad and Zine ElAabidine, Amal and Andrau, Jean-Christophe and Lebre, Sophie and Brehelin,Laurent and Parrinello, Hughes and Rohmer,', 'description' => '<p>The ubiquitous family of dimeric transcription factors AP-1 is made up of Fos and Jun family proteins. It has long been thought to operate principally at gene promoters and how it controls transcription is still ill-understood. The Fos family protein Fra-1 is overexpressed in triple negative breast cancers (TNBCs) where it contributes to tumor aggressiveness. To address its transcriptional actions in TNBCs, we combined transcriptomics, ChIP-seqs, machine learning and NG Capture-C. Additionally, we studied its Fos family kin Fra-2 also expressed in TNBCs, albeit much less. Consistently with their pleiotropic effects, Fra-1 and Fra-2 up- and downregulate individually, together or redundantly many genes associated with a wide range of biological processes. Target gene regulation is principally due to binding of Fra-1 and Fra-2 at regulatory elements located distantly from cognate promoters where Fra-1 modulates the recruitment of the transcriptional co-regulator p300/CBP and where differences in AP-1 variant motif recognition can underlie preferential Fra-1- or Fra-2 bindings. Our work also shows no major role for Fra-1 in chromatin architecture control at target gene loci, but suggests collaboration between Fra-1-bound and -unbound enhancers within chromatin hubs sometimes including promoters for other Fra-1-regulated genes. Our work impacts our view of AP-1.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33533919', 'doi' => '10.1093/nar/gkab053', 'modified' => '2021-12-07 10:09:23', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 43 => array( 'id' => '4139', 'name' => 'Cell-specific alterations inPitx1regulatory landscape activation caused bythe loss of a single enhancer', 'authors' => 'Rouco, R. et al.', 'description' => '<p>Most developmental genes rely on multiple transcriptional enhancers for their accurate expression during embryogenesis. Because enhancers may have partially redundant activities, the loss of one of them often leads to a partial loss of gene expression and concurrent moderate phenotypic outcome, if any. While such a phenomenon has been observed in many instances, the nature of the underlying mechanisms remains elusive. We used the Pitx1 testbed locus to characterize in detail the regulatory and cellular identity alterations following the deletion in vivo of one of its enhancers (Pen), which normally accounts for 30 percent of Pitx1 expression in hindlimb buds. By combining single cell transcriptomics and a novel in embryo cell tracing approach, we observed that this global decrease in Pitx1 expression results from both an increase in the number of non- or low-expressing cells, and a decrease in the number of high-expressing cells. We found that the over-representation of Pitx1 non/low-expressing cells originates from a failure of the Pitx1 locus to coordinate enhancer activities and 3D chromatin changes. The resulting increase in Pitx1 non/low-expressing cells eventually affects the proximal limb more severely than the distal limb, leading to a clubfoot phenotype likely produced through a localized heterochrony and concurrent loss of irregular connective tissue. This data suggests that, in some cases, redundant enhancers may be used to locally enforce a robust activation of their host regulatory landscapes.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.10.434611', 'doi' => '10.1101/2021.03.10.434611', 'modified' => '2021-12-13 09:18:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 44 => array( 'id' => '4141', 'name' => 'Transgenic mice for in vivo epigenome editing with CRISPR-based systems', 'authors' => 'Gemberling, M. et al.', 'description' => '<p>The discovery, characterization, and adaptation of the RNA-guided clustered regularly interspersed short palindromic repeat (CRISPR)-Cas9 system has greatly increased the ease with which genome and epigenome editing can be performed. Fusion of chromatin-modifying domains to the nuclease-deactivated form of Cas9 (dCas9) has enabled targeted gene activation or repression in both cultured cells and in vivo in animal models. However, delivery of the large dCas9 fusion proteins to target cell types and tissues is an obstacle to widespread adoption of these tools for in vivo studies. Here we describe the generation and validation of two conditional transgenic mouse lines for targeted gene regulation, Rosa26:LSL-dCas9-p300 for gene activation and Rosa26:LSL-dCas9-KRAB for gene repression. Using the dCas9p300 and dCas9KRAB transgenic mice we demonstrate activation or repression of genes in both the brain and liver in vivo, and T cells and fibroblasts ex vivo. We show gene regulation and targeted epigenetic modification with gRNAs targeting either transcriptional start sites (TSS) or distal enhancer elements, as well as corresponding changes to downstream phenotypes. These mouse lines are convenient and valuable tools for facile, temporally controlled, and tissue-restricted epigenome editing and manipulation of gene expression in vivo.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.08.434430', 'doi' => '10.1101/2021.03.08.434430', 'modified' => '2021-12-13 09:23:10', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 45 => array( 'id' => '4163', 'name' => 'Transcriptional programming drives Ibrutinib-resistance evolution in mantlecell lymphoma.', 'authors' => 'Zhao, Xiaohong et al.', 'description' => '<p>Ibrutinib, a bruton's tyrosine kinase (BTK) inhibitor, provokes robust clinical responses in aggressive mantle cell lymphoma (MCL), yet many patients relapse with lethal Ibrutinib-resistant (IR) disease. Here, using genomic, chemical proteomic, and drug screen profiling, we report that enhancer remodeling-mediated transcriptional activation and adaptive signaling changes drive the aggressive phenotypes of IR. Accordingly, IR MCL cells are vulnerable to inhibitors of the transcriptional machinery and especially so to inhibitors of cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the positive transcription elongation factor b (P-TEFb) of RNA polymerase II (RNAPII). Further, CDK9 inhibition disables reprogrammed signaling circuits and prevents the emergence of IR in MCL. Finally, and importantly, we find that a robust and facile ex vivo image-based functional drug screening platform can predict clinical therapeutic responses of IR MCL and identify vulnerabilities that can be targeted to disable the evolution of IR.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33730585', 'doi' => '10.1016/j.celrep.2021.108870', 'modified' => '2021-12-21 15:28:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 46 => array( 'id' => '4119', 'name' => 'Coordinated changes in gene expression, H1 variant distribution and genome3D conformation in response to H1 depletion', 'authors' => 'Serna-Pujol, Nuria and Salinas-Pena, Monica and Mugianesi, Francesca and LeDily, François and Marti-Renom, Marc A. and Jordan, Albert', 'description' => '<p>Up to seven members of the histone H1 family may contribute to chromatin compaction and its regulation in human somatic cells. In breast cancer cells, knock-down of multiple H1 variants deregulates many genes, promotes the appearance of genome-wide accessibility sites and triggers an interferon response via activation of heterochromatic repeats. However, how these changes in the expression profile relate to the re-distribution of H1 variants as well as to genome conformational changes have not been yet studied. Here, we combined ChIP-seq of five endogenous H1 variants with Chromosome Conformation Capture analysis in wild-type and H1 knock-down T47D cells. The results indicate that H1 variants coexist in the genome in two large groups depending on the local DNA GC content and that their distribution is robust with respect to multiple H1 depletion. Despite the small changes in H1 variants distribution, knock-down of H1 translated into more isolated but de-compacted chromatin structures at the scale of Topologically Associating Domains or TADs. Such changes in TAD structure correlated with a coordinated gene expression response of their resident genes. This is the first report describing simultaneous profiling of five endogenous H1 variants within a cell line and giving functional evidence of genome topology alterations upon H1 depletion in human cancer cells.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.12.429879', 'doi' => '10.1101/2021.02.12.429879', 'modified' => '2021-12-07 09:43:11', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 47 => array( 'id' => '4144', 'name' => 'REPROGRAMMING CBX8-PRC1 FUNCTION WITH A POSITIVE ALLOSTERICMODULATOR', 'authors' => 'Suh, J. L. et al.', 'description' => '<p>Canonical targeting of Polycomb Repressive Complex 1 (PRC1) to repress developmental genes is mediated by cell type-specific, paralogous chromobox (CBX) proteins (CBX2, 4, 6, 7 and 8). Based on their central role in silencing and their misregulation associated with human disease including cancer, CBX proteins are attractive targets for small molecule chemical probe development. Here, we have used a quantitative and target-specific cellular assay to discover a potent positive allosteric modulator (PAM) of CBX8. The PAM activity of UNC7040 antagonizes H3K27me3 binding by CBX8 while increasing interactions with nucleic acids and participation in variant PRC1. We show that treatment with UNC7040 leads to efficient PRC1 chromatin eviction, loss of silencing and reduced proliferation across different cancer cell lines. Our discovery and characterization of UNC7040 not only revealed the most cellularly potent CBX8-specific chemical probe to date, but also corroborates a mechanism of polycomb regulation by non-histone lysine methylated interaction partners.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.23.432388', 'doi' => '10.1101/2021.02.23.432388', 'modified' => '2021-12-13 09:35:04', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 48 => array( 'id' => '4145', 'name' => 'Germline activity of the heat shock factor HSF-1 programs theinsulin-receptor daf-2 in C. elegans', 'authors' => 'Das, S. et al.', 'description' => '<p>The mechanisms by which maternal stress alters offspring phenotypes remain poorly understood. Here we report that the heat shock transcription factor HSF-1, activated in the C. elegans maternal germline upon stress, epigenetically programs the insulin-like receptor daf-2 by increasing repressive H3K9me2 levels throughout the daf-2 gene. This increase occurs by the recruitment of the C. elegans SETDB1 homolog MET-2 by HSF-1. Increased H3K9me2 levels at daf-2 persist in offspring to downregulate daf-2, activate the C. elegans FOXO ortholog DAF-16 and enhance offspring stress resilience. Thus, HSF-1 activity in the mother promotes the early life programming of the insulin/IGF-1 signaling (IIS) pathway and determines the strategy of stress resilience in progeny.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.22.432344', 'doi' => '10.1101/2021.02.22.432344', 'modified' => '2021-12-14 09:13:54', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 49 => array( 'id' => '4151', 'name' => 'The epigenetic landscape in purified myonuclei from fast and slow muscles', 'authors' => 'Bengtsen, M. et al.', 'description' => '<p>Muscle cells have different phenotypes adapted to different usage and can be grossly divided into fast/glycolytic and slow/oxidative types. While most muscles contain a mixture of such fiber types, we aimed at providing a genome-wide analysis of chromatin environment by ChIP-Seq in two muscle extremes, the almost completely fast/glycolytic extensor digitorum longus (EDL) and slow/oxidative soleus muscles. Muscle is a heterogeneous tissue where less than 60\% of the nuclei are inside muscle fibers. Since cellular homogeneity is critical in epigenome-wide association studies we devised a new method for purifying skeletal muscle nuclei from whole tissue based on the nuclear envelope protein Pericentriolar material 1 (PCM1) being a specific marker for myonuclei. Using antibody labeling and a magnetic-assisted sorting approach we were able to sort out myonuclei with 95\% purity. The sorting eliminated influence from other cell types in the tissue and improved the myo-specific signal. A genome-wide comparison of the epigenetic landscape in EDL and soleus reflected the functional properties of the two muscles each with a distinct regulatory program involving distal enhancers, including a glycolytic super-enhancer in the EDL. The two muscles are also regulated by different sets of transcription factors; e.g. in soleus binding sites for MEF2C, NFATC2 and PPARA were enriched, while in EDL MYOD1 and SOX1 binding sites were found to be overrepresented. In addition, novel factors for muscle regulation such as MAF, ZFX and ZBTB14 were identified.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.04.429545', 'doi' => '10.1101/2021.02.04.429545', 'modified' => '2021-12-14 09:40:02', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 50 => array( 'id' => '4166', 'name' => 'The glucocorticoid receptor recruits the COMPASS complex to regulateinflammatory transcription at macrophage enhancers.', 'authors' => 'Greulich, Franziska et al.', 'description' => '<p>Glucocorticoids (GCs) are effective anti-inflammatory drugs; yet, their mechanisms of action are poorly understood. GCs bind to the glucocorticoid receptor (GR), a ligand-gated transcription factor controlling gene expression in numerous cell types. Here, we characterize GR's protein interactome and find the SETD1A (SET domain containing 1A)/COMPASS (complex of proteins associated with Set1) histone H3 lysine 4 (H3K4) methyltransferase complex highly enriched in activated mouse macrophages. We show that SETD1A/COMPASS is recruited by GR to specific cis-regulatory elements, coinciding with H3K4 methylation dynamics at subsets of sites, upon treatment with lipopolysaccharide (LPS) and GCs. By chromatin immunoprecipitation sequencing (ChIP-seq) and RNA-seq, we identify subsets of GR target loci that display SETD1A occupancy, H3K4 mono-, di-, or tri-methylation patterns, and transcriptional changes. However, our data on methylation status and COMPASS recruitment suggest that SETD1A has additional transcriptional functions. Setd1a loss-of-function studies reveal that SETD1A/COMPASS is required for GR-controlled transcription of subsets of macrophage target genes. We demonstrate that the SETD1A/COMPASS complex cooperates with GR to mediate anti-inflammatory effects.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33567280', 'doi' => '10.1016/j.celrep.2021.108742', 'modified' => '2021-12-21 15:42:49', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 51 => array( 'id' => '4185', 'name' => 'A distinct metabolic response characterizes sensitivity to EZH2inhibition in multiple myeloma.', 'authors' => 'Nylund P. et al.', 'description' => '<p>Multiple myeloma (MM) is a heterogeneous haematological disease that remains clinically challenging. Increased activity of the epigenetic silencer EZH2 is a common feature in patients with poor prognosis. Previous findings have demonstrated that metabolic profiles can be sensitive markers for response to treatment in cancer. While EZH2 inhibition (EZH2i) has proven efficient in inducing cell death in a number of human MM cell lines, we hereby identified a subset of cell lines that despite a global loss of H3K27me3, remains viable after EZH2i. By coupling liquid chromatography-mass spectrometry with gene and miRNA expression profiling, we found that sensitivity to EZH2i correlated with distinct metabolic signatures resulting from a dysregulation of genes involved in methionine cycling. Specifically, EZH2i resulted in a miRNA-mediated downregulation of methionine cycling-associated genes in responsive cells. This induced metabolite accumulation and DNA damage, leading to G2 arrest and apoptosis. Altogether, we unveiled that sensitivity to EZH2i in human MM cell lines is associated with a specific metabolic and gene expression profile post-treatment.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33579905', 'doi' => '10.1038/s41419-021-03447-8', 'modified' => '2022-01-05 14:59:39', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 52 => array( 'id' => '4108', 'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma', 'authors' => 'Laubscher et. al.', 'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that </span><em>SMARCA4</em><span><span> </span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span> </span></span><em>de novo</em><span><span> </span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>', 'date' => '2021-01-07', 'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1', 'doi' => ' 10.21203/rs.3.rs-131009/v1', 'modified' => '2021-07-07 11:52:23', 'created' => '2021-07-07 06:38:34', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 53 => array( 'id' => '4098', 'name' => 'A Tumor Suppressor Enhancer of PTEN in T-cell development and leukemia', 'authors' => 'L. Tottone at al.', 'description' => '<p>Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss of expression of PTEN is associated with the pathogenesis of various cancers, including T-cell leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts with the <em>PTEN</em> promoter in multiple hematopoietic populations, including T-cells, and acts as a hub of relevant transcription factors in T-ALL. Consistently, loss of PE leads to reduced <em>PTEN</em> levels in T-ALL cells. Moreover, PE-null mice show reduced <em>Pten</em> levels in thymocytes and accelerated development of NOTCH1-induced T-ALL. Furthermore, secondary loss of PE in established leukemias leads to accelerated progression and a gene expression signature driven by <em>Pten</em> loss. Finally, we uncovered recurrent deletions encompassing PE in T-ALL, which are associated with decreased <em>PTEN</em> levels. Altogether, our results identify PE as the first long-range tumor suppressor enhancer directly implicated in cancer.</p>', 'date' => '2021-01-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33458694/', 'doi' => '10.1158/2643-3230.BCD-20-0201 ', 'modified' => '2021-05-04 09:51:10', 'created' => '2021-05-04 09:51:10', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 54 => array( 'id' => '4157', 'name' => 'Stronger induction of trained immunity by mucosal BCG or MTBVAC vaccination compared to standard intradermal vaccination.', 'authors' => 'Vierboom, M.P.M. et al. ', 'description' => '<p>BCG vaccination can strengthen protection against pathogens through the induction of epigenetic and metabolic reprogramming of innate immune cells, a process called trained immunity. We and others recently demonstrated that mucosal or intravenous BCG better protects rhesus macaques from infection and TB disease than standard intradermal vaccination, correlating with local adaptive immune signatures. In line with prior mouse data, here, we show in rhesus macaques that intravenous BCG enhances innate cytokine production associated with changes in H3K27 acetylation typical of trained immunity. Alternative delivery of BCG does not alter the cytokine production of unfractionated bronchial lavage cells. However, mucosal but not intradermal vaccination, either with BCG or the -derived candidate MTBVAC, enhances innate cytokine production by blood- and bone marrow-derived monocytes associated with metabolic rewiring, typical of trained immunity. These results provide support to strategies for improving TB vaccination and, more broadly, modulating innate immunity via mucosal surfaces.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33521699', 'doi' => '10.1016/j.xcrm.2020.100185', 'modified' => '2021-12-16 10:50:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 55 => array( 'id' => '4193', 'name' => 'Postoperative abdominal sepsis induces selective and persistent changes inCTCF binding within the MHC-II region of human monocytes.', 'authors' => 'Siegler B. et al.', 'description' => '<p>BACKGROUND: Postoperative abdominal infections belong to the most common triggers of sepsis and septic shock in intensive care units worldwide. While monocytes play a central role in mediating the initial host response to infections, sepsis-induced immune dysregulation is characterized by a defective antigen presentation to T-cells via loss of Major Histocompatibility Complex Class II DR (HLA-DR) surface expression. Here, we hypothesized a sepsis-induced differential occupancy of the CCCTC-Binding Factor (CTCF), an architectural protein and superordinate regulator of transcription, inside the Major Histocompatibility Complex Class II (MHC-II) region in patients with postoperative sepsis, contributing to an altered monocytic transcriptional response during critical illness. RESULTS: Compared to a matched surgical control cohort, postoperative sepsis was associated with selective and enduring increase in CTCF binding within the MHC-II. In detail, increased CTCF binding was detected at four sites adjacent to classical HLA class II genes coding for proteins expressed on monocyte surface. Gene expression analysis revealed a sepsis-associated decreased transcription of (i) the classical HLA genes HLA-DRA, HLA-DRB1, HLA-DPA1 and HLA-DPB1 and (ii) the gene of the MHC-II master regulator, CIITA (Class II Major Histocompatibility Complex Transactivator). Increased CTCF binding persisted in all sepsis patients, while transcriptional recovery CIITA was exclusively found in long-term survivors. CONCLUSION: Our experiments demonstrate differential and persisting alterations of CTCF occupancy within the MHC-II, accompanied by selective changes in the expression of spatially related HLA class II genes, indicating an important role of CTCF in modulating the transcriptional response of immunocompromised human monocytes during critical illness.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33939725', 'doi' => '10.1371/journal.pone.0250818', 'modified' => '2022-01-06 14:22:15', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 56 => array( 'id' => '4204', 'name' => 'S-adenosyl-l-homocysteine hydrolase links methionine metabolism to thecircadian clock and chromatin remodeling.', 'authors' => 'Greco C. M. et al. ', 'description' => '<p>Circadian gene expression driven by transcription activators CLOCK and BMAL1 is intimately associated with dynamic chromatin remodeling. However, how cellular metabolism directs circadian chromatin remodeling is virtually unexplored. We report that the S-adenosylhomocysteine (SAH) hydrolyzing enzyme adenosylhomocysteinase (AHCY) cyclically associates to CLOCK-BMAL1 at chromatin sites and promotes circadian transcriptional activity. SAH is a potent feedback inhibitor of S-adenosylmethionine (SAM)-dependent methyltransferases, and timely hydrolysis of SAH by AHCY is critical to sustain methylation reactions. We show that AHCY is essential for cyclic H3K4 trimethylation, genome-wide recruitment of BMAL1 to chromatin, and subsequent circadian transcription. Depletion or targeted pharmacological inhibition of AHCY in mammalian cells markedly decreases the amplitude of circadian gene expression. In mice, pharmacological inhibition of AHCY in the hypothalamus alters circadian locomotor activity and rhythmic transcription within the suprachiasmatic nucleus. These results reveal a previously unappreciated connection between cellular metabolism, chromatin dynamics, and circadian regulation.</p>', 'date' => '2020-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33328229', 'doi' => '10.1126/sciadv.abc5629', 'modified' => '2022-01-06 14:59:48', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 57 => array( 'id' => '4040', 'name' => 'Genomic profiling of T-cell activation suggests increased sensitivity ofmemory T cells to CD28 costimulation.', 'authors' => 'Glinos, Dafni A and Soskic, Blagoje and Williams, Cayman and Kennedy, Alanand Jostins, Luke and Sansom, David M and Trynka, Gosia', 'description' => '<p>T-cell activation is a critical driver of immune responses. The CD28 costimulation is an essential regulator of CD4 T-cell responses, however, its relative importance in naive and memory T cells is not fully understood. Using different model systems, we observe that human memory T cells are more sensitive to CD28 costimulation than naive T cells. To deconvolute how the T-cell receptor (TCR) and CD28 orchestrate activation of human T cells, we stimulate cells using varying intensities of TCR and CD28 and profiled gene expression. We show that genes involved in cell cycle progression and division are CD28-driven in memory cells, but under TCR control in naive cells. We further demonstrate that T-helper differentiation and cytokine expression are controlled by CD28. Using chromatin accessibility profiling, we observe that AP1 transcriptional regulation is enriched when both TCR and CD28 are engaged, whereas open chromatin near CD28-sensitive genes is enriched for NF-kB motifs. Lastly, we show that CD28-sensitive genes are enriched in GWAS regions associated with immune diseases, implicating a role for CD28 in disease development. Our study provides important insights into the differential role of costimulation in naive and memory T-cell responses and disease susceptibility.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33223527', 'doi' => '10.1038/s41435-020-00118-0', 'modified' => '2021-02-19 12:08:04', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 58 => array( 'id' => '4060', 'name' => 'A genetic variant controls interferon-β gene expression in human myeloidcells by preventing C/EBP-β binding on a conserved enhancer.', 'authors' => 'Assouvie, Anaïs and Rotival, Maxime and Hamroune, Juliette and Busso,Didier and Romeo, Paul-Henri and Quintana-Murci, Lluis and Rousselet,Germain', 'description' => '<p>Interferon β (IFN-β) is a cytokine that induces a global antiviral proteome, and regulates the adaptive immune response to infections and tumors. Its effects strongly depend on its level and timing of expression. Therefore, the transcription of its coding gene IFNB1 is strictly controlled. We have previously shown that in mice, the TRIM33 protein restrains Ifnb1 transcription in activated myeloid cells through an upstream inhibitory sequence called ICE. Here, we show that the deregulation of Ifnb1 expression observed in murine Trim33-/- macrophages correlates with abnormal looping of both ICE and the Ifnb1 gene to a 100 kb downstream region overlapping the Ptplad2/Hacd4 gene. This region is a predicted myeloid super-enhancer in which we could characterize 3 myeloid-specific active enhancers, one of which (E5) increases the response of the Ifnb1 promoter to activation. In humans, the orthologous region contains several single nucleotide polymorphisms (SNPs) known to be associated with decreased expression of IFNB1 in activated monocytes, and loops to the IFNB1 gene. The strongest association is found for the rs12553564 SNP, located in the E5 orthologous region. The minor allele of rs12553564 disrupts a conserved C/EBP-β binding motif, prevents binding of C/EBP-β, and abolishes the activation-induced enhancer activity of E5. Altogether, these results establish a link between a genetic variant preventing binding of a transcription factor and a higher order phenotype, and suggest that the frequent minor allele (around 30\% worldwide) might be associated with phenotypes regulated by IFN-β expression in myeloid cells.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147208', 'doi' => '10.1371/journal.pgen.1009090', 'modified' => '2021-02-19 17:29:34', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 59 => array( 'id' => '4084', 'name' => 'BCG Vaccination Induces Long-Term Functional Reprogramming of HumanNeutrophils.', 'authors' => 'Moorlag, Simone J C F M and Rodriguez-Rosales, Yessica Alina and Gillard,Joshua and Fanucchi, Stephanie and Theunissen, Kate and Novakovic, Borisand de Bont, Cynthia M and Negishi, Yutaka and Fok, Ezio T and Kalafati,Lydia and Verginis, Panayotis and M', 'description' => '<p>The tuberculosis vaccine bacillus Calmette-Guérin (BCG) protects against some heterologous infections, probably via induction of non-specific innate immune memory in monocytes and natural killer (NK) cells, a process known as trained immunity. Recent studies have revealed that the induction of trained immunity is associated with a bias toward granulopoiesis in bone marrow hematopoietic progenitor cells, but it is unknown whether BCG vaccination also leads to functional reprogramming of mature neutrophils. Here, we show that BCG vaccination of healthy humans induces long-lasting changes in neutrophil phenotype, characterized by increased expression of activation markers and antimicrobial function. The enhanced function of human neutrophils persists for at least 3 months after vaccination and is associated with genome-wide epigenetic modifications in trimethylation at histone 3 lysine 4. Functional reprogramming of neutrophils by the induction of trained immunity might offer novel therapeutic strategies in clinical conditions that could benefit from modulation of neutrophil effector function.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33207187', 'doi' => '10.1016/j.celrep.2020.108387', 'modified' => '2021-03-15 17:07:29', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 60 => array( 'id' => '4086', 'name' => 'Macrophage Immune Memory Controls Endometriosis in Mice and Humans.', 'authors' => 'Jeljeli, Mohamed and Riccio, Luiza G C and Chouzenoux, Sandrine and Moresi,Fabiana and Toullec, Laurie and Doridot, Ludivine and Nicco, Carole andBourdon, Mathilde and Marcellin, Louis and Santulli, Pietro and Abrão,Mauricio S and Chapron, Charles and ', 'description' => '<p>Endometriosis is a frequent, chronic, inflammatory gynecological disease characterized by the presence of ectopic endometrial tissue causing pain and infertility. Macrophages have a central role in lesion establishment and maintenance by driving chronic inflammation and tissue remodeling. Macrophages can be reprogrammed to acquire memory-like characteristics after antigenic challenge to reinforce or inhibit a subsequent immune response, a phenomenon termed "trained immunity." Here, whereas bacille Calmette-Guérin (BCG) training enhances the lesion growth in a mice model of endometriosis, tolerization with repeated low doses of lipopolysaccharide (LPS) or adoptive transfer of LPS-tolerized macrophages elicits a suppressor effect. LPS-tolerized human macrophages mitigate the fibro-inflammatory phenotype of endometriotic cells in an interleukin-10 (IL-10)-dependent manner. A history of severe Gram-negative infection is associated with reduced infertility duration and alleviated symptoms, in contrast to patients with Gram-positive infection history. Thus, the manipulation of innate immune memory may be effective in dampening hyper-inflammatory conditions, opening the way to promising therapeutic approaches.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147452', 'doi' => '10.1016/j.celrep.2020.108325', 'modified' => '2021-03-15 17:14:08', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 61 => array( 'id' => '4050', 'name' => 'UTX/KDM6A suppresses AP-1 and a gliogenesis program during neuraldifferentiation of human pluripotent stem cells.', 'authors' => 'Xu, Beisi and Mulvey, Brett and Salie, Muneeb and Yang, Xiaoyang andMatsui, Yurika and Nityanandam, Anjana and Fan, Yiping and Peng, Jamy C', 'description' => '<p>BACKGROUND: UTX/KDM6A is known to interact and influence multiple different chromatin modifiers to promote an open chromatin environment to facilitate gene activation, but its molecular activities in developmental gene regulation remain unclear. RESULTS: We report that in human neural stem cells, UTX binding correlates with both promotion and suppression of gene expression. These activities enable UTX to modulate neural stem cell self-renewal, promote neurogenesis, and suppress gliogenesis. In neural stem cells, UTX has a less influence over histone H3 lysine 27 and lysine 4 methylation but more predominantly affects histone H3 lysine 27 acetylation and chromatin accessibility. Furthermore, UTX suppresses components of AP-1 and, in turn, a gliogenesis program. CONCLUSIONS: Our findings revealed that UTX coordinates dualistic gene regulation to govern neural stem cell properties and neurogenesis-gliogenesis switch.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32977832', 'doi' => '10.1186/s13072-020-00359-3', 'modified' => '2021-02-19 14:46:42', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 62 => array( 'id' => '4091', 'name' => 'Epigenetic regulation of the lineage specificity of primary human dermallymphatic and blood vascular endothelial cells.', 'authors' => 'Tacconi, Carlotta and He, Yuliang and Ducoli, Luca and Detmar, Michael', 'description' => '<p>Lymphatic and blood vascular endothelial cells (ECs) share several molecular and developmental features. However, these two cell types possess distinct phenotypic signatures, reflecting their different biological functions. Despite significant advances in elucidating how the specification of lymphatic and blood vascular ECs is regulated at the transcriptional level during development, the key molecular mechanisms governing their lineage identity under physiological or pathological conditions remain poorly understood. To explore the epigenomic signatures in the maintenance of EC lineage specificity, we compared the transcriptomic landscapes, histone composition (H3K4me3 and H3K27me3) and DNA methylomes of cultured matched human primary dermal lymphatic and blood vascular ECs. Our findings reveal that blood vascular lineage genes manifest a more 'repressed' histone composition in lymphatic ECs, whereas DNA methylation at promoters is less linked to the differential transcriptomes of lymphatic versus blood vascular ECs. Meta-analyses identified two transcriptional regulators, BCL6 and MEF2C, which potentially govern endothelial lineage specificity. Notably, the blood vascular endothelial lineage markers CD34, ESAM and FLT1 and the lymphatic endothelial lineage markers PROX1, PDPN and FLT4 exhibited highly differential epigenetic profiles and responded in distinct manners to epigenetic drug treatments. The perturbation of histone and DNA methylation selectively promoted the expression of blood vascular endothelial markers in lymphatic endothelial cells, but not vice versa. Overall, our study reveals that the fine regulation of lymphatic and blood vascular endothelial transcriptomes is maintained via several epigenetic mechanisms, which are crucial to the maintenance of endothelial cell identity.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32918672', 'doi' => '10.1007/s10456-020-09743-9', 'modified' => '2021-03-17 17:09:36', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 63 => array( 'id' => '4010', 'name' => 'Combined treatment with CBP and BET inhibitors reverses inadvertentactivation of detrimental super enhancer programs in DIPG cells.', 'authors' => 'Wiese, M and Hamdan, FH and Kubiak, K and Diederichs, C and Gielen, GHand Nussbaumer, G and Carcaboso, AM and Hulleman, E and Johnsen, SA andKramm, CM', 'description' => '<p>Diffuse intrinsic pontine gliomas (DIPG) are the most aggressive brain tumors in children with 5-year survival rates of only 2%. About 85% of all DIPG are characterized by a lysine-to-methionine substitution in histone 3, which leads to global H3K27 hypomethylation accompanied by H3K27 hyperacetylation. Hyperacetylation in DIPG favors the action of the Bromodomain and Extra-Terminal (BET) protein BRD4, and leads to the reprogramming of the enhancer landscape contributing to the activation of DIPG super enhancer-driven oncogenes. The activity of the acetyltransferase CREB-binding protein (CBP) is enhanced by BRD4 and associated with acetylation of nucleosomes at super enhancers (SE). In addition, CBP contributes to transcriptional activation through its function as a scaffold and protein bridge. Monotherapy with either a CBP (ICG-001) or BET inhibitor (JQ1) led to the reduction of tumor-related characteristics. Interestingly, combined treatment induced strong cytotoxic effects in H3.3K27M-mutated DIPG cell lines. RNA sequencing and chromatin immunoprecipitation revealed that these effects were caused by the inactivation of DIPG SE-controlled tumor-related genes. However, single treatment with ICG-001 or JQ1, respectively, led to activation of a subgroup of detrimental super enhancers. Combinatorial treatment reversed the inadvertent activation of these super enhancers and rescued the effect of ICG-001 and JQ1 single treatment on enhancer-driven oncogenes in H3K27M-mutated DIPG, but not in H3 wild-type pedHGG cells. In conclusion, combinatorial treatment with CBP and BET inhibitors is highly efficient in H3K27M-mutant DIPG due to reversal of inadvertent activation of detrimental SE programs in comparison with monotherapy.</p>', 'date' => '2020-08-21', 'pmid' => 'http://www.pubmed.gov/32826850', 'doi' => '10.1038/s41419-020-02800-7', 'modified' => '2020-12-18 13:25:09', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 64 => array( 'id' => '4028', 'name' => 'Methylation in pericytes after acute injury promotes chronic kidneydisease.', 'authors' => 'Chou, YH and Pan, SY and Shao, YH and Shih, HM and Wei, SY andLai, CF and Chiang, WC and Schrimpf, C and Yang, KC and Lai, LC andChen, YM and Chu, TS and Lin, SL', 'description' => '<p>The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury-induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-β1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD.</p>', 'date' => '2020-08-04', 'pmid' => 'http://www.pubmed.gov/32749240', 'doi' => '10.1172/JCI135773.', 'modified' => '2020-12-18 13:25:55', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 65 => array( 'id' => '4011', 'name' => 'Exploring the virulence gene interactome with CRISPR/dCas9 in the humanmalaria parasite.', 'authors' => 'Bryant, JM and Baumgarten, S and Dingli, F and Loew, D and Sinha, A andClaës, A and Preiser, PR and Dedon, PC and Scherf, A', 'description' => '<p>Mutually exclusive expression of the var multigene family is key to immune evasion and pathogenesis in Plasmodium falciparum, but few factors have been shown to play a direct role. We adapted a CRISPR-based proteomics approach to identify novel factors associated with var genes in their natural chromatin context. Catalytically inactive Cas9 ("dCas9") was targeted to var gene regulatory elements, immunoprecipitated, and analyzed with mass spectrometry. Known and novel factors were enriched including structural proteins, DNA helicases, and chromatin remodelers. Functional characterization of PfISWI, an evolutionarily divergent putative chromatin remodeler enriched at the var gene promoter, revealed a role in transcriptional activation. Proteomics of PfISWI identified several proteins enriched at the var gene promoter such as acetyl-CoA synthetase, a putative MORC protein, and an ApiAP2 transcription factor. These findings validate the CRISPR/dCas9 proteomics method and define a new var gene-associated chromatin complex. This study establishes a tool for targeted chromatin purification of unaltered genomic loci and identifies novel chromatin-associated factors potentially involved in transcriptional control and/or chromatin organization of virulence genes in the human malaria parasite.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32816370', 'doi' => 'https://dx.doi.org/10.15252%2Fmsb.20209569', 'modified' => '2020-12-18 13:26:33', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 66 => array( 'id' => '4019', 'name' => 'Targeted bisulfite sequencing for biomarker discovery.', 'authors' => 'Morselli, M and Farrell, C and Rubbi, L and Fehling, HL and Henkhaus, Rand Pellegrini, M', 'description' => '<p>Cytosine methylation is one of the best studied epigenetic modifications. In mammals, DNA methylation patterns vary among cells and is mainly found in the CpG context. DNA methylation is involved in important processes during development and differentiation and its dysregulation can lead to or is associated with diseases, such as cancer, loss-of-imprinting syndromes and neurological disorders. It has been also shown that DNA methylation at the cellular, tissue and organism level varies with age. To overcome the costs of Whole-Genome Bisulfite Sequencing, the gold standard method to detect 5-methylcytosines at a single base resolution, DNA methylation arrays have been developed and extensively used. This method allows one to assess the status of a fraction of the CpG sites present in the genome of an organism. In order to combine the relatively low cost of Methylation Arrays and digital signals of bisulfite sequencing, we developed a Targeted Bisulfite Sequencing method that can be applied to biomarker discovery for virtually any phenotype. Here we describe a comprehensive step-by-step protocol to build a DNA methylation-based epigenetic clock.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32755621', 'doi' => '10.1016/j.ymeth.2020.07.006', 'modified' => '2020-12-18 13:27:14', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 67 => array( 'id' => '4031', 'name' => 'Battle of the sex chromosomes: competition between X- and Y-chromosomeencoded proteins for partner interaction and chromatin occupancy drivesmulti-copy gene expression and evolution in muroid rodents.', 'authors' => 'Moretti, C and Blanco, M and Ialy-Radio, C and Serrentino, ME and Gobé,C and Friedman, R and Battail, C and Leduc, M and Ward, MA and Vaiman, Dand Tores, F and Cocquet, J', 'description' => '<p>Transmission distorters (TDs) are genetic elements that favor their own transmission to the detriments of others. Slx/Slxl1 (Sycp3-like-X-linked and Slx-like1) and Sly (Sycp3-like-Y-linked) are TDs which have been co-amplified on the X and Y chromosomes of Mus species. They are involved in an intragenomic conflict in which each favors its own transmission, resulting in sex ratio distortion of the progeny when Slx/Slxl1 vs. Sly copy number is unbalanced. They are specifically expressed in male postmeiotic gametes (spermatids) and have opposite effects on gene expression: Sly knockdown leads to the upregulation of hundreds of spermatid-expressed genes, while Slx/Slxl1-deficiency downregulates them. When both Slx/Slxl1 and Sly are knocked-down, sex ratio distortion and gene deregulation are corrected. Slx/Slxl1 and Sly are, therefore, in competition but the molecular mechanism remains unknown. By comparing their chromatin binding profiles and protein partners, we show that SLX/SLXL1 and SLY proteins compete for interaction with H3K4me3-reader SSTY1 (Spermiogenesis-specific-transcript-on-the-Y1) at the promoter of thousands of genes to drive their expression, and that the opposite effect they have on gene expression is mediated by different abilities to recruit SMRT/N-Cor transcriptional complex. Their target genes are predominantly spermatid-specific multicopy genes encoded by the sex chromosomes and the autosomal Speer/Takusan. Many of them have co-amplified with Slx/Slxl1/Sly but also Ssty during muroid rodent evolution. Overall, we identify Ssty as a key element of the X vs. Y intragenomic conflict, which may have influenced gene content and hybrid sterility beyond Mus lineage since Ssty amplification on the Y pre-dated that of Slx/Slxl1/Sly.</p>', 'date' => '2020-07-13', 'pmid' => 'http://www.pubmed.gov/32658962', 'doi' => '10.1093/molbev/msaa175/5870835', 'modified' => '2020-12-18 13:27:51', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 68 => array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ) ), 'Testimonial' => array(), 'Area' => array() ) $country = 'US' $countries_allowed = array( (int) 0 => 'CA', (int) 1 => 'US', (int) 2 => 'IE', (int) 3 => 'GB', (int) 4 => 'DK', (int) 5 => 'NO', (int) 6 => 'SE', (int) 7 => 'FI', (int) 8 => 'NL', (int) 9 => 'BE', (int) 10 => 'LU', (int) 11 => 'FR', (int) 12 => 'DE', (int) 13 => 'CH', (int) 14 => 'AT', (int) 15 => 'ES', (int) 16 => 'IT', (int) 17 => 'PT' ) $outsource = false $other_formats = array() $edit = '' $testimonials = '' $featured_testimonials = '' $related_products = '<li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201140</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-3047" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <form action="/en/carts/add/3047" id="CartAdd/3047Form" method="post" accept-charset="utf-8"><div style="display:none;"><input type="hidden" name="_method" value="POST"/></div><input type="hidden" name="data[Cart][product_id]" value="3047" id="CartProductId"/> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p>Add <input name="data[Cart][quantity]" placeholder="1" value="1" min="1" style="width:60px;display:inline" type="number" id="CartQuantity" required="required"/> <strong> Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico</strong> to my shopping cart.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="checkout" id="checkout" value="checkout" type="submit">Checkout</button> </div> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="keepshop" id="keepshop" type="submit">Keep shopping</button> </div> </div> </div> </div> </form><a class="close-reveal-modal" aria-label="Close">×</a></div><!-- END: ADD TO CART MODAL --><a href="#" id="1-5-ml-tube-holder-dock-for-bioruptor-pico" data-reveal-id="cartModal-3047" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 1.5 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201143</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: QUOTE MODAL --><div id="quoteModal-3048" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h3>Get a quote</h3><p class="lead">You are about to request a quote for <strong>Tube holder for 0.65 ml tubes - Bioruptor<sup>®</sup> Pico</strong>. 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data-reveal-id="cartModal-3049" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 0.2 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack"><img src="/img/product/shearing_technologies/B01200016_tube_holder.jpg" alt="some alt" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01200016</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-1796" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" 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'name' => 'product/shearing_technologies/B01200016_tube_holder.jpg', 'alt' => 'some alt', 'modified' => '2015-06-10 17:28:55', 'created' => '2015-06-10 17:28:55', 'ProductsImage' => array( [maximum depth reached] ) ) ) ) $list = '<div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-1.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-2.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-3.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-4.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-5.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B010600010.jpg" /></div>' $img = array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => 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=> '3046', 'protocol_id' => '73' ) ) $document = array( 'id' => '1170', 'name' => 'Critical steps for Bioruptor® maintenance and efficient shearing', 'description' => '', 'image_id' => null, 'type' => 'Document', 'url' => 'files/products/shearing_technology/critical-steps-bioruptor-web.pdf', 'slug' => 'critical-steps-bioruptor-maintenance', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2023-08-31 14:27:41', 'created' => '2023-08-31 14:27:41', 'ProductsDocument' => array( 'id' => '3264', 'product_id' => '3046', 'document_id' => '1170' ) ) $publication = array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( 'id' => '6424', 'product_id' => '3046', 'publication_id' => '4549' ) ) $externalLink = ' <a href="https://www.researchsquare.com/article/rs-1832996/v1" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755 View::_evaluate() - CORE/Cake/View/View.php, line 971 View::_render() - CORE/Cake/View/View.php, line 933 View::render() - CORE/Cake/View/View.php, line 473 Controller::render() - CORE/Cake/Controller/Controller.php, line 963 Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 200 Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167 [main] - APP/webroot/index.php, line 118
Notice (8): Undefined variable: header [APP/View/Products/view.ctp, line 755]Code Context<!-- BEGIN: REQUEST_FORM MODAL --><div id="request_formModal" class="reveal-modal medium" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"><?= $this->element('Forms/simple_form', array('solution_of_interest' => $solution_of_interest, 'header' => $header, 'message' => $message, 'campaign_id' => $campaign_id)) ?>$viewFile = '/home/website-server/www/app/View/Products/view.ctp' $dataForView = array( 'language' => 'en', 'noindex' => 'noindex', 'meta_keywords' => '', 'meta_description' => 'Bioruptor® Pico sonication device', 'meta_title' => 'Bioruptor® Pico sonication device', 'product' => array( 'Product' => array( 'id' => '3046', 'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa fa-arrow-circle-right"></i> <a href="https://www.diagenode.com/pages/chromatin-prep-easyshear-kit-guide">Read more</a></h3> </div> <p> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> </p> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'format' => '1 unit', 'catalog_number' => 'B01080010', 'old_catalog_number' => '', 'sf_code' => 'B01080010-', 'type' => 'ACC', 'search_order' => '00-Machine', 'price_EUR' => '27000', 'price_USD' => '30000', 'price_GBP' => '23500', 'price_JPY' => '4229550', 'price_CNY' => '/', 'price_AUD' => '75000', 'country' => 'ALL', 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'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa fa-arrow-circle-right"></i> <a href="https://www.diagenode.com/pages/chromatin-prep-easyshear-kit-guide">Read more</a></h3> </div> <p> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> </p> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'format' => '1 unit', 'catalog_number' => 'B01080010', 'old_catalog_number' => '', 'sf_code' => 'B01080010-', 'type' => 'ACC', 'search_order' => '00-Machine', 'price_EUR' => '27000', 'price_USD' => '30000', 'price_GBP' => '23500', 'price_JPY' => '4229550', 'price_CNY' => '/', 'price_AUD' => '75000', 'country' => 'ALL', 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Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>®</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>®</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>®</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div> <div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 µl volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.1 ml Bioruptor® Microtubes (Cat. No. B01200041). <strong>Panel B, 100 µl volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.65 ml Bioruptor® Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 µl volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016). Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37°C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 µl of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div> <div class="small-12 medium-12 large-12 columns"><br /><br /></div> <div class="small-12 medium-12 large-12 columns"> <p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p> </div> <div class="small-12 medium-12 large-12 columns"> <div class="page" title="Page 7"> <table> <tbody> <tr valign="middle"> <td></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>SDS concentration</strong></p> </td> <td style="text-align: center;"> <p>< 0.1%</p> </td> <td style="text-align: center;"> <p>0.2%</p> </td> <td style="text-align: center;"> <p>1%</p> </td> <td style="text-align: center;"> <p>0.5%</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Nuclei isolation</strong></p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>No</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Allows for shearing of... cells/tissue</strong></p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>up to 25 g of tissue</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Corresponding to shearing buffers from</strong></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p> <p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p> </td> </tr> </tbody> </table> <p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor® Pico</span></a></em></p> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'chromatin-shearing', 'meta_keywords' => 'Chromatin shearing,Chromatin Immunoprecipitation,Bioruptor,Sonication,Sonicator', 'meta_description' => 'Diagenode's Bioruptor® is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.', 'meta_title' => 'Chromatin shearing using Bioruptor® sonication device | Diagenode', 'modified' => '2017-11-15 10:14:02', 'created' => '2015-03-05 15:56:30', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3', 'position' => '10', 'parent_id' => null, 'name' => '次世代シーケンシング', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2 style="font-size: 22px;">DNA断片化、ライブラリー調製、自動化：NGSのワンストップショップ</h2> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-12 medium-12 large-12 columns"> <h4>1. 断片化装置を選択してください：150 bp〜75 kbの範囲でDNAを断片化します。</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-pico-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/bioruptor_pico.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/megaruptor2-1-unit"><img src="https://www.diagenode.com/img/product/shearing_technologies/B06010001_megaruptor2.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-one-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/br-one-profil.png" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns">5μlまで断片化：150 bp〜2 kb<br />NGS DNAライブラリー調製およびFFPE核酸抽出に最適で、</td> <td class="small-4 medium-4 large-4 columns">2 kb〜75 kbの範囲をできます。<br />メイトペアライブラリー調製および長いフラグメントDNAシーケンシングに最適で、この軽量デスクトップデバイスで</td> <td class="small-4 medium-4 large-4 columns">20または50μlの断片化が可能です。</td> </tr> </tbody> </table> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-8 medium-8 large-8 columns"> <h4>2. 最適化されたライブラリー調整キットを選択してください。</h4> </th> <th class="small-4 medium-4 large-4 columns"> <h4>3. ライブラリー前処理自動化を選択して、比類のないデータ再現性を実感</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><img src="https://www.diagenode.com/img/product/kits/microPlex_library_preparation.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns"><img src="https://www.diagenode.com/img/product/kits/box_kit.jpg" style="display: block; margin-left: auto; margin-right: auto;" height="173" width="250" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/sx-8g-ip-star-compact-automated-system-1-unit"><img src="https://www.diagenode.com/img/product/automation/B03000002%20_ipstar_compact.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">50pgの低入力：MicroPlex Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">5ng以上：iDeal Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">Achieve great NGS data easily</td> </tr> </tbody> </table> </div> </div> <blockquote> <div class="row"> <div class="small-12 medium-12 large-12 columns"><span class="label" style="margin-bottom: 16px; margin-left: -22px; font-size: 15px;">DiagenodeがNGS研究にぴったりなプロバイダーである理由</span> <p>Diagenodeは15年以上もエピジェネティクス研究に専念、専門としています。 ChIP研究クロマチン用のユニークな断片化システムの開発から始まり、 専門知識を活かし、5μlのせん断体積まで可能で、NGS DNAライブラリーの調製に最適な最先端DNA断片化装置の開発にたどり着きました。 我々は以来、ChIP-seq、Methyl-seq、NGSライブラリー調製用キットを研究開発し、業界をリードする免疫沈降研究と同様に、ライブラリー調製を自動化および完結させる独自の自動化システムを開発にも成功しました。</p> <ul> <li>信頼されるせん断装置</li> <li>様々なインプットからのライブラリ作成キット</li> <li>独自の自動化デバイス</li> </ul> </div> </div> </blockquote> <div class="row"> <div class="small-12 columns"> <ul class="accordion" data-accordion=""> <li class="accordion-navigation"><a href="#panel1a">次世代シーケンシングへの理解とその専門知識</a> <div id="panel1a" class="content"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p><strong>次世代シーケンシング (NGS)</strong> ）は、著しいスケールとハイスループットでシーケンシングを行い、1日に数十億もの塩基生成を可能にします。 NGSのハイスループットは迅速でありながら正確で、再現性のあるデータセットを実現し、さらにシーケンシング費用を削減します。 NGSは、ゲノムシーケンシング、ゲノム再シーケンシング、デノボシーケンシング、トランスクリプトームシーケンシング、その他にDNA-タンパク質相互作用の検出やエピゲノムなどを示します。 指数関数的に増加するシーケンシングデータの需要は、計算分析の障害や解釈、データストレージなどの課題を解決します。</p> <p>アプリケーションおよび出発物質に応じて、数百万から数十億の鋳型DNA分子を大規模に並行してシーケンシングすることが可能です。その為に、異なる化学物質を使用するいくつかの市販のNGSプラットフォームを利用することができます。 NGSプラットフォームの種類によっては、事前準備とライブラリー作成が必要です。</p> <p>NGSにとっても、特にデータ処理と分析に関した大きな課題はあります。第3世代技術はゲノミクス研究にさらに革命を起こすであろうと大きく期待されています。</p> </div> </div> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <p><strong>NGS アプリケーション</strong></p> <ul> <li>全ゲノム配列決定</li> <li>デノボシーケンシング</li> <li>標的配列</li> <li>Exomeシーケンシング</li> <li>トランスクリプトーム配列決定</li> <li>ゲノム配列決定</li> <li>ミトコンドリア配列決定</li> <li>DNA-タンパク質相互作用（ChIP-seq</li> <li>バリアント検出</li> <li>ゲノム仕上げ</li> </ul> </div> <div class="small-6 medium-6 large-6 columns"> <p><strong>研究分野におけるNGS:</strong></p> <ul> <li>腫瘍学</li> <li>リプロダクティブ・ヘルス</li> <li>法医学ゲノミクス</li> <li>アグリゲノミックス</li> <li>複雑な病気</li> <li>微生物ゲノミクス</li> <li>食品・環境ゲノミクス</li> <li>創薬ゲノミクス - パーソナライズド・メディカル</li> </ul> </div> <div class="small-12 medium-12 large-12 columns"> <p><strong>NGSの用語</strong></p> <dl> <dt>リード（読み取り）</dt> <dd>この装置から得られた連続した単一のストレッチ</dd> <dt>断片リード</dt> <dd>フラグメントライブラリからの読み込み。 シーケンシングプラットフォームに応じて、読み取りは通常約100〜300bp。</dd> <dt>断片ペアエンドリード</dt> <dd>断片ライブラリーからDNA断片の各末端2つの読み取り。</dd> <dt>メイトペアリード</dt> <dd>大きなDNA断片（通常は予め定義されたサイズ範囲）の各末端から2つの読み取り。</dd> <dt>カバレッジ（例）</dt> <dd>30×適用範囲とは、参照ゲノム中の各塩基対が平均30回の読み取りを示す。</dd> </dl> </div> </div> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2>NGSプラットフォーム</h2> <h3><a href="http://www.illumina.com" target="_blank">イルミナ</a></h3> <p>イルミナは、クローン的に増幅された鋳型DNA（クラスター）上に位置する、蛍光標識された可逆的鎖ターミネーターヌクレオチドを用いた配列別合成技術を使用。 DNAクラスターは、ガラスフローセルの表面上に固定化され、 ワークフローは、4つのヌクレオチド（それぞれ異なる蛍光色素で標識された）の組み込み、4色イメージング、色素や末端基の切断、取り込み、イメージングなどを繰り返します。フローセルは大規模な並列配列決定を受ける。 この方法により、単一蛍光標識されたヌクレオチドの制御添加によるモノヌクレオチドのエラーを回避する可能性があります。 読み取りの長さは、通常約100〜150 bpです。</p> <h3><a href="http://www.lifetechnologies.com" target="_blank">イオン トレント</a></h3> <p>イオントレントは、半導体技術チップを用いて、合成中にヌクレオチドを取り込む際に放出されたプロトンを検出します。 これは、イオン球粒子と呼ばれるビーズの表面にエマルションPCR（emPCR）を使用し、リンクされた特定のアダプターを用いてDNA断片を増幅します。 各ビーズは1種類のDNA断片で覆われていて、異なるDNA断片を有するビーズは次いで、チップの陽子感知ウェル内に配置されます。 チップには一度に4つのヌクレオチドのうちの1つが浸水し、このプロセスは異なるヌクレオチドで15秒ごとに繰り返されます。 配列決定の間に4つの塩基の各々が1つずつ導入されます、組み込みの場合はプロトンが放出され、電圧信号が取り込みに比例して検出されます。.</p> <h3><a href="http://www.pacificbiosciences.com" target="_blank">パシフィック バイオサイエンス</a></h3> <p>パシフィックバイオサイエンスでは、20kbを超える塩基対の読み取りも、単一分子リアルタイム（SMRT）シーケンシングによる構造および細胞タイプの変化を観察することができます。 このプラットフォームでは、超長鎖二本鎖DNA（dsDNA）断片が、Megaruptor（登録商標）のようなDiagenode装置を用いたランダムシアリングまたは目的の標的領域の増幅によって生成されます。 SMRTbellライブラリーは、ユニバーサルヘアピンアダプターをDNA断片の各末端に連結することによって生成します。 サイズ選択条件による洗浄ステップの後、配列決定プライマーをSMRTbellテンプレートにアニーリングし、鋳型DNAに結合したDNAポリメラーゼを含む配列決定を、蛍光標識ヌクレオチドの存在下で開始。 各塩基が取り込まれると、異なる蛍光のパルスをリアルタイムで検出します。</p> <h3><a href="https://nanoporetech.com" target="_blank">オックスフォード ナノポア</a></h3> <p>Oxford Nanoporeは、単一のDNA分子配列決定に基づく技術を開発します。その技術により生物学的分子、すなわちDNAが一群の電気抵抗性高分子膜として位置するナノスケールの孔（ナノ細孔）またはその近くを通過し、イオン電流が変化します。 この変化に関する情報は、例えば4つのヌクレオチド（AまたはG r CまたはT）ならびに修飾されたヌクレオチドすべてを区別することによって分子情報に訳されます。 シーケンシングミニオンデバイスのフローセルは、数百個のナノポアチャネルのセンサアレイを含みます。 DNAサンプルは、Diagenode社のMegaruptor（登録商標）を用いてランダムシアリングによって生成され得る超長鎖DNAフラグメントが必要です。</p> <h3><a href="http://www.lifetechnologies.com/be/en/home/life-science/sequencing/next-generation-sequencing/solid-next-generation-sequencing.html" target="_blank">SOLiD</a></h3> <p>SOLiDは、ユニークな化学作用により、何千という個々のDNA分子の同時配列決定を可能にします。 それは、アダプター対ライブラリーのフラグメントが適切で、せん断されたゲノムDNAへのアダプターのライゲーションによるライブラリー作製から始まります。 次のステップでは、エマルジョンPCR（emPCR）を実施して、ビーズの表面上の個々の鋳型DNA分子をクローン的に増幅。 emPCRでは、個々の鋳型DNAをPCR試薬と混合し、水中油型エマルジョン内の疎水性シェルで囲まれた水性液滴内のプライマーコートビーズを、配列決定のためにロードするスライドガラスの表面にランダムに付着。 この技術は、シークエンシングプライマーへのライゲーションで競合する4つの蛍光標識されたジ塩基プローブのセットを使用します。</p> <h3><a href="http://454.com/products/technology.asp" target="_blank">454</a></h3> <p>454は、大規模並列パイロシーケンシングを利用しています。 始めに全ゲノムDNAまたは標的遺伝子断片の300〜800bp断片のライブラリー調製します。 次に、DNAフラグメントへのアダプターの付着および単一のDNA鎖の分離。 その後アダプターに連結されたDNAフラグメントをエマルジョンベースのクローン増幅（emPCR）で処理し、DNAライブラリーフラグメントをミクロンサイズのビーズ上に配置します。 各DNA結合ビーズを光ファイバーチップ上のウェルに入れ、器具に挿入します。 4つのDNAヌクレオチドは、配列決定操作中に固定された順序で連続して加えられ、並行して配列決定されます。</p> </div> </div> </div> </li> </ul> </div> </div>', 'in_footer' => true, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'next-generation-sequencing', 'meta_keywords' => 'Next-generation sequencing,NGS,Whole genome sequencing,NGS platforms,DNA/RNA shearing', 'meta_description' => 'Diagenode offers kits and DNA/RNA shearing technology prior to next-generation sequencing, many Next-generation sequencing platforms require preparation of the DNA.', 'meta_title' => 'Next-generation sequencing (NGS) Applications and Methods | Diagenode', 'modified' => '2018-07-26 05:24:29', 'created' => '2015-04-01 22:47:04', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '13', 'position' => '10', 'parent_id' => '3', 'name' => 'DNA/RNA shearing', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns">In recent years, advances in Next-Generation Sequencing (NGS) have revolutionized genomics and biology. This growth has fueled demands on upstream techniques for optimal sample preparation and genomic library construction. One of the most critical aspects of optimal library preparation is the quality of the DNA to be sequenced. The DNA must first be effectively and consistently sheared into the appropriate fragment size (depending on the sequencing platform) to enable sensitive and reliable NGS results. The <strong>Bioruptor</strong><sup>®</sup> <strong>Pico</strong> and the <strong>Megaruptor</strong><sup>®</sup> provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows. Follow our guidelines and find the good parameters for your expected DNA size: <a href="https://pybrevet.typeform.com/to/o8cQfM">DNA shearing with the Bioruptor<sup>®</sup></a>.</div> </div> <p></p> <div class="row"> <div class="small-7 medium-7 large-7 columns text-center"><img src="https://www.diagenode.com/img/applications/true-flexibility-with-br-ngs.jpg" /></div> <div class="small-5 medium-5 large-5 columns"><small><strong>Programmable DNA size distribution and high reproducibility with Bioruptor<sup>®</sup> Pico using 0.65 (panel A) or 0.1 ml (panel B) microtubes</strong>. <b>Panel A:</b> 200 bp after 13 cycles (13 sec ON/OFF) using 100 µl volume. Average size: 204; CV%:1.89%). <b>Panel B:</b> 200 bp after 20 cycles (30 sec ON/OFF) using 10 µl volume. (Average size: 215 bp; CV%: 6.6%). <b>Panel A & B:</b> peak electropherogram view. <b>Panel C & D:</b> virtual gel view.</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-10 medium-10 large-10 columns text-center end small-offset-1"><img src="https://www.diagenode.com/img/applications/megaruptor-short-frag.jpg" /></div> <div class="small-12 medium-12 large-12 columns"><small><strong> Reproducible and narrow DNA size distribution with Megaruptor® using short fragment size Hydropores Validation using two different DNA sources and two different methods of analysis. A:</strong> Shearing of lambda phage genomic DNA (20 ng/μl; 150 μl/sample) sheared at different speed settings and analyzed on 1% agarose gel. <strong>B:</strong> Bioanalyzer profiles of human genomic DNA (20 ng/μl; 150 μl/sample) sheared at different software settings of 2 and 5 kb. Three independent experiments were run for each setting. (Agilent DNA 12000 kit was used for separation and fragment sizing).</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-4 medium-4 large-4 columns text-center"><img src="https://www.diagenode.com/img/applications/megaruptor-long-frag.jpg" /></div> <div class="small-8 medium-8 large-8 columns"><small><strong> Demonstrated shearing to fragment sizes between 15 kb and 75 kb with Megaruptor® using long fragment size Hydropores. </strong>Image shows DNA size distribution of human genomic DNA sheared with long fragment Hydropores. DNA was analyzed by pulsed field gel electrophoresis (PFGE) in 1% agarose gel and a mean size of smears was estimated using Image Lab 4.1 software.<br /> * indicates unsheared DNA </small></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'dna-rna-shearing', 'meta_keywords' => 'DNA/RNA shearing,Bioruptor® Pico,Megaruptor®,Next-Generation Sequencing ', 'meta_description' => 'Bioruptor® Pico and the Megaruptor® provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows.', 'meta_title' => 'DNA shearing & RNA shearing for Next-Generation Sequencing (NGS) | Diagenode', 'modified' => '2017-12-08 14:44:11', 'created' => '2014-10-29 12:45:41', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '17', 'position' => '10', 'parent_id' => '4', 'name' => 'Protein extraction', 'description' => '<div class="row"> <div class="large-12 columns">Various biochemical and analytical techniques require the extraction of protein from tissues or mammalian, yeast and bacterial cells. Obtaining high quality and yields of proteins is important for further downstream protein characterization such as in PAGE, western blotting, mass spectrometry or protein purification. The efficient disruption and homogenization of tissues and cultured cells obtained in just one step using <strong>Diagenode's Bioruptor</strong><sup>®</sup> deliver high quality protein.</div> </div> <p></p> <div class="row"> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_standard_plus.png" /> <p><small>Western blot analysis of GAPDH and HSP90 proteins in tissues (various mouse tissues) and cultured cell extracts (HeLA).</small></p> </div> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_pico.png" /> <p><small>Western blot analysis of GAPDH and ß-tubulin proteins in tissues (mouse liver) and cultured cell extracts (HeLA).</small></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'protein-extraction', 'meta_keywords' => 'Protein extraction,Bioruptor,Sonication,Protein Analysis', 'meta_description' => 'Diagenode provides efficient disruption and homogenization of tissues and cultured cells obtained in just one step using Bioruptor® deliver high quality protein.', 'meta_title' => 'Protein extraction using Bioruptor® Sonication device | Diagenode', 'modified' => '2017-10-16 14:39:42', 'created' => '2014-07-02 04:41:03', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '6', 'position' => '10', 'parent_id' => '1', 'name' => 'メチル化DNA結合タンパク質', 'description' => '<div class="row"> <div class="large-12 columns">MBD方法は、メチル化DNAに対するH6-GST-MBD融合タンパク質の非常に高い親和性に基づいています。 このタンパク質は、N末端His6タグを含むグルタチオン-S-トランスフェラーゼ（GST）とのC末端融合物として、ヒトMeCP2のメチル結合ドメイン（MBD）を含有します。 このH6-GST-MBD融合タンパク質を用いて、メチル化CpGを含むDNAを特異的に単離する事が可能です。<br /><br />DiagenodeのMethylCap®キットは、二本鎖DNAの高濃縮と、メチル化CpG密度の関数における微分分画を可能にします。 分画はサンプルの複雑さを軽減し、次世代のシーケンシングを容易にします。 MethylCapアッセイに先立ち、DNAを最初に抽出し、Picoruptorソニケーターを用いて断片化します。<br /> <h3>概要</h3> <p class="text-center"><br /><img src="https://www.diagenode.com/img/applications/methyl_binding_domain_overview.jpg" /></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'methylbinding-domain-protein', 'meta_keywords' => 'Epigenetic,Methylbinding Domain Protein,MBD,DNA methylation,DNA replication,MethylCap,MethylCap assay,', 'meta_description' => 'Methylbinding Domain Protein(MBD) approach is based on the very high affinity of a H6-GST-MBD fusion protein for methylated DNA. This protein consists of the methyl binding domain (MBD) of human MeCP2, as a C-terminal fusion with Glutathione-S-transferase', 'meta_title' => 'Epigenetic Methylbinding Domain Protein(MBD) - DNA methylation | Diagenode', 'modified' => '2019-03-22 12:32:12', 'created' => '2015-06-02 17:05:42', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '9', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-seq', 'description' => '<div class="row"> <div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div> <div class="large-12 columns"></div> <h5 class="large-12 columns"><strong></strong></h5> <h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div> <div class="large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by sonication to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with <strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: Reverse cross-links, elute, and purify </li> <li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify IP'd material</li> <li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chromatin-immunoprecipitation-sequencing', 'meta_keywords' => 'Chromatin Immunoprecipitation Sequencing,ChIP-Seq,ChIP-seq grade antibodies,DNA purification,qPCR,Shearing of chromatin', 'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing', 'meta_title' => 'Chromatin Immunoprecipitation - ChIP-seq Kits - Dna methylation | Diagenode', 'modified' => '2017-11-14 09:57:16', 'created' => '2015-04-12 18:08:46', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '11', 'position' => '10', 'parent_id' => '3', 'name' => 'FFPE DNA extraction', 'description' => '<div class="row"> <div class="large-12 columns">Diagenode's high yields FFPE DNA extraction using Bioruptor<sup><span>®</span></sup> is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no toxic reagents, digest tissues, and purify DNA with high yields and low sample degradation. The DNA can then be analyzed by traditional methods or can be sheared with the Bioruptor<sup>®</sup> Pico ultrasonicator for downstream NGS library prep using the MicroPlex Library Preparation Kit.</div> <div class="small-12 medium-12 large-12 columns text-center"><img src="https://www.diagenode.com/img/applications/ffpe_workflow.png" /></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'ffpe-dna-extraction', 'meta_keywords' => 'FFPE DNA extraction,Next-Gen Sequencing,Bioruptor® ultrasonicator', 'meta_description' => 'Diagenode's high yields FFPE DNA extraction using Bioruptor is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no tox', 'meta_title' => 'FFPE DNA extraction using Bioruptor® ultrasonicator | Diagenode', 'modified' => '2017-10-16 14:34:57', 'created' => '2014-10-01 01:24:40', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '10', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-qPCR', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns text-justify"> <p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p> <p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p> </div> <div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div> <div class="small-12 medium-12 large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li> <li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chip-qpcr', 'meta_keywords' => 'Chromatin immunoprecipitation,ChIP Quantitative PCR,polymerase chain reaction (PCR)', 'meta_description' => 'Diagenode's ChIP qPCR kits can be used to quantify enriched DNA after chromatin immunoprecipitation. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of', 'meta_title' => 'ChIP Quantitative PCR (ChIP-qPCR) | Diagenode', 'modified' => '2018-01-09 16:46:56', 'created' => '2014-12-11 00:22:08', 'ProductsApplication' => array( [maximum depth reached] ) ) ), 'Category' => array( (int) 0 => array( 'id' => '6', 'position' => '1', 'parent_id' => '1', 'name' => 'Bioruptor<sup>®</sup>', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"><br /> <p><span>Diagenode focuses on state-of-the-art preparation of high quality biological and chemical samples by developing the industry’s most advanced water bath sonicators and hydrodynamic devices. Our instruments are ideal for a number of applications in various fields of studies including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</span></p> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor/TAB-BR-comparaison.pdf" target="_blank"><img src="https://www.diagenode.com/img/bouton-comparaison.png" /></a></p> </div> <!-- <center> <div class="small-12 medium-4 large-4 columns"> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </div> </center></div> <p><span></span></p> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;"></h2> <h2 style="text-align: center;">Technology explained</h2> <div class="container-wrapper-genially" style="position: relative; min-height: 400px; max-width: 80%; margin: 0 auto;"><video width="300" height="150" style="position: absolute; top: 45%; left: 50%; transform: translate(-50%, -50%); width: 80px; height: 80px; margin-bottom: 10%;" class="loader-genially" autoplay="autoplay" loop="loop" playsinline="playsInline" muted="muted"><source src="https://static.genial.ly/resources/panel-loader-low.mp4" type="video/mp4" />Your browser does not support the video tag.</video> <div id="601970a2edea170d2af29118" class="genially-embed" style="margin: 0px auto; position: relative; height: auto; width: 100%;"></div> </div> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script>// <![CDATA[ (function (d) { var js, id = "genially-embed-js", ref = d.getElementsByTagName("script")[0]; if (d.getElementById(id)) { return; } js = d.createElement("script"); js.id = id; js.async = true; js.src = "https://view.genial.ly/static/embed/embed.js"; ref.parentNode.insertBefore(js, ref); }(document)); // ]]></script> </div> </div>--> <p><span> <br /></span></p> <div class="spacer"></div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">Reproductibility is our priority</h2> </div> </div> <div><img src="https://www.diagenode.com/img/shearing/reproductibility.png" alt="reproductibility" /> <p class="bottom_note"></p> </div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">An affordable instrument for wide range of applications</h2> </div> </div> <p style="text-align: center;">Designed for any researchers, the Bioruptor gives the user the right level of flexibility.</p> <table style="width: 972px;"> <tbody> <tr style="height: 56px;"> <th style="width: 380px; height: 56px;"></th> <th class="text-center" style="width: 126px; height: 56px;">Bioruptor</th> <th class="text-center" style="width: 141px; height: 56px;">Cup Horn Sonicators</th> <th class="text-center" style="width: 156px; height: 56px;">Focused <br />ultra-sonicators</th> <th class="text-center" style="width: 155px; height: 56px;">Multi Sample Sonicator</th> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Instrument pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Consumables pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Range of applications</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Scalable and sample volume flexibility</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Throughput</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> </tbody> </table> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;"></h2> <h2 style="text-align: center;">Bioruptor ultrasonication for best results in:</h2> <p><b><span>✓ Chromatin shearing</span><span> </span><span style="font-weight: 400;">- Industry leader in accurate and tight fragment ranges</span></b></p> <p><b><span>✓ DNA shearing</span><span> </span><span style="font-weight: 400;">- Excellent results for optimal fragment lengths in NGS library prep</span></b></p> <p><b><span>✓<span> </span></span>Protein aggregation studies </b><span style="font-weight: 400;">- Standardizing seeding with the robust Bioruptor.<br /></span><i><span style="font-weight: 400;">Read the app note by Dr. Kelvin Luk at the University of Pennsylvania </span></i><a href="https://www.diagenode.com/en/documents/standardizing-seeding-experiments-for-the-understanding-of-parkinson-disease" style="color: #13b29c;"><i><span style="font-weight: 400;">“Standardizing seeding experiments using the Bioruptor® for the understanding of the neuronal alpha-synuclein pathology”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>3D genome analysis with Hi-C</b><span style="font-weight: 400;"> - Preparing chromatin libraries with high-quality sonication.<br /></span><i><span style="font-weight: 400;">Read the app note, “</span></i><a href="https://www.diagenode.com/en/documents/applicationnote-arima-low-input" style="color: #13b29c;"><i><span style="font-weight: 400;">Unlock Low-Input 3D Genome Analysis with the Arima-HiC Kit”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>Mass spectrometry</b> <b>and increasing protein identification</b><span style="font-weight: 400;">- Sample preparation using Preomics iST and Bioruptor sonication.<br /></span><i><span style="font-weight: 400;">Read the app note “</span></i><a href="https://www.diagenode.com/en/documents/wp-ist-adaptators" style="color: #13b29c;"><i><span style="font-weight: 400;">Increase your iST ultrasonication throughput with the new Bioruptor® Pico cartridge holder”</span></i></a></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>Cell lysis, liposome prep, protein extraction, RNA extraction and more</b></span></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>CUT&RUN –Sonication of input DNA (for enrichment comparison) for NGS</b></span></p> </div> </div> <p><a href="https://www.diagenode.com/en/categories/bioruptor-maintenance"><img src="https://www.diagenode.com/img/banners/maintenance-banner-br.png" /></a></p> <p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> </div>', 'no_promo' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'hide' => false, 'all_format' => false, 'is_antibody' => false, 'slug' => 'bioruptor-shearing-device', 'cookies_tag_id' => null, 'meta_keywords' => 'Bioruptor,ultrasonicator devices,probe sonicator,Next-Generation Sequencing', 'meta_description' => 'Bioruptor Sonication is ideal for Chromatin Shearing for Chromatin Immunoprecipitation (ChIP), Genomic DNA Shearing for next Generation Sequencing, RNA Shearing, Cell and Tissue Disruption', 'meta_title' => 'Bioruptor Sonication for Chromatin, DNA / RNA Shearing, Cell and Tissue Disruption | Diagenode', 'modified' => '2024-08-28 14:03:21', 'created' => '2014-12-18 22:08:39', 'ProductsCategory' => array( [maximum depth reached] ), 'CookiesTag' => array([maximum depth reached]) ) ), 'Document' => array( (int) 0 => array( 'id' => '1067', 'name' => 'Chromatin Shearing Guide', 'description' => '<p>Guide for successful chromatin preparation using the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/products/shearing_technology/bioruptor/chromatin-shearing-guide-Pico.pdf', 'slug' => 'chromatin-shearing-guide-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-01-21 15:27:22', 'created' => '2020-01-21 15:27:22', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '1068', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:13:24', 'created' => '2020-01-21 15:30:32', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '1072', 'name' => 'Which tubes for Bioruptor<sup>®</sup> Pico', 'description' => '', 'image_id' => null, 'type' => 'Document', 'url' => 'files/products/shearing_technology/bioruptor/org-tubes-pico-01_20.pdf', 'slug' => 'org-tubes-pico-01-20', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-02-10 11:16:30', 'created' => '2020-02-10 10:55:30', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1127', 'name' => 'Unlock Low-Input 3D Genome Analysis with the Arima-HiC Kit', 'description' => '<p><span>By combining the optimized chemistry of the Arima-HiC kit along with new low input protocols, the potential applications of powerful Hi-C technology are unlocked. When studying samples that are difficult to obtain or grow, low input solutions can help you understand genome structure across a new range of low input samples. In addition, the Diagenode Bioruptor Pico assures that chromatin is sheared to optimal fragment lengths.</span></p>', 'image_id' => '247', 'type' => 'Application Note', 'url' => 'files/application_notes/ApplicationNote-Arima-Low-Input.pdf', 'slug' => 'applicationnote-arima-low-input', 'meta_keywords' => 'application note arima low input', 'meta_description' => 'application note arima low input', 'modified' => '2021-02-09 09:55:59', 'created' => '2021-02-09 09:55:59', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1074', 'name' => 'Datasheet of Bioruptor tubes', 'description' => '<p>Datasheet of Diagenode tubes for Bioruptor Pico and Bioruptor Plus.</p>', 'image_id' => null, 'type' => 'Datasheet', 'url' => 'files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf', 'slug' => 'tds-bioruptor-tubes', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2022-02-23 12:21:44', 'created' => '2020-03-23 10:41:46', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '1170', 'name' => 'Critical steps for Bioruptor® maintenance and efficient shearing', 'description' => '', 'image_id' => null, 'type' => 'Document', 'url' => 'files/products/shearing_technology/critical-steps-bioruptor-web.pdf', 'slug' => 'critical-steps-bioruptor-maintenance', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2023-08-31 14:27:41', 'created' => '2023-08-31 14:27:41', 'ProductsDocument' => array( [maximum depth reached] ) ) ), 'Feature' => array( (int) 0 => array( 'id' => '6', 'name' => 'All-in-one solution', 'slug' => '', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2015-07-24 11:50:41', 'created' => '2014-06-21 12:07:09', 'ProductsFeature' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '16', 'name' => 'Highly reproducible', 'slug' => '', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2015-11-09 14:21:15', 'created' => '2015-05-11 05:24:25', 'ProductsFeature' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '7', 'name' => 'Processing of 6-16 samples', 'slug' => '', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2018-03-13 11:10:21', 'created' => '2014-11-09 09:21:21', 'ProductsFeature' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1', 'name' => 'User friendly software', 'slug' => '', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2015-07-24 17:39:16', 'created' => '2014-06-27 10:32:35', 'ProductsFeature' => array( [maximum depth reached] ) ) ), 'Image' => array( (int) 0 => array( 'id' => '1803', 'name' => 'product/shearing_technologies/B01080000-1.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:55:07', 'created' => '2020-01-10 10:52:54', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '1804', 'name' => 'product/shearing_technologies/B01080000-2.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:08', 'created' => '2020-01-10 10:53:08', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '1805', 'name' => 'product/shearing_technologies/B01080000-3.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:46', 'created' => '2020-01-10 10:53:46', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1806', 'name' => 'product/shearing_technologies/B01080000-4.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:56', 'created' => '2020-01-10 10:53:56', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1807', 'name' => 'product/shearing_technologies/B01080000-5.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:54:06', 'created' => '2020-01-10 10:54:06', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => '2018-02-14 15:41:46', 'ProductsImage' => array( [maximum depth reached] ) ) ), 'Promotion' => array(), 'Protocol' => array( (int) 0 => array( 'id' => '73', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:16:00', 'created' => '0000-00-00 00:00:00', 'ProductsProtocol' => array( [maximum depth reached] ) ) ), 'Publication' => array( (int) 0 => array( 'id' => '4881', 'name' => 'LEO1 Is Required for Efficient Entry into Quiescence, Control of H3K9 Methylation and Gene Expression in Human Fibroblasts', 'authors' => 'Laurent M. et al.', 'description' => '<p><span>(1) Background: The LEO1 (Left open reading frame 1) protein is a conserved subunit of the PAF1C complex (RNA polymerase II-associated factor 1 complex). PAF1C has well-established mechanistic functions in elongation of transcription and RNA processing. We previously showed, in fission yeast, that LEO1 controls histone H3K9 methylation levels by affecting the turnover of histone H3 in chromatin, and that it is essential for the proper regulation of gene expression during cellular quiescence. Human fibroblasts enter a reversible quiescence state upon serum deprivation in the growth media. Here we investigate the function of LEO1 in human fibroblasts. (2) Methods: We knocked out the </span><span class="html-italic">LEO1</span><span><span> </span>gene using CRISPR/Cas9 methodology in human fibroblasts and verified that the LEO1 protein was undetectable by Western blot. We characterized the phenotype of the<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout cells with FACS analysis and cell growth assays. We used RNA-sequencing using spike-in controls to measure gene expression and spike-in controlled ChIP-sequencing experiments to measure the histone modification H3K9me2 genome-wide. (3) Results: Gene expression levels are altered in quiescent cells, however factors controlling chromatin and gene expression changes in quiescent human cells are largely unknown. The<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout fibroblasts are viable but have reduced metabolic activity compared to wild-type cells.<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells showed a slower entry into quiescence and a different morphology compared to wild-type cells. Gene expression was generally reduced in quiescent wild-type cells. The downregulated genes included genes involved in cell proliferation. A small number of genes were upregulated in quiescent wild-type cells including several genes involved in ERK1/ERK2 and Wnt signaling. In quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells, many genes were mis-regulated compared to wild-type cells. This included genes involved in Calcium ion transport and cell morphogenesis. Finally, spike-in controlled ChIP-sequencing experiments demonstrated that the histone modification H3K9me2 levels are globally increased in quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells. (4) Conclusions: Thus, LEO1 is important for proper entry into cellular quiescence, control of H3K9me2 levels, and gene expression in human fibroblasts.</span></p>', 'date' => '2023-11-17', 'pmid' => 'https://www.mdpi.com/2218-273X/13/11/1662', 'doi' => 'https://doi.org/10.3390/biom13111662', 'modified' => '2023-11-21 12:01:53', 'created' => '2023-11-21 12:01:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '4845', 'name' => 'DeSUMOylation of chromatin-bound proteins limits the rapidtranscriptional reprogramming induced by daunorubicin in acute myeloidleukemias.', 'authors' => 'Boulanger M. et al.', 'description' => '<p>Genotoxicants have been used for decades as front-line therapies against cancer on the basis of their DNA-damaging actions. However, some of their non-DNA-damaging effects are also instrumental for killing dividing cells. We report here that the anthracycline Daunorubicin (DNR), one of the main drugs used to treat Acute Myeloid Leukemia (AML), induces rapid (3 h) and broad transcriptional changes in AML cells. The regulated genes are particularly enriched in genes controlling cell proliferation and death, as well as inflammation and immunity. These transcriptional changes are preceded by DNR-dependent deSUMOylation of chromatin proteins, in particular at active promoters and enhancers. Surprisingly, inhibition of SUMOylation with ML-792 (SUMO E1 inhibitor), dampens DNR-induced transcriptional reprogramming. Quantitative proteomics shows that the proteins deSUMOylated in response to DNR are mostly transcription factors, transcriptional co-regulators and chromatin organizers. Among them, the CCCTC-binding factor CTCF is highly enriched at SUMO-binding sites found in cis-regulatory regions. This is notably the case at the promoter of the DNR-induced NFKB2 gene. DNR leads to a reconfiguration of chromatin loops engaging CTCF- and SUMO-bound NFKB2 promoter with a distal cis-regulatory region and inhibition of SUMOylation with ML-792 prevents these changes.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37462077', 'doi' => '10.1093/nar/gkad581', 'modified' => '2023-08-01 14:16:43', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '4846', 'name' => 'RNA polymerase II CTD is dispensable for transcription and requiredfor termination in human cells.', 'authors' => 'Yahia Y. et al.', 'description' => '<p>The largest subunit of RNA polymerase (Pol) II harbors an evolutionarily conserved C-terminal domain (CTD), composed of heptapeptide repeats, central to the transcriptional process. Here, we analyze the transcriptional phenotypes of a CTD-Δ5 mutant that carries a large CTD truncation in human cells. Our data show that this mutant can transcribe genes in living cells but displays a pervasive phenotype with impaired termination, similar to but more severe than previously characterized mutations of CTD tyrosine residues. The CTD-Δ5 mutant does not interact with the Mediator and Integrator complexes involved in the activation of transcription and processing of RNAs. Examination of long-distance interactions and CTCF-binding patterns in CTD-Δ5 mutant cells reveals no changes in TAD domains or borders. Our data demonstrate that the CTD is largely dispensable for the act of transcription in living cells. We propose a model in which CTD-depleted Pol II has a lower entry rate onto DNA but becomes pervasive once engaged in transcription, resulting in a defect in termination.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37424514', 'doi' => '10.15252/embr.202256150', 'modified' => '2023-08-01 14:17:54', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '4793', 'name' => 'Targeting lymphoid-derived IL-17 signaling to delay skin aging.', 'authors' => 'Paloma S. et al.', 'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, γδ T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-κB in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218', 'doi' => '10.1038/s43587-023-00431-z', 'modified' => '2023-06-14 15:56:56', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '4796', 'name' => 'Nicotinamide N-methyltransferase sustains a core epigenetic programthat promotes metastatic colonization in breast cancer.', 'authors' => 'Couto J.P. et al.', 'description' => '<p><span>Metastatic colonization of distant organs accounts for over 90% of deaths related to solid cancers, yet the molecular determinants of metastasis remain poorly understood. Here, we unveil a mechanism of colonization in the aggressive basal-like subtype of breast cancer that is driven by the NAD</span><sup>+</sup><span><span> </span>metabolic enzyme nicotinamide N-methyltransferase (NNMT). We demonstrate that NNMT imprints a basal genetic program into cancer cells, enhancing their plasticity. In line, NNMT expression is associated with poor clinical outcomes in patients with breast cancer. Accordingly, ablation of NNMT dramatically suppresses metastasis formation in pre-clinical mouse models. Mechanistically, NNMT depletion results in a methyl overflow that increases histone H3K9 trimethylation (H3K9me3) and DNA methylation at the promoters of PR/SET Domain-5 (PRDM5) and extracellular matrix-related genes. PRDM5 emerged in this study as a pro-metastatic gene acting via induction of cancer-cell intrinsic transcription of collagens. Depletion of PRDM5 in tumor cells decreases COL1A1 deposition and impairs metastatic colonization of the lungs. These findings reveal a critical activity of the NNMT-PRDM5-COL1A1 axis for cancer cell plasticity and metastasis in basal-like breast cancer.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37259596', 'doi' => '10.15252/embj.2022112559', 'modified' => '2023-06-15 08:35:19', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '4812', 'name' => 'SOX expression in prostate cancer drives resistance to nuclear hormonereceptor signaling inhibition through the WEE1/CDK1 signaling axis.', 'authors' => 'Williams A. et al.', 'description' => '<p><span>The development of androgen receptor signaling inhibitor (ARSI) drug resistance in prostate cancer (PC) remains therapeutically challenging. Our group has described the role of sex determining region Y-box 2 (SOX2) overexpression in ARSI-resistant PC. Continuing this work, we report that NR3C1, the gene encoding glucocorticoid receptor (GR), is a novel SOX2 target in PC, positively regulating its expression. Similar to ARSI treatment, SOX2-positive PC cells are insensitive to GR signaling inhibition using a GR modulating therapy. To understand SOX2-mediated nuclear hormone receptor signaling inhibitor (NHRSI) insensitivity, we performed RNA-seq in SOX2-positive and -negative PC cells following NHRSI treatment. RNA-seq prioritized differentially regulated genes mediating the cell cycle, including G2 checkpoint WEE1 Kinase (WEE1) and cyclin-dependent kinase 1 (CDK1). Additionally, WEE1 and CDK1 were differentially expressed in PC patient tumors dichotomized by high vs low SOX2 gene expression. Importantly, pharmacological targeting of WEE1 (WEE1i) in combination with an ARSI or GR modulator re-sensitizes SOX2-positive PC cells to nuclear hormone receptor signaling inhibition in vitro, and WEE1i combined with ARSI significantly slowed tumor growth in vivo. Collectively, our data suggest SOX2 predicts NHRSI resistance, and simultaneously indicates the addition of WEE1i to improve therapeutic efficacy of NHRSIs in SOX2-positive PC.</span></p>', 'date' => '2023-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37169162', 'doi' => '10.1016/j.canlet.2023.216209', 'modified' => '2023-06-15 08:58:59', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '4787', 'name' => 'The Effect of Metformin and Carbohydrate-Controlled Diet onDNA Methylation and Gene Expression in the Endometrium of Womenwith Polycystic Ovary Syndrome.', 'authors' => 'Garcia-Gomez E. et al.', 'description' => '<p>Polycystic ovary syndrome (PCOS) is an endocrine disease associated with infertility and metabolic disorders in reproductive-aged women. In this study, we evaluated the expression of eight genes related to endometrial function and their DNA methylation levels in the endometrium of PCOS patients and women without the disease (control group). In addition, eight of the PCOS patients underwent intervention with metformin (1500 mg/day) and a carbohydrate-controlled diet (type and quantity) for three months. Clinical and metabolic parameters were determined, and RT-qPCR and MeDIP-qPCR were used to evaluate gene expression and DNA methylation levels, respectively. Decreased expression levels of , , and genes and increased DNA methylation levels of the promoter were found in the endometrium of PCOS patients compared to controls. After metformin and nutritional intervention, some metabolic and clinical variables improved in PCOS patients. This intervention was associated with increased expression of , , and genes and reduced DNA methylation levels of the promoter in the endometrium of PCOS women. Our preliminary findings suggest that metformin and a carbohydrate-controlled diet improve endometrial function in PCOS patients, partly by modulating DNA methylation of the gene promoter and the expression of genes implicated in endometrial receptivity and insulin signaling.</p>', 'date' => '2023-04-01', 'pmid' => 'https://doi.org/10.3390%2Fijms24076857', 'doi' => '10.3390/ijms24076857', 'modified' => '2023-06-12 08:58:33', 'created' => '2023-05-05 12:34:24', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '4763', 'name' => 'Chromatin profiling identifies transcriptional readthrough as a conservedmechanism for piRNA biogenesis in mosquitoes.', 'authors' => 'Qu J. et al.', 'description' => '<p>The piRNA pathway in mosquitoes differs substantially from other model organisms, with an expanded PIWI gene family and functions in antiviral defense. Here, we define core piRNA clusters as genomic loci that show ubiquitous piRNA expression in both somatic and germline tissues. These core piRNA clusters are enriched for non-retroviral endogenous viral elements (nrEVEs) in antisense orientation and depend on key biogenesis factors, Veneno, Tejas, Yb, and Shutdown. Combined transcriptome and chromatin state analyses identify transcriptional readthrough as a conserved mechanism for cluster-derived piRNA biogenesis in the vector mosquitoes Aedes aegypti, Aedes albopictus, Culex quinquefasciatus, and Anopheles gambiae. Comparative analyses between the two Aedes species suggest that piRNA clusters function as traps for nrEVEs, allowing adaptation to environmental challenges such as virus infection. Our systematic transcriptome and chromatin state analyses lay the foundation for studies of gene regulation, genome evolution, and piRNA function in these important vector species.</p>', 'date' => '2023-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36930642', 'doi' => '10.1016/j.celrep.2023.112257', 'modified' => '2023-04-17 09:12:37', 'created' => '2023-04-14 13:41:22', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 8 => array( 'id' => '4720', 'name' => 'Activation of AKT induces EZH2-mediated β-catenin trimethylation incolorectal cancer.', 'authors' => 'Ghobashi A. H. et al.', 'description' => '<p>Colorectal cancer (CRC) develops in part through the deregulation of different signaling pathways, including activation of the WNT/β-catenin and PI3K/AKT pathways. Enhancer of zeste homolog 2 (EZH2) is a lysine methyltransferase that is involved in regulating stem cell development and differentiation and is overexpressed in CRC. However, depending on the study EZH2 has been found to be both positively and negatively correlated with the survival of CRC patients suggesting that EZH2's role in CRC may be context specific. In this study, we explored how PI3K/AKT activation alters EZH2's role in CRC. We found that activation of AKT by PTEN knockdown or by hydrogen peroxide treatment induced EZH2 phosphorylation at serine 21. Phosphorylation of EZH2 resulted in EZH2-mediated methylation of β-catenin and an associated increased interaction between β-catenin, TCF1, and RNA polymerase II. AKT activation increased β-catenin's enrichment across the genome and EZH2 inhibition reduced this enrichment by reducing the methylation of β-catenin. Furthermore, PTEN knockdown increased the expression of epithelial-mesenchymal transition (EMT)-related genes, and somewhat unexpectedly EZH2 inhibition further increased the expression of these genes. Consistent with these findings, EZH2 inhibition enhanced the migratory phenotype of PTEN knockdown cells. Overall, we demonstrated that EZH2 modulates AKT-induced changes in gene expression through the AKT/EZH2/ β-catenin axis in CRC with active PI3K/AKT signaling. Therefore, it is important to consider the use of EZH2 inhibitors in CRC with caution as these inhibitors will inhibit EZH2-mediated methylation of histone and non-histone targets such as β-catenin, which can have tumor-promoting effects.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1101%2F2023.01.31.526429', 'doi' => '10.1101/2023.01.31.526429', 'modified' => '2023-03-28 09:13:16', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 9 => array( 'id' => '4667', 'name' => 'Detailed molecular and epigenetic characterization of the Pig IPECJ2and Chicken SL-29 cell lines', 'authors' => 'de Vos J. et al.', 'description' => '<p>The pig IPECJ2 and chicken SL-29 cell lines are of interest because of their untransformed nature and wide use in functional studies. Molecular characterization of these cell lines is important to gain insight into possible molecular aberrations. The aims of this paper are providing a molecular and epigenetic characterization of the IPEC-J2 and SL-29 cell lines and providing a cell-line reference for the FAANG community, and future biomedical research. Whole genome sequencing , gene expression, DNA methylation , chromatin accessibility and ChIP-seq of four histone marks (H3K4me1, H3K4me3, H3K27ac, H3K27me3) and an insulator (CTCF) are used to achieve these aims. Heteroploidy (aneuploidy) of various chromosomes was observed from whole genome sequencing analysis in both cell lines. Furthermore, higher gene expression for genes located on chromosomes with aneuploidy in comparison to diploid chromosomes was observed. Regulatory complexity of gene expression, DNA methylation and chromatin accessibility was investigated through an integrative approach.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.isci.2023.106252', 'doi' => '10.1016/j.isci.2023.106252', 'modified' => '2023-04-07 16:52:26', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 10 => array( 'id' => '4673', 'name' => 'Signal-induced enhancer activation requires Ku70 to readtopoisomerase1-DNA covalent complexes.', 'authors' => 'Tan Y. et al.', 'description' => '<p>Enhancer activation serves as the main mechanism regulating signal-dependent transcriptional programs, ensuring cellular plasticity, yet central questions persist regarding their mechanism of activation. Here, by successfully mapping topoisomerase I-DNA covalent complexes genome-wide, we find that most, if not all, acutely activated enhancers, including those induced by 17β-estradiol, dihydrotestosterone, tumor necrosis factor alpha and neuronal depolarization, are hotspots for topoisomerase I-DNA covalent complexes, functioning as epigenomic signatures read by the classic DNA damage sensor protein, Ku70. Ku70 in turn nucleates a heterochromatin protein 1 gamma (HP1γ)-mediator subunit Med26 complex to facilitate acute, but not chronic, transcriptional activation programs. Together, our data uncover a broad, unappreciated transcriptional code, required for most, if not all, acute signal-dependent enhancer activation events in both mitotic and postmitotic cells.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36747093', 'doi' => '10.1038/s41594-022-00883-8', 'modified' => '2023-04-14 09:24:10', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 11 => array( 'id' => '4668', 'name' => 'Cotranscriptional demethylation induces global loss of H3K4me2 fromactive genes in Arabidopsis', 'authors' => 'Mori S. et al.', 'description' => '<p>Based on studies of animals and yeasts, methylation of histone H3 lysine 4 (H3K4me1/2/3, for mono-, di-, and tri-methylation, respectively) is regarded as the key epigenetic modification of transcriptionally active genes. In plants, however, H3K4me2 correlates negatively with transcription, and the regulatory mechanisms of this counterintuitive H3K4me2 distribution in plants remain largely unexplored. A previous genetic screen for factors regulating plant regeneration identified Arabidopsis LYSINE-SPECIFIC DEMETHYLASE 1-LIKE 3 (LDL3), which is a major H3K4me2 demethylase. Here, we show that LDL3-mediated H3K4me2 demethylation depends on the transcription elongation factor Paf1C and phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII). In addition, LDL3 binds to phosphorylated RNAPII. These results suggest that LDL3 is recruited to transcribed genes by binding to elongating RNAPII and demethylates H3K4me2 cotranscriptionally. Importantly, the negative correlation between H3K4me2 and transcription is disrupted in the ldl3 mutant, demonstrating the genome-wide impacts of the transcription-driven LDL3 pathway to control H3K4me2 in plants. Our findings implicate H3K4me2 in plants as chromatin memory for transcriptionally repressive states, which ensures robust gene control.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.02.17.528985v1', 'doi' => '10.1101/2023.02.17.528985', 'modified' => '2023-04-14 09:31:55', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 12 => array( 'id' => '4670', 'name' => 'Epigenetic regulation of plastin 3 expression by the macrosatelliteDXZ4 and the transcriptional regulator CHD4.', 'authors' => 'Strathmann E. A. et al.', 'description' => '<p>Dysregulated Plastin 3 (PLS3) levels associate with a wide range of skeletal and neuromuscular disorders and the most common types of solid and hematopoietic cancer. Most importantly, PLS3 overexpression protects against spinal muscular atrophy. Despite its crucial role in F-actin dynamics in healthy cells and its involvement in many diseases, the mechanisms that regulate PLS3 expression are unknown. Interestingly, PLS3 is an X-linked gene and all asymptomatic SMN1-deleted individuals in SMA-discordant families who exhibit PLS3 upregulation are female, suggesting that PLS3 may escape X chromosome inactivation. To elucidate mechanisms contributing to PLS3 regulation, we performed a multi-omics analysis in two SMA-discordant families using lymphoblastoid cell lines and iPSC-derived spinal motor neurons originated from fibroblasts. We show that PLS3 tissue-specifically escapes X-inactivation. PLS3 is located ∼500 kb proximal to the DXZ4 macrosatellite, which is essential for X chromosome inactivation. By applying molecular combing in a total of 25 lymphoblastoid cell lines (asymptomatic individuals, individuals with SMA, control subjects) with variable PLS3 expression, we found a significant correlation between the copy number of DXZ4 monomers and PLS3 levels. Additionally, we identified chromodomain helicase DNA binding protein 4 (CHD4) as an epigenetic transcriptional regulator of PLS3 and validated co-regulation of the two genes by siRNA-mediated knock-down and overexpression of CHD4. We show that CHD4 binds the PLS3 promoter by performing chromatin immunoprecipitation and that CHD4/NuRD activates the transcription of PLS3 by dual-luciferase promoter assays. Thus, we provide evidence for a multilevel epigenetic regulation of PLS3 that may help to understand the protective or disease-associated PLS3 dysregulation.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.ajhg.2023.02.004', 'doi' => '10.1016/j.ajhg.2023.02.004', 'modified' => '2023-04-14 09:36:04', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 13 => array( 'id' => '4672', 'name' => 'A dataset of definitive endoderm and hepatocyte differentiations fromhuman induced pluripotent stem cells.', 'authors' => 'Tanaka Y. et al.', 'description' => '<p>Hepatocytes are a major parenchymal cell type in the liver and play an essential role in liver function. Hepatocyte-like cells can be differentiated in vitro from induced pluripotent stem cells (iPSCs) via definitive endoderm (DE)-like cells and hepatoblast-like cells. Here, we explored the in vitro differentiation time-course of hepatocyte-like cells. We performed methylome and transcriptome analyses for hepatocyte-like cell differentiation. We also analyzed DE-like cell differentiation by methylome, transcriptome, chromatin accessibility, and GATA6 binding profiles, using finer time-course samples. In this manuscript, we provide a detailed description of the dataset and the technical validations. Our data may be valuable for the analysis of the molecular mechanisms underlying hepatocyte and DE differentiations.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36788249', 'doi' => '10.1038/s41597-023-02001-9', 'modified' => '2023-04-14 09:41:29', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 14 => array( 'id' => '4643', 'name' => 'The mineralocorticoid receptor modulates timing and location of genomicbinding by glucocorticoid receptor in response to synthetic glucocorticoidsin keratinocytes.', 'authors' => 'Carceller-Zazo E. et al.', 'description' => '<p>Glucocorticoids (GCs) exert potent antiproliferative and anti-inflammatory properties, explaining their therapeutic efficacy for skin diseases. GCs act by binding to the GC receptor (GR) and the mineralocorticoid receptor (MR), co-expressed in classical and non-classical targets including keratinocytes. Using knockout mice, we previously demonstrated that GR and MR exert essential nonoverlapping functions in skin homeostasis. These closely related receptors may homo- or heterodimerize to regulate transcription, and theoretically bind identical GC-response elements (GRE). We assessed the contribution of MR to GR genomic binding and the transcriptional response to the synthetic GC dexamethasone (Dex) using control (CO) and MR knockout (MR ) keratinocytes. GR chromatin immunoprecipitation (ChIP)-seq identified peaks common and unique to both genotypes upon Dex treatment (1 h). GREs, AP-1, TEAD, and p53 motifs were enriched in CO and MR peaks. However, GR genomic binding was 35\% reduced in MR , with significantly decreased GRE enrichment, and reduced nuclear GR. Surface plasmon resonance determined steady state affinity constants, suggesting preferred dimer formation as MR-MR > GR-MR ~ GR-GR; however, kinetic studies demonstrated that GR-containing dimers had the longest lifetimes. Despite GR-binding differences, RNA-seq identified largely similar subsets of differentially expressed genes in both genotypes upon Dex treatment (3 h). However, time-course experiments showed gene-dependent differences in the magnitude of expression, which correlated with earlier and more pronounced GR binding to GRE sites unique to CO including near Nr3c1. Our data show that endogenous MR has an impact on the kinetics and differential genomic binding of GR, affecting the time-course, specificity, and magnitude of GC transcriptional responses in keratinocytes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36527388', 'doi' => '10.1096/fj.202201199RR', 'modified' => '2023-03-28 08:55:08', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 15 => array( 'id' => '4605', 'name' => 'Gene Regulatory Interactions at Lamina-Associated Domains', 'authors' => 'Madsen-Østerbye J. et al.', 'description' => '<p>The nuclear lamina provides a repressive chromatin environment at the nuclear periphery. However, whereas most genes in lamina-associated domains (LADs) are inactive, over ten percent reside in local euchromatic contexts and are expressed. How these genes are regulated and whether they are able to interact with regulatory elements remain unclear. Here, we integrate publicly available enhancer-capture Hi-C data with our own chromatin state and transcriptomic datasets to show that inferred enhancers of active genes in LADs are able to form connections with other enhancers within LADs and outside LADs. Fluorescence in situ hybridization analyses show proximity changes between differentially expressed genes in LADs and distant enhancers upon the induction of adipogenic differentiation. We also provide evidence of involvement of lamin A/C, but not lamin B1, in repressing genes at the border of an in-LAD active region within a topological domain. Our data favor a model where the spatial topology of chromatin at the nuclear lamina is compatible with gene expression in this dynamic nuclear compartment.</p>', 'date' => '2023-01-01', 'pmid' => 'https://doi.org/10.3390%2Fgenes14020334', 'doi' => '10.3390/genes14020334', 'modified' => '2023-04-04 08:57:32', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 16 => array( 'id' => '4578', 'name' => 'The aryl hydrocarbon receptor cell intrinsically promotes resident memoryCD8 T cell differentiation and function.', 'authors' => 'Dean J. W. et al.', 'description' => '<p>The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4 T cells; however, its cell-intrinsic role in CD8 T cells remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8 T cell (T) differentiation and function. Genetic ablation of Ahr in mouse CD8 T cells leads to increased CD127KLRG1 short-lived effector cells and CD44CD62L T central memory cells but reduced granzyme-B-producing CD69CD103 T cells. Genome-wide analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8 T cell population, revealed by single-cell RNA-seq, is diminished upon Ahr deletion, compromising anti-tumor immunity. Human intestinal intraepithelial CD8 T cells also highly express AHR that regulates in vitro T differentiation and granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8 T cell immunity.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36640340', 'doi' => '10.1016/j.celrep.2022.111963', 'modified' => '2023-04-11 10:14:26', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 17 => array( 'id' => '4577', 'name' => 'Impact of Fetal Exposure to Endocrine Disrupting ChemicalMixtures on FOXA3 Gene and Protein Expression in Adult RatTestes.', 'authors' => 'Walker C. et al.', 'description' => '<p>Perinatal exposure to endocrine disrupting chemicals (EDCs) has been shown to affect male reproductive functions. However, the effects on male reproduction of exposure to EDC mixtures at doses relevant to humans have not been fully characterized. In previous studies, we found that in utero exposure to mixtures of the plasticizer di(2-ethylhexyl) phthalate (DEHP) and the soy-based phytoestrogen genistein (Gen) induced abnormal testis development in rats. In the present study, we investigated the molecular basis of these effects in adult testes from the offspring of pregnant SD rats gavaged with corn oil or Gen + DEHP mixtures at 0.1 or 10 mg/kg/day. Testicular transcriptomes were determined by microarray and RNA-seq analyses. A protein analysis was performed on paraffin and frozen testis sections, mainly by immunofluorescence. The transcription factor forkhead box protein 3 (FOXA3), a key regulator of Leydig cell function, was identified as the most significantly downregulated gene in testes from rats exposed in utero to Gen + DEHP mixtures. FOXA3 protein levels were decreased in testicular interstitium at a dose previously found to reduce testosterone levels, suggesting a primary effect of fetal exposure to Gen + DEHP on adult Leydig cells, rather than on spermatids and Sertoli cells, also expressing FOXA3. Thus, FOXA3 downregulation in adult testes following fetal exposure to Gen + DEHP may contribute to adverse male reproductive outcomes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36674726', 'doi' => '10.3390/ijms24021211', 'modified' => '2023-04-11 10:18:58', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 18 => array( 'id' => '4721', 'name' => 'Transfer of blocker-based qPCR reactions for DNA methylation analysisinto a microfluidic LoC system using thermal modeling.', 'authors' => 'Kärcher J.et al.', 'description' => '<p>Changes in the DNA methylation landscape are associated with many diseases like cancer. Therefore, DNA methylation analysis is of great interest for molecular diagnostics and can be applied, e.g., for minimally invasive diagnostics in liquid biopsy samples like blood plasma. Sensitive detection of local methylation, which occurs in various cancer types, can be achieved with quantitative HeavyMethyl-PCR using oligonucleotides that block the amplification of unmethylated DNA. A transfer of these quantitative PCRs (qPCRs) into point-of-care (PoC) devices like microfluidic Lab-on-Chip (LoC) cartridges can be challenging as LoC systems show significantly different thermal properties than qPCR cyclers. We demonstrate how an adequate thermal model of the specific LoC system can help us to identify a suitable thermal profile, even for complex HeavyMethyl qPCRs, with reduced experimental effort. Using a simulation-based approach, we demonstrate a proof-of-principle for the successful LoC transfer of colorectal /-qPCR from Epi Procolon® colorectal carcinoma test, by avoidance of oligonucleotide interactions.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36506005', 'doi' => '10.1063/5.0108374', 'modified' => '2023-03-28 09:15:30', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 19 => array( 'id' => '4575', 'name' => 'Intranasal administration of Acinetobacter lwoffii in a murine model ofasthma induces IL-6-mediated protection associated with cecal microbiotachanges.', 'authors' => 'Alashkar A. B. et al.', 'description' => '<p>BACKGROUND: Early-life exposure to certain environmental bacteria including Acinetobacter lwoffii (AL) has been implicated in protection from chronic inflammatory diseases including asthma later in life. However, the underlying mechanisms at the immune-microbe interface remain largely unknown. METHODS: The effects of repeated intranasal AL exposure on local and systemic innate immune responses were investigated in wild-type and Il6 , Il10 , and Il17 mice exposed to ovalbumin-induced allergic airway inflammation. Those investigations were expanded by microbiome analyses. To assess for AL-associated changes in gene expression, the picture arising from animal data was supplemented by in vitro experiments of macrophage and T-cell responses, yielding expression and epigenetic data. RESULTS: The asthma preventive effect of AL was confirmed in the lung. Repeated intranasal AL administration triggered a proinflammatory immune response particularly characterized by elevated levels of IL-6, and consequently, IL-6 induced IL-10 production in CD4 T-cells. Both IL-6 and IL-10, but not IL-17, were required for asthma protection. AL had a profound impact on the gene regulatory landscape of CD4 T-cells which could be largely recapitulated by recombinant IL-6. AL administration also induced marked changes in the gastrointestinal microbiome but not in the lung microbiome. By comparing the effects on the microbiota according to mouse genotype and AL-treatment status, we have identified microbial taxa that were associated with either disease protection or activity. CONCLUSION: These experiments provide a novel mechanism of Acinetobacter lwoffii-induced asthma protection operating through IL-6-mediated epigenetic activation of IL-10 production and with associated effects on the intestinal microbiome.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36458896', 'doi' => '10.1111/all.15606', 'modified' => '2023-04-11 10:23:07', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 20 => array( 'id' => '4574', 'name' => 'Trichoderma root colonization triggers epigenetic changes in jasmonic andsalicylic acid pathway-related genes.', 'authors' => 'Agostini R. B. et al.', 'description' => '<p>Beneficial interactions between plant-roots and Trichoderma spp. lead to a local and systemic enhancement of the plant immune system through a mechanism known as priming of defenses. In recent reports, we outlined a repertoire of genes and proteins differentially regulated in distant tissues of maize plants previously inoculated with Trichoderma atroviride. To further investigate the mechanisms involved in the systemic activation of plant responses, we continued evaluating the regulatory aspects of a selected group of genes when priming is triggered in maize plants. We conducted a time-course expression experiment from the beginning of the interaction between T. atroviride and maize roots, along plant vegetative growth and during Colletotrichum graminicola leaf infection. In addition to gene expression studies, the levels of jasmonic and salicylic acid were determined in the same samples for a comprehensive understanding of the gene expression results. Lastly, chromatin structure and modification assays were designed to evaluate the role of epigenetic marks during the long-lasting activation of the primed state of maize plants. The overall analysis of the results allowed us to shed some light on the interplay between the phytohormones and epigenetic regulatory events in the systemic and long-lasting regulation of maize plant defenses after Trichoderma inoculation.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36575905', 'doi' => '10.1093/jxb/erac518', 'modified' => '2023-04-14 09:08:14', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 21 => array( 'id' => '4474', 'name' => 'DNA sequence and chromatin modifiers cooperate to confer epigeneticbistability at imprinting control regions.', 'authors' => 'Butz S. et al.', 'description' => '<p>Genomic imprinting is regulated by parental-specific DNA methylation of imprinting control regions (ICRs). Despite an identical DNA sequence, ICRs can exist in two distinct epigenetic states that are memorized throughout unlimited cell divisions and reset during germline formation. Here, we systematically study the genetic and epigenetic determinants of this epigenetic bistability. By iterative integration of ICRs and related DNA sequences to an ectopic location in the mouse genome, we first identify the DNA sequence features required for maintenance of epigenetic states in embryonic stem cells. The autonomous regulatory properties of ICRs further enabled us to create DNA-methylation-sensitive reporters and to screen for key components involved in regulating their epigenetic memory. Besides DNMT1, UHRF1 and ZFP57, we identify factors that prevent switching from methylated to unmethylated states and show that two of these candidates, ATF7IP and ZMYM2, are important for the stability of DNA and H3K9 methylation at ICRs in embryonic stem cells.</p>', 'date' => '2022-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36333500', 'doi' => '10.1038/s41588-022-01210-z', 'modified' => '2022-11-18 12:20:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 22 => array( 'id' => '4493', 'name' => 'Smc5/6 silences episomal transcription by a three-step function.', 'authors' => 'Abdul F. et al.', 'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36097294', 'doi' => '10.1038/s41594-022-00829-0', 'modified' => '2022-11-18 12:41:42', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 23 => array( 'id' => '4495', 'name' => 'Exploration of nuclear body-enhanced sumoylation reveals that PMLrepresses 2-cell features of embryonic stem cells.', 'authors' => 'Tessier S. et al.', 'description' => '<p>Membrane-less organelles are condensates formed by phase separation whose functions often remain enigmatic. Upon oxidative stress, PML scaffolds Nuclear Bodies (NBs) to regulate senescence or metabolic adaptation. PML NBs recruit many partner proteins, but the actual biochemical mechanism underlying their pleiotropic functions remains elusive. Similarly, PML role in embryonic stem cell (ESC) and retro-element biology is unsettled. Here we demonstrate that PML is essential for oxidative stress-driven partner SUMO2/3 conjugation in mouse ESCs (mESCs) or leukemia, a process often followed by their poly-ubiquitination and degradation. Functionally, PML is required for stress responses in mESCs. Differential proteomics unravel the KAP1 complex as a PML NB-dependent SUMO2-target in arsenic-treated APL mice or mESCs. PML-driven KAP1 sumoylation enables activation of this key epigenetic repressor implicated in retro-element silencing. Accordingly, Pml mESCs re-express transposable elements and display 2-Cell-Like features, the latter enforced by PML-controlled SUMO2-conjugation of DPPA2. Thus, PML orchestrates mESC state by coordinating SUMO2-conjugation of different transcriptional regulators, raising new hypotheses about PML roles in cancer.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36175410', 'doi' => '10.1038/s41467-022-33147-6', 'modified' => '2022-11-21 10:21:48', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 24 => array( 'id' => '4502', 'name' => 'Loss of epigenetic regulation disrupts lineage integrity, inducesaberrant alveogenesis and promotes breast cancer.', 'authors' => 'Langille E. et al.', 'description' => '<p>Systematically investigating the scores of genes mutated in cancer and discerning disease drivers from inconsequential bystanders is a prerequisite for Precision Medicine but remains challenging. Here, we developed a somatic CRISPR/Cas9 mutagenesis screen to study 215 recurrent 'long-tail' breast cancer genes, which revealed epigenetic regulation as a major tumor suppressive mechanism. We report that components of the BAP1 and the COMPASS-like complexes, including KMT2C/D, KDM6A, BAP1 and ASXL1/2 ("EpiDrivers"), cooperate with PIK3CAH1047R to transform mouse and human breast epithelial cells. Mechanistically, we find that activation of PIK3CAH1047R and concomitant EpiDriver loss triggered an alveolar-like lineage conversion of basal mammary epithelial cells and accelerated formation of luminal-like tumors, suggesting a basal origin for luminal tumors. EpiDrivers mutations are found in ~39\% of human breast cancers and ~50\% of ductal-carcinoma-in-situ express casein suggesting that lineage infidelity and alveogenic mimicry may significantly contribute to early steps of breast cancer etiology.</p>', 'date' => '2022-09-01', 'pmid' => 'https://aacrjournals.org/cancerdiscovery/article-abstract/doi/10.1158/2159-8290.CD-21-0865/709222/Loss-of-epigenetic-regulation-disrupts-lineage?redirectedFrom=fulltext', 'doi' => '10.1158/2159-8290.CD-21-0865', 'modified' => '2022-11-21 10:34:24', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 25 => array( 'id' => '4449', 'name' => 'RAD51 protects human cells from transcription-replication conflicts.', 'authors' => 'Bhowmick R. et al.', 'description' => '<p>Oncogene activation during tumorigenesis promotes DNA replication stress (RS), which subsequently drives the formation of cancer-associated chromosomal rearrangements. Many episodes of physiological RS likely arise due to conflicts between the DNA replication and transcription machineries operating simultaneously at the same loci. One role of the RAD51 recombinase in human cells is to protect replication forks undergoing RS. Here, we have identified a key role for RAD51 in preventing transcription-replication conflicts (TRCs) from triggering replication fork breakage. The genomic regions most affected by RAD51 deficiency are characterized by being replicated and transcribed in early S-phase and show significant overlap with loci prone to cancer-associated amplification. Consistent with a role for RAD51 in protecting against transcription-replication conflicts, many of the adverse effects of RAD51 depletion are ameliorated by inhibiting early S-phase transcription. We propose a model whereby RAD51 suppresses fork breakage and subsequent inadvertent amplification of genomic loci prone to experiencing TRCs.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36002000', 'doi' => '10.1016/j.molcel.2022.07.010', 'modified' => '2022-10-14 16:44:54', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 26 => array( 'id' => '4511', 'name' => 'The Arabidopsis APOLO and human UPAT sequence-unrelated longnoncoding RNAs can modulate DNA and histone methylation machineries inplants.', 'authors' => 'Fonouni-Farde C. et al.', 'description' => '<p>BACKGROUND: RNA-DNA hybrid (R-loop)-associated long noncoding RNAs (lncRNAs), including the Arabidopsis lncRNA AUXIN-REGULATED PROMOTER LOOP (APOLO), are emerging as important regulators of three-dimensional chromatin conformation and gene transcriptional activity. RESULTS: Here, we show that in addition to the PRC1-component LIKE HETEROCHROMATIN PROTEIN 1 (LHP1), APOLO interacts with the methylcytosine-binding protein VARIANT IN METHYLATION 1 (VIM1), a conserved homolog of the mammalian DNA methylation regulator UBIQUITIN-LIKE CONTAINING PHD AND RING FINGER DOMAINS 1 (UHRF1). The APOLO-VIM1-LHP1 complex directly regulates the transcription of the auxin biosynthesis gene YUCCA2 by dynamically determining DNA methylation and H3K27me3 deposition over its promoter during the plant thermomorphogenic response. Strikingly, we demonstrate that the lncRNA UHRF1 Protein Associated Transcript (UPAT), a direct interactor of UHRF1 in humans, can be recognized by VIM1 and LHP1 in plant cells, despite the lack of sequence homology between UPAT and APOLO. In addition, we show that increased levels of APOLO or UPAT hamper VIM1 and LHP1 binding to YUCCA2 promoter and globally alter the Arabidopsis transcriptome in a similar manner. CONCLUSIONS: Collectively, our results uncover a new mechanism in which a plant lncRNA coordinates Polycomb action and DNA methylation through the interaction with VIM1, and indicates that evolutionary unrelated lncRNAs with potentially conserved structures may exert similar functions by interacting with homolog partners.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36038910', 'doi' => '10.1186/s13059-022-02750-7', 'modified' => '2022-11-21 10:43:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 27 => array( 'id' => '4552', 'name' => 'Prolonged FOS activity disrupts a global myogenic transcriptionalprogram by altering 3D chromatin architecture in primary muscleprogenitor cells.', 'authors' => 'Barutcu A Rasim et al.', 'description' => '<p>BACKGROUND: The AP-1 transcription factor, FBJ osteosarcoma oncogene (FOS), is induced in adult muscle satellite cells (SCs) within hours following muscle damage and is required for effective stem cell activation and muscle repair. However, why FOS is rapidly downregulated before SCs enter cell cycle as progenitor cells (i.e., transiently expressed) remains unclear. Further, whether boosting FOS levels in the proliferating progeny of SCs can enhance their myogenic properties needs further evaluation. METHODS: We established an inducible, FOS expression system to evaluate the impact of persistent FOS activity in muscle progenitor cells ex vivo. We performed various assays to measure cellular proliferation and differentiation, as well as uncover changes in RNA levels and three-dimensional (3D) chromatin interactions. RESULTS: Persistent FOS activity in primary muscle progenitor cells severely antagonizes their ability to differentiate and form myotubes within the first 2 weeks in culture. RNA-seq analysis revealed that ectopic FOS activity in muscle progenitor cells suppressed a global pro-myogenic transcriptional program, while activating a stress-induced, mitogen-activated protein kinase (MAPK) transcriptional signature. Additionally, we observed various FOS-dependent, chromosomal re-organization events in A/B compartments, topologically associated domains (TADs), and genomic loops near FOS-regulated genes. CONCLUSIONS: Our results suggest that elevated FOS activity in recently activated muscle progenitor cells perturbs cellular differentiation by altering the 3D chromosome organization near critical pro-myogenic genes. This work highlights the crucial importance of tightly controlling FOS expression in the muscle lineage and suggests that in states of chronic stress or disease, persistent FOS activity in muscle precursor cells may disrupt the muscle-forming process.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35971133', 'doi' => '10.1186/s13395-022-00303-x', 'modified' => '2022-11-24 10:11:55', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 28 => array( 'id' => '4452', 'name' => 'Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.', 'authors' => 'Schomann T. et al.', 'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>', 'date' => '2022-07-01', 'pmid' => 'https://doi.org/10.3390%2Fbiom12081048', 'doi' => '10.3390/biom12081048', 'modified' => '2022-10-21 09:33:25', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 29 => array( 'id' => '4446', 'name' => 'Variation in PU.1 binding and chromatin looping at neutrophil enhancersinfluences autoimmune disease susceptibility', 'authors' => 'Watt S. et al. ', 'description' => '<p>Neutrophils play fundamental roles in innate inflammatory response, shape adaptive immunity1, and have been identified as a potentially causal cell type underpinning genetic associations with immune system traits and diseases2,3 The majority of these variants are non-coding and the underlying mechanisms are not fully understood. Here, we profiled the binding of one of the principal myeloid transcriptional regulators, PU.1, in primary neutrophils across nearly a hundred volunteers, and elucidate the coordinated genetic effects of PU.1 binding variation, local chromatin state, promoter-enhancer interactions and gene expression. We show that PU.1 binding and the associated chain of molecular changes underlie genetically-driven differences in cell count and autoimmune disease susceptibility. Our results advance interpretation for genetic loci associated with neutrophil biology and immune disease.</p>', 'date' => '2022-05-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/620260v1.abstract', 'doi' => '10.1101/620260', 'modified' => '2022-10-14 16:39:03', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 30 => array( 'id' => '4217', 'name' => 'CREBBP/EP300 acetyltransferase inhibition disrupts FOXA1-bound enhancers to inhibit the proliferation of ER+ breast cancer cells.', 'authors' => 'Bommi-Reddy A. et al.', 'description' => '<p><span>Therapeutic targeting of the estrogen receptor (ER) is a clinically validated approach for estrogen receptor positive breast cancer (ER+ BC), but sustained response is limited by acquired resistance. Targeting the transcriptional coactivators required for estrogen receptor activity represents an alternative approach that is not subject to the same limitations as targeting estrogen receptor itself. In this report we demonstrate that the acetyltransferase activity of coactivator paralogs CREBBP/EP300 represents a promising therapeutic target in ER+ BC. Using the potent and selective inhibitor CPI-1612, we show that CREBBP/EP300 acetyltransferase inhibition potently suppresses in vitro and in vivo growth of breast cancer cell line models and acts in a manner orthogonal to directly targeting ER. CREBBP/EP300 acetyltransferase inhibition suppresses ER-dependent transcription by targeting lineage-specific enhancers defined by the pioneer transcription factor FOXA1. These results validate CREBBP/EP300 acetyltransferase activity as a viable target for clinical development in ER+ breast cancer.</span></p>', 'date' => '2022-03-30', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/35353838/', 'doi' => '10.1371/journal.pone.0262378', 'modified' => '2022-04-12 10:56:54', 'created' => '2022-04-12 10:56:54', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 31 => array( 'id' => '4407', 'name' => 'Transient regulation of focal adhesion via Tensin3 is required fornascent oligodendrocyte differentiation', 'authors' => 'Merour E. et al.', 'description' => '<p>The differentiation of oligodendroglia from oligodendrocyte precursor cells (OPCs) to complex and extensive myelinating oligodendrocytes (OLs) is a multistep process that involves largescale morphological changes with significant strain on the cytoskeleton. While key chromatin and transcriptional regulators of differentiation have been identified, their target genes responsible for the morphological changes occurring during OL myelination are still largely unknown. Here, we show that the regulator of focal adhesion, Tensin3 (Tns3), is a direct target gene of Olig2, Chd7, and Chd8, transcriptional regulators of OL differentiation. Tns3 is transiently upregulated and localized to cell processes of immature OLs, together with integrin-β1, a key mediator of survival at this transient stage. Constitutive Tns3 loss-of-function leads to reduced viability in mouse and humans, with surviving knockout mice still expressing Tns3 in oligodendroglia. Acute deletion of Tns3 in vivo, either in postnatal neural stem cells (NSCs) or in OPCs, leads to a two-fold reduction in OL numbers. We find that the transient upregulation of Tns3 is required to protect differentiating OPCs and immature OLs from cell death by preventing the upregulation of p53, a key regulator of apoptosis. Altogether, our findings reveal a specific time window during which transcriptional upregulation of Tns3 in immature OLs is required for OL differentiation likely by mediating integrin-β1 survival signaling to the actin cytoskeleton as OL undergo the large morphological changes required for their terminal differentiation.</p>', 'date' => '2022-02-01', 'pmid' => 'https://doi.org/10.1101%2F2022.02.25.481980', 'doi' => '10.1101/2022.02.25.481980', 'modified' => '2022-08-11 15:05:41', 'created' => '2022-08-11 12:14:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 32 => array( 'id' => '4238', 'name' => 'The long noncoding RNA H19 regulates tumor plasticity inneuroendocrine prostate cancer', 'authors' => 'Singh N. et al.', 'description' => '<p>Neuroendocrine (NE) prostate cancer (NEPC) is a lethal subtype of castration-resistant prostate cancer (PCa) arising either de novo or from transdifferentiated prostate adenocarcinoma following androgen deprivation therapy (ADT). Extensive computational analysis has identified a high degree of association between the long noncoding RNA (lncRNA) H19 and NEPC, with the longest isoform highly expressed in NEPC. H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown). It contributes to treatment resistance, with the knockdown of H19 re-sensitizing PCa to ADT. It is also essential for the proliferation and invasion of NEPC. H19 levels are negatively regulated by androgen signaling via androgen receptor (AR). When androgen is absent SOX2 levels increase, driving H19 transcription and facilitating transdifferentiation. H19 facilitates the PRC2 complex in regulating methylation changes at H3K27me3/H3K4me3 histone sites of AR-driven and NEPC-related genes. Additionally, this lncRNA induces alterations in genome-wide DNA methylation on CpG sites, further regulating genes associated with the NEPC phenotype. Our clinical data identify H19 as a candidate diagnostic marker and predictive marker of NEPC with elevated H19 levels associated with an increased probability of biochemical recurrence and metastatic disease in patients receiving ADT. Here we report H19 as an early upstream regulator of cell fate, plasticity, and treatment resistance in NEPC that can reverse/transform cells to a treatable form of PCa once therapeutically deactivated.</p>', 'date' => '2021-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34934057', 'doi' => '10.1038/s41467-021-26901-9', 'modified' => '2022-05-19 17:06:50', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 33 => array( 'id' => '4239', 'name' => 'Epromoters function as a hub to recruit key transcription factorsrequired for the inflammatory response', 'authors' => 'Santiago-Algarra D. et al. ', 'description' => '<p>Gene expression is controlled by the involvement of gene-proximal (promoters) and distal (enhancers) regulatory elements. Our previous results demonstrated that a subset of gene promoters, termed Epromoters, work as bona fide enhancers and regulate distal gene expression. Here, we hypothesized that Epromoters play a key role in the coordination of rapid gene induction during the inflammatory response. Using a high-throughput reporter assay we explored the function of Epromoters in response to type I interferon. We find that clusters of IFNa-induced genes are frequently associated with Epromoters and that these regulatory elements preferentially recruit the STAT1/2 and IRF transcription factors and distally regulate the activation of interferon-response genes. Consistently, we identified and validated the involvement of Epromoter-containing clusters in the regulation of LPS-stimulated macrophages. Our findings suggest that Epromoters function as a local hub recruiting the key TFs required for coordinated regulation of gene clusters during the inflammatory response.</p>', 'date' => '2021-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34795220', 'doi' => '10.1038/s41467-021-26861-0', 'modified' => '2022-05-19 17:10:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 34 => array( 'id' => '4231', 'name' => 'Differential contribution to gene expression prediction of histonemodifications at enhancers or promoters.', 'authors' => 'González-Ramírez M. et al.', 'description' => '<p>The ChIP-seq signal of histone modifications at promoters is a good predictor of gene expression in different cellular contexts, but whether this is also true at enhancers is not clear. To address this issue, we develop quantitative models to characterize the relationship of gene expression with histone modifications at enhancers or promoters. We use embryonic stem cells (ESCs), which contain a full spectrum of active and repressed (poised) enhancers, to train predictive models. As many poised enhancers in ESCs switch towards an active state during differentiation, predictive models can also be trained on poised enhancers throughout differentiation and in development. Remarkably, we determine that histone modifications at enhancers, as well as promoters, are predictive of gene expression in ESCs and throughout differentiation and development. Importantly, we demonstrate that their contribution to the predictive models varies depending on their location in enhancers or promoters. Moreover, we use a local regression (LOESS) to normalize sequencing data from different sources, which allows us to apply predictive models trained in a specific cellular context to a different one. We conclude that the relationship between gene expression and histone modifications at enhancers is universal and different from promoters. Our study provides new insight into how histone modifications relate to gene expression based on their location in enhancers or promoters.</p>', 'date' => '2021-09-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473698/', 'doi' => '10.1371/journal.pcbi.1009368', 'modified' => '2022-05-19 16:50:59', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 35 => array( 'id' => '4315', 'name' => 'Atg7 deficiency in microglia drives an altered transcriptomic profileassociated with an impaired neuroinflammatory response', 'authors' => 'Friess L. et al.', 'description' => '<p>Microglia, resident immunocompetent cells of the central nervous system, can display a range of reaction states and thereby exhibit distinct biological functions across development, adulthood and under disease conditions. Distinct gene expression profiles are reported to define each of these microglial reaction states. Hence, the identification of modulators of selective microglial transcriptomic signature, which have the potential to regulate unique microglial function has gained interest. Here, we report the identification of ATG7 (Autophagy-related 7) as a selective modulator of an NF-κB-dependent transcriptional program controlling the pro-inflammatory response of microglia. We also uncover that microglial Atg7-deficiency was associated with reduced microglia-mediated neurotoxicity, and thus a loss of biological function associated with the pro-inflammatory microglial reactive state. Further, we show that Atg7-deficiency in microglia did not impact on their ability to respond to alternative stimulus, such as one driving them towards an anti-inflammatory/tumor supportive phenotype. The identification of distinct regulators, such as Atg7, controlling specific microglial transcriptional programs could lead to developing novel therapeutic strategies aiming to manipulate selected microglial phenotypes, instead of the whole microglial population with is associated with several pitfalls. Supplementary Information The online version contains supplementary material available at 10.1186/s13041-021-00794-7.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34082793', 'doi' => '10.1186/s13041-021-00794-7', 'modified' => '2022-08-02 16:47:13', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 36 => array( 'id' => '4349', 'name' => 'Lasp1 regulates adherens junction dynamics and fibroblast transformationin destructive arthritis', 'authors' => 'Beckmann D. et al.', 'description' => '<p>The LIM and SH3 domain protein 1 (Lasp1) was originally cloned from metastatic breast cancer and characterised as an adaptor molecule associated with tumourigenesis and cancer cell invasion. However, the regulation of Lasp1 and its function in the aggressive transformation of cells is unclear. Here we use integrative epigenomic profiling of invasive fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA) and from mouse models of the disease, to identify Lasp1 as an epigenomically co-modified region in chronic inflammatory arthritis and a functionally important binding partner of the Cadherin-11/β-Catenin complex in zipper-like cell-to-cell contacts. In vitro, loss or blocking of Lasp1 alters pathological tissue formation, migratory behaviour and platelet-derived growth factor response of arthritic FLS. In arthritic human TNF transgenic mice, deletion of Lasp1 reduces arthritic joint destruction. Therefore, we show a function of Lasp1 in cellular junction formation and inflammatory tissue remodelling and identify Lasp1 as a potential target for treating inflammatory joint disorders associated with aggressive cellular transformation.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34131132', 'doi' => '10.1038/s41467-021-23706-8', 'modified' => '2022-08-03 17:02:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 37 => array( 'id' => '4136', 'name' => 'The lncRNA and the transcription factor WRKY42 target common cell wallEXTENSIN encoding genes to trigger root hair cell elongation.', 'authors' => 'Pacheco, J. M. et al.', 'description' => '<p>Plant long noncoding RNAs (lncRNAs) are key chromatin dynamics regulators, directing the transcriptional programs driving a wide variety of developmental outputs. Recently, we uncovered how the lncRNA () directly recognizes the locus encoding the root hair (RH) master regulator () modulating its transcriptional activation and leading to low temperature-induced RH elongation. We further demonstrated that interacts with the transcription factor WRKY42 in a novel ribonucleoprotein complex shaping epigenetic environment and integrating signals governing RH growth and development. In this work, we expand this model showing that is able to bind and positively control the expression of several cell wall EXTENSIN (EXT) encoding genes, including , a key regulator for RH growth. Interestingly, emerged as a novel common target of and WRKY42. Furthermore, we showed that the ROS homeostasis-related gene is deregulated upon overexpression, likely through the RHD6-RSL4 pathway, and that is required for low temperature-dependent enhancement of RH growth. Collectively, our results uncover an intricate regulatory network involving the /WRKY42 hub in the control of master and effector genes during RH development.</p>', 'date' => '2021-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33944666', 'doi' => '10.1080/15592324.2021.1920191', 'modified' => '2021-12-13 09:06:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 38 => array( 'id' => '4143', 'name' => 'Placental uptake and metabolism of 25(OH)Vitamin D determines itsactivity within the fetoplacental unit', 'authors' => 'Ashley, B. et al.', 'description' => '<p>Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes, but the underlying mechanisms have not been elucidated. Using physiological human placental perfusion approaches and intact villous explants we demonstrate a role for the placenta in regulating the relationships between maternal 25(OH)D concentrations and fetal physiology. Here, we demonstrate active placental uptake of 25(OH)D3 by endocytosis and placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the fetal and maternal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than solely the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer, including transcriptional activation and inflammatory responses. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta; with widespread effects on the placenta itself. These data show complex and synergistic interplay between vitamin D and the placenta, and inform possible interventions to optimise placental function to better support fetal growth and the maternal adaptations to pregnancy.</p>', 'date' => '2021-05-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.01.431439', 'doi' => '10.1101/2021.03.01.431439', 'modified' => '2021-12-13 09:29:25', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 39 => array( 'id' => '4147', 'name' => 'Waves of sumoylation support transcription dynamics during adipocytedifferentiation', 'authors' => 'Zhao, X. et al.', 'description' => '<p>Tight control of gene expression networks required for adipose tissue formation and plasticity is essential for adaptation to energy needs and environmental cues. However, little is known about the mechanisms that orchestrate the dramatic transcriptional changes leading to adipocyte differentiation. We investigated the regulation of nascent transcription by the sumoylation pathway during adipocyte differentiation using SLAMseq and ChIPseq. We discovered that the sumoylation pathway has a dual function in differentiation; it supports the initial downregulation of pre-adipocyte-specific genes, while it promotes the establishment of the mature adipocyte transcriptional program. By characterizing sumoylome dynamics in differentiating adipocytes by mass spectrometry, we found that sumoylation of specific transcription factors like Pparγ/RXR and their co-factors is associated with the transcription of adipogenic genes. Our data demonstrate that the sumoylation pathway coordinates the rewiring of transcriptional networks required for formation of functional adipocytes. This study also provides an in-depth resource of gene transcription dynamics, SUMO-regulated genes and sumoylation sites during adipogenesis.</p>', 'date' => '2021-04-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.20.432084', 'doi' => '10.1101/2021.02.20.432084', 'modified' => '2021-12-14 09:23:28', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 40 => array( 'id' => '4171', 'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.', 'authors' => 'Ryan, Genevieve E. et al.', 'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse LβT2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733', 'doi' => '10.1016/j.mce.2021.111286', 'modified' => '2021-12-21 15:57:35', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 41 => array( 'id' => '4181', 'name' => 'Genetic perturbation of PU.1 binding and chromatin looping at neutrophilenhancers associates with autoimmune disease.', 'authors' => 'Watt, Stephen et al.', 'description' => '<p>Neutrophils play fundamental roles in innate immune response, shape adaptive immunity, and are a potentially causal cell type underpinning genetic associations with immune system traits and diseases. Here, we profile the binding of myeloid master regulator PU.1 in primary neutrophils across nearly a hundred volunteers. We show that variants associated with differential PU.1 binding underlie genetically-driven differences in cell count and susceptibility to autoimmune and inflammatory diseases. We integrate these results with other multi-individual genomic readouts, revealing coordinated effects of PU.1 binding variants on the local chromatin state, enhancer-promoter contacts and downstream gene expression, and providing a functional interpretation for 27 genes underlying immune traits. Collectively, these results demonstrate the functional role of PU.1 and its target enhancers in neutrophil transcriptional control and immune disease susceptibility.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863903', 'doi' => '10.1038/s41467-021-22548-8', 'modified' => '2021-12-21 16:50:30', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 42 => array( 'id' => '4126', 'name' => 'Fra-1 regulates its target genes via binding to remote enhancers withoutexerting major control on chromatin architecture in triple negative breastcancers.', 'authors' => 'Bejjani, Fabienne and Tolza, Claire and Boulanger, Mathias and Downes,Damien and Romero, Raphaël and Maqbool, Muhammad Ahmad and Zine ElAabidine, Amal and Andrau, Jean-Christophe and Lebre, Sophie and Brehelin,Laurent and Parrinello, Hughes and Rohmer,', 'description' => '<p>The ubiquitous family of dimeric transcription factors AP-1 is made up of Fos and Jun family proteins. It has long been thought to operate principally at gene promoters and how it controls transcription is still ill-understood. The Fos family protein Fra-1 is overexpressed in triple negative breast cancers (TNBCs) where it contributes to tumor aggressiveness. To address its transcriptional actions in TNBCs, we combined transcriptomics, ChIP-seqs, machine learning and NG Capture-C. Additionally, we studied its Fos family kin Fra-2 also expressed in TNBCs, albeit much less. Consistently with their pleiotropic effects, Fra-1 and Fra-2 up- and downregulate individually, together or redundantly many genes associated with a wide range of biological processes. Target gene regulation is principally due to binding of Fra-1 and Fra-2 at regulatory elements located distantly from cognate promoters where Fra-1 modulates the recruitment of the transcriptional co-regulator p300/CBP and where differences in AP-1 variant motif recognition can underlie preferential Fra-1- or Fra-2 bindings. Our work also shows no major role for Fra-1 in chromatin architecture control at target gene loci, but suggests collaboration between Fra-1-bound and -unbound enhancers within chromatin hubs sometimes including promoters for other Fra-1-regulated genes. Our work impacts our view of AP-1.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33533919', 'doi' => '10.1093/nar/gkab053', 'modified' => '2021-12-07 10:09:23', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 43 => array( 'id' => '4139', 'name' => 'Cell-specific alterations inPitx1regulatory landscape activation caused bythe loss of a single enhancer', 'authors' => 'Rouco, R. et al.', 'description' => '<p>Most developmental genes rely on multiple transcriptional enhancers for their accurate expression during embryogenesis. Because enhancers may have partially redundant activities, the loss of one of them often leads to a partial loss of gene expression and concurrent moderate phenotypic outcome, if any. While such a phenomenon has been observed in many instances, the nature of the underlying mechanisms remains elusive. We used the Pitx1 testbed locus to characterize in detail the regulatory and cellular identity alterations following the deletion in vivo of one of its enhancers (Pen), which normally accounts for 30 percent of Pitx1 expression in hindlimb buds. By combining single cell transcriptomics and a novel in embryo cell tracing approach, we observed that this global decrease in Pitx1 expression results from both an increase in the number of non- or low-expressing cells, and a decrease in the number of high-expressing cells. We found that the over-representation of Pitx1 non/low-expressing cells originates from a failure of the Pitx1 locus to coordinate enhancer activities and 3D chromatin changes. The resulting increase in Pitx1 non/low-expressing cells eventually affects the proximal limb more severely than the distal limb, leading to a clubfoot phenotype likely produced through a localized heterochrony and concurrent loss of irregular connective tissue. This data suggests that, in some cases, redundant enhancers may be used to locally enforce a robust activation of their host regulatory landscapes.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.10.434611', 'doi' => '10.1101/2021.03.10.434611', 'modified' => '2021-12-13 09:18:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 44 => array( 'id' => '4141', 'name' => 'Transgenic mice for in vivo epigenome editing with CRISPR-based systems', 'authors' => 'Gemberling, M. et al.', 'description' => '<p>The discovery, characterization, and adaptation of the RNA-guided clustered regularly interspersed short palindromic repeat (CRISPR)-Cas9 system has greatly increased the ease with which genome and epigenome editing can be performed. Fusion of chromatin-modifying domains to the nuclease-deactivated form of Cas9 (dCas9) has enabled targeted gene activation or repression in both cultured cells and in vivo in animal models. However, delivery of the large dCas9 fusion proteins to target cell types and tissues is an obstacle to widespread adoption of these tools for in vivo studies. Here we describe the generation and validation of two conditional transgenic mouse lines for targeted gene regulation, Rosa26:LSL-dCas9-p300 for gene activation and Rosa26:LSL-dCas9-KRAB for gene repression. Using the dCas9p300 and dCas9KRAB transgenic mice we demonstrate activation or repression of genes in both the brain and liver in vivo, and T cells and fibroblasts ex vivo. We show gene regulation and targeted epigenetic modification with gRNAs targeting either transcriptional start sites (TSS) or distal enhancer elements, as well as corresponding changes to downstream phenotypes. These mouse lines are convenient and valuable tools for facile, temporally controlled, and tissue-restricted epigenome editing and manipulation of gene expression in vivo.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.08.434430', 'doi' => '10.1101/2021.03.08.434430', 'modified' => '2021-12-13 09:23:10', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 45 => array( 'id' => '4163', 'name' => 'Transcriptional programming drives Ibrutinib-resistance evolution in mantlecell lymphoma.', 'authors' => 'Zhao, Xiaohong et al.', 'description' => '<p>Ibrutinib, a bruton's tyrosine kinase (BTK) inhibitor, provokes robust clinical responses in aggressive mantle cell lymphoma (MCL), yet many patients relapse with lethal Ibrutinib-resistant (IR) disease. Here, using genomic, chemical proteomic, and drug screen profiling, we report that enhancer remodeling-mediated transcriptional activation and adaptive signaling changes drive the aggressive phenotypes of IR. Accordingly, IR MCL cells are vulnerable to inhibitors of the transcriptional machinery and especially so to inhibitors of cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the positive transcription elongation factor b (P-TEFb) of RNA polymerase II (RNAPII). Further, CDK9 inhibition disables reprogrammed signaling circuits and prevents the emergence of IR in MCL. Finally, and importantly, we find that a robust and facile ex vivo image-based functional drug screening platform can predict clinical therapeutic responses of IR MCL and identify vulnerabilities that can be targeted to disable the evolution of IR.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33730585', 'doi' => '10.1016/j.celrep.2021.108870', 'modified' => '2021-12-21 15:28:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 46 => array( 'id' => '4119', 'name' => 'Coordinated changes in gene expression, H1 variant distribution and genome3D conformation in response to H1 depletion', 'authors' => 'Serna-Pujol, Nuria and Salinas-Pena, Monica and Mugianesi, Francesca and LeDily, François and Marti-Renom, Marc A. and Jordan, Albert', 'description' => '<p>Up to seven members of the histone H1 family may contribute to chromatin compaction and its regulation in human somatic cells. In breast cancer cells, knock-down of multiple H1 variants deregulates many genes, promotes the appearance of genome-wide accessibility sites and triggers an interferon response via activation of heterochromatic repeats. However, how these changes in the expression profile relate to the re-distribution of H1 variants as well as to genome conformational changes have not been yet studied. Here, we combined ChIP-seq of five endogenous H1 variants with Chromosome Conformation Capture analysis in wild-type and H1 knock-down T47D cells. The results indicate that H1 variants coexist in the genome in two large groups depending on the local DNA GC content and that their distribution is robust with respect to multiple H1 depletion. Despite the small changes in H1 variants distribution, knock-down of H1 translated into more isolated but de-compacted chromatin structures at the scale of Topologically Associating Domains or TADs. Such changes in TAD structure correlated with a coordinated gene expression response of their resident genes. This is the first report describing simultaneous profiling of five endogenous H1 variants within a cell line and giving functional evidence of genome topology alterations upon H1 depletion in human cancer cells.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.12.429879', 'doi' => '10.1101/2021.02.12.429879', 'modified' => '2021-12-07 09:43:11', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 47 => array( 'id' => '4144', 'name' => 'REPROGRAMMING CBX8-PRC1 FUNCTION WITH A POSITIVE ALLOSTERICMODULATOR', 'authors' => 'Suh, J. L. et al.', 'description' => '<p>Canonical targeting of Polycomb Repressive Complex 1 (PRC1) to repress developmental genes is mediated by cell type-specific, paralogous chromobox (CBX) proteins (CBX2, 4, 6, 7 and 8). Based on their central role in silencing and their misregulation associated with human disease including cancer, CBX proteins are attractive targets for small molecule chemical probe development. Here, we have used a quantitative and target-specific cellular assay to discover a potent positive allosteric modulator (PAM) of CBX8. The PAM activity of UNC7040 antagonizes H3K27me3 binding by CBX8 while increasing interactions with nucleic acids and participation in variant PRC1. We show that treatment with UNC7040 leads to efficient PRC1 chromatin eviction, loss of silencing and reduced proliferation across different cancer cell lines. Our discovery and characterization of UNC7040 not only revealed the most cellularly potent CBX8-specific chemical probe to date, but also corroborates a mechanism of polycomb regulation by non-histone lysine methylated interaction partners.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.23.432388', 'doi' => '10.1101/2021.02.23.432388', 'modified' => '2021-12-13 09:35:04', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 48 => array( 'id' => '4145', 'name' => 'Germline activity of the heat shock factor HSF-1 programs theinsulin-receptor daf-2 in C. elegans', 'authors' => 'Das, S. et al.', 'description' => '<p>The mechanisms by which maternal stress alters offspring phenotypes remain poorly understood. Here we report that the heat shock transcription factor HSF-1, activated in the C. elegans maternal germline upon stress, epigenetically programs the insulin-like receptor daf-2 by increasing repressive H3K9me2 levels throughout the daf-2 gene. This increase occurs by the recruitment of the C. elegans SETDB1 homolog MET-2 by HSF-1. Increased H3K9me2 levels at daf-2 persist in offspring to downregulate daf-2, activate the C. elegans FOXO ortholog DAF-16 and enhance offspring stress resilience. Thus, HSF-1 activity in the mother promotes the early life programming of the insulin/IGF-1 signaling (IIS) pathway and determines the strategy of stress resilience in progeny.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.22.432344', 'doi' => '10.1101/2021.02.22.432344', 'modified' => '2021-12-14 09:13:54', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 49 => array( 'id' => '4151', 'name' => 'The epigenetic landscape in purified myonuclei from fast and slow muscles', 'authors' => 'Bengtsen, M. et al.', 'description' => '<p>Muscle cells have different phenotypes adapted to different usage and can be grossly divided into fast/glycolytic and slow/oxidative types. While most muscles contain a mixture of such fiber types, we aimed at providing a genome-wide analysis of chromatin environment by ChIP-Seq in two muscle extremes, the almost completely fast/glycolytic extensor digitorum longus (EDL) and slow/oxidative soleus muscles. Muscle is a heterogeneous tissue where less than 60\% of the nuclei are inside muscle fibers. Since cellular homogeneity is critical in epigenome-wide association studies we devised a new method for purifying skeletal muscle nuclei from whole tissue based on the nuclear envelope protein Pericentriolar material 1 (PCM1) being a specific marker for myonuclei. Using antibody labeling and a magnetic-assisted sorting approach we were able to sort out myonuclei with 95\% purity. The sorting eliminated influence from other cell types in the tissue and improved the myo-specific signal. A genome-wide comparison of the epigenetic landscape in EDL and soleus reflected the functional properties of the two muscles each with a distinct regulatory program involving distal enhancers, including a glycolytic super-enhancer in the EDL. The two muscles are also regulated by different sets of transcription factors; e.g. in soleus binding sites for MEF2C, NFATC2 and PPARA were enriched, while in EDL MYOD1 and SOX1 binding sites were found to be overrepresented. In addition, novel factors for muscle regulation such as MAF, ZFX and ZBTB14 were identified.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.04.429545', 'doi' => '10.1101/2021.02.04.429545', 'modified' => '2021-12-14 09:40:02', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 50 => array( 'id' => '4166', 'name' => 'The glucocorticoid receptor recruits the COMPASS complex to regulateinflammatory transcription at macrophage enhancers.', 'authors' => 'Greulich, Franziska et al.', 'description' => '<p>Glucocorticoids (GCs) are effective anti-inflammatory drugs; yet, their mechanisms of action are poorly understood. GCs bind to the glucocorticoid receptor (GR), a ligand-gated transcription factor controlling gene expression in numerous cell types. Here, we characterize GR's protein interactome and find the SETD1A (SET domain containing 1A)/COMPASS (complex of proteins associated with Set1) histone H3 lysine 4 (H3K4) methyltransferase complex highly enriched in activated mouse macrophages. We show that SETD1A/COMPASS is recruited by GR to specific cis-regulatory elements, coinciding with H3K4 methylation dynamics at subsets of sites, upon treatment with lipopolysaccharide (LPS) and GCs. By chromatin immunoprecipitation sequencing (ChIP-seq) and RNA-seq, we identify subsets of GR target loci that display SETD1A occupancy, H3K4 mono-, di-, or tri-methylation patterns, and transcriptional changes. However, our data on methylation status and COMPASS recruitment suggest that SETD1A has additional transcriptional functions. Setd1a loss-of-function studies reveal that SETD1A/COMPASS is required for GR-controlled transcription of subsets of macrophage target genes. We demonstrate that the SETD1A/COMPASS complex cooperates with GR to mediate anti-inflammatory effects.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33567280', 'doi' => '10.1016/j.celrep.2021.108742', 'modified' => '2021-12-21 15:42:49', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 51 => array( 'id' => '4185', 'name' => 'A distinct metabolic response characterizes sensitivity to EZH2inhibition in multiple myeloma.', 'authors' => 'Nylund P. et al.', 'description' => '<p>Multiple myeloma (MM) is a heterogeneous haematological disease that remains clinically challenging. Increased activity of the epigenetic silencer EZH2 is a common feature in patients with poor prognosis. Previous findings have demonstrated that metabolic profiles can be sensitive markers for response to treatment in cancer. While EZH2 inhibition (EZH2i) has proven efficient in inducing cell death in a number of human MM cell lines, we hereby identified a subset of cell lines that despite a global loss of H3K27me3, remains viable after EZH2i. By coupling liquid chromatography-mass spectrometry with gene and miRNA expression profiling, we found that sensitivity to EZH2i correlated with distinct metabolic signatures resulting from a dysregulation of genes involved in methionine cycling. Specifically, EZH2i resulted in a miRNA-mediated downregulation of methionine cycling-associated genes in responsive cells. This induced metabolite accumulation and DNA damage, leading to G2 arrest and apoptosis. Altogether, we unveiled that sensitivity to EZH2i in human MM cell lines is associated with a specific metabolic and gene expression profile post-treatment.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33579905', 'doi' => '10.1038/s41419-021-03447-8', 'modified' => '2022-01-05 14:59:39', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 52 => array( 'id' => '4108', 'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma', 'authors' => 'Laubscher et. al.', 'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that </span><em>SMARCA4</em><span><span> </span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span> </span></span><em>de novo</em><span><span> </span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>', 'date' => '2021-01-07', 'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1', 'doi' => ' 10.21203/rs.3.rs-131009/v1', 'modified' => '2021-07-07 11:52:23', 'created' => '2021-07-07 06:38:34', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 53 => array( 'id' => '4098', 'name' => 'A Tumor Suppressor Enhancer of PTEN in T-cell development and leukemia', 'authors' => 'L. Tottone at al.', 'description' => '<p>Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss of expression of PTEN is associated with the pathogenesis of various cancers, including T-cell leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts with the <em>PTEN</em> promoter in multiple hematopoietic populations, including T-cells, and acts as a hub of relevant transcription factors in T-ALL. Consistently, loss of PE leads to reduced <em>PTEN</em> levels in T-ALL cells. Moreover, PE-null mice show reduced <em>Pten</em> levels in thymocytes and accelerated development of NOTCH1-induced T-ALL. Furthermore, secondary loss of PE in established leukemias leads to accelerated progression and a gene expression signature driven by <em>Pten</em> loss. Finally, we uncovered recurrent deletions encompassing PE in T-ALL, which are associated with decreased <em>PTEN</em> levels. Altogether, our results identify PE as the first long-range tumor suppressor enhancer directly implicated in cancer.</p>', 'date' => '2021-01-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33458694/', 'doi' => '10.1158/2643-3230.BCD-20-0201 ', 'modified' => '2021-05-04 09:51:10', 'created' => '2021-05-04 09:51:10', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 54 => array( 'id' => '4157', 'name' => 'Stronger induction of trained immunity by mucosal BCG or MTBVAC vaccination compared to standard intradermal vaccination.', 'authors' => 'Vierboom, M.P.M. et al. ', 'description' => '<p>BCG vaccination can strengthen protection against pathogens through the induction of epigenetic and metabolic reprogramming of innate immune cells, a process called trained immunity. We and others recently demonstrated that mucosal or intravenous BCG better protects rhesus macaques from infection and TB disease than standard intradermal vaccination, correlating with local adaptive immune signatures. In line with prior mouse data, here, we show in rhesus macaques that intravenous BCG enhances innate cytokine production associated with changes in H3K27 acetylation typical of trained immunity. Alternative delivery of BCG does not alter the cytokine production of unfractionated bronchial lavage cells. However, mucosal but not intradermal vaccination, either with BCG or the -derived candidate MTBVAC, enhances innate cytokine production by blood- and bone marrow-derived monocytes associated with metabolic rewiring, typical of trained immunity. These results provide support to strategies for improving TB vaccination and, more broadly, modulating innate immunity via mucosal surfaces.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33521699', 'doi' => '10.1016/j.xcrm.2020.100185', 'modified' => '2021-12-16 10:50:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 55 => array( 'id' => '4193', 'name' => 'Postoperative abdominal sepsis induces selective and persistent changes inCTCF binding within the MHC-II region of human monocytes.', 'authors' => 'Siegler B. et al.', 'description' => '<p>BACKGROUND: Postoperative abdominal infections belong to the most common triggers of sepsis and septic shock in intensive care units worldwide. While monocytes play a central role in mediating the initial host response to infections, sepsis-induced immune dysregulation is characterized by a defective antigen presentation to T-cells via loss of Major Histocompatibility Complex Class II DR (HLA-DR) surface expression. Here, we hypothesized a sepsis-induced differential occupancy of the CCCTC-Binding Factor (CTCF), an architectural protein and superordinate regulator of transcription, inside the Major Histocompatibility Complex Class II (MHC-II) region in patients with postoperative sepsis, contributing to an altered monocytic transcriptional response during critical illness. RESULTS: Compared to a matched surgical control cohort, postoperative sepsis was associated with selective and enduring increase in CTCF binding within the MHC-II. In detail, increased CTCF binding was detected at four sites adjacent to classical HLA class II genes coding for proteins expressed on monocyte surface. Gene expression analysis revealed a sepsis-associated decreased transcription of (i) the classical HLA genes HLA-DRA, HLA-DRB1, HLA-DPA1 and HLA-DPB1 and (ii) the gene of the MHC-II master regulator, CIITA (Class II Major Histocompatibility Complex Transactivator). Increased CTCF binding persisted in all sepsis patients, while transcriptional recovery CIITA was exclusively found in long-term survivors. CONCLUSION: Our experiments demonstrate differential and persisting alterations of CTCF occupancy within the MHC-II, accompanied by selective changes in the expression of spatially related HLA class II genes, indicating an important role of CTCF in modulating the transcriptional response of immunocompromised human monocytes during critical illness.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33939725', 'doi' => '10.1371/journal.pone.0250818', 'modified' => '2022-01-06 14:22:15', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 56 => array( 'id' => '4204', 'name' => 'S-adenosyl-l-homocysteine hydrolase links methionine metabolism to thecircadian clock and chromatin remodeling.', 'authors' => 'Greco C. M. et al. ', 'description' => '<p>Circadian gene expression driven by transcription activators CLOCK and BMAL1 is intimately associated with dynamic chromatin remodeling. However, how cellular metabolism directs circadian chromatin remodeling is virtually unexplored. We report that the S-adenosylhomocysteine (SAH) hydrolyzing enzyme adenosylhomocysteinase (AHCY) cyclically associates to CLOCK-BMAL1 at chromatin sites and promotes circadian transcriptional activity. SAH is a potent feedback inhibitor of S-adenosylmethionine (SAM)-dependent methyltransferases, and timely hydrolysis of SAH by AHCY is critical to sustain methylation reactions. We show that AHCY is essential for cyclic H3K4 trimethylation, genome-wide recruitment of BMAL1 to chromatin, and subsequent circadian transcription. Depletion or targeted pharmacological inhibition of AHCY in mammalian cells markedly decreases the amplitude of circadian gene expression. In mice, pharmacological inhibition of AHCY in the hypothalamus alters circadian locomotor activity and rhythmic transcription within the suprachiasmatic nucleus. These results reveal a previously unappreciated connection between cellular metabolism, chromatin dynamics, and circadian regulation.</p>', 'date' => '2020-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33328229', 'doi' => '10.1126/sciadv.abc5629', 'modified' => '2022-01-06 14:59:48', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 57 => array( 'id' => '4040', 'name' => 'Genomic profiling of T-cell activation suggests increased sensitivity ofmemory T cells to CD28 costimulation.', 'authors' => 'Glinos, Dafni A and Soskic, Blagoje and Williams, Cayman and Kennedy, Alanand Jostins, Luke and Sansom, David M and Trynka, Gosia', 'description' => '<p>T-cell activation is a critical driver of immune responses. The CD28 costimulation is an essential regulator of CD4 T-cell responses, however, its relative importance in naive and memory T cells is not fully understood. Using different model systems, we observe that human memory T cells are more sensitive to CD28 costimulation than naive T cells. To deconvolute how the T-cell receptor (TCR) and CD28 orchestrate activation of human T cells, we stimulate cells using varying intensities of TCR and CD28 and profiled gene expression. We show that genes involved in cell cycle progression and division are CD28-driven in memory cells, but under TCR control in naive cells. We further demonstrate that T-helper differentiation and cytokine expression are controlled by CD28. Using chromatin accessibility profiling, we observe that AP1 transcriptional regulation is enriched when both TCR and CD28 are engaged, whereas open chromatin near CD28-sensitive genes is enriched for NF-kB motifs. Lastly, we show that CD28-sensitive genes are enriched in GWAS regions associated with immune diseases, implicating a role for CD28 in disease development. Our study provides important insights into the differential role of costimulation in naive and memory T-cell responses and disease susceptibility.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33223527', 'doi' => '10.1038/s41435-020-00118-0', 'modified' => '2021-02-19 12:08:04', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 58 => array( 'id' => '4060', 'name' => 'A genetic variant controls interferon-β gene expression in human myeloidcells by preventing C/EBP-β binding on a conserved enhancer.', 'authors' => 'Assouvie, Anaïs and Rotival, Maxime and Hamroune, Juliette and Busso,Didier and Romeo, Paul-Henri and Quintana-Murci, Lluis and Rousselet,Germain', 'description' => '<p>Interferon β (IFN-β) is a cytokine that induces a global antiviral proteome, and regulates the adaptive immune response to infections and tumors. Its effects strongly depend on its level and timing of expression. Therefore, the transcription of its coding gene IFNB1 is strictly controlled. We have previously shown that in mice, the TRIM33 protein restrains Ifnb1 transcription in activated myeloid cells through an upstream inhibitory sequence called ICE. Here, we show that the deregulation of Ifnb1 expression observed in murine Trim33-/- macrophages correlates with abnormal looping of both ICE and the Ifnb1 gene to a 100 kb downstream region overlapping the Ptplad2/Hacd4 gene. This region is a predicted myeloid super-enhancer in which we could characterize 3 myeloid-specific active enhancers, one of which (E5) increases the response of the Ifnb1 promoter to activation. In humans, the orthologous region contains several single nucleotide polymorphisms (SNPs) known to be associated with decreased expression of IFNB1 in activated monocytes, and loops to the IFNB1 gene. The strongest association is found for the rs12553564 SNP, located in the E5 orthologous region. The minor allele of rs12553564 disrupts a conserved C/EBP-β binding motif, prevents binding of C/EBP-β, and abolishes the activation-induced enhancer activity of E5. Altogether, these results establish a link between a genetic variant preventing binding of a transcription factor and a higher order phenotype, and suggest that the frequent minor allele (around 30\% worldwide) might be associated with phenotypes regulated by IFN-β expression in myeloid cells.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147208', 'doi' => '10.1371/journal.pgen.1009090', 'modified' => '2021-02-19 17:29:34', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 59 => array( 'id' => '4084', 'name' => 'BCG Vaccination Induces Long-Term Functional Reprogramming of HumanNeutrophils.', 'authors' => 'Moorlag, Simone J C F M and Rodriguez-Rosales, Yessica Alina and Gillard,Joshua and Fanucchi, Stephanie and Theunissen, Kate and Novakovic, Borisand de Bont, Cynthia M and Negishi, Yutaka and Fok, Ezio T and Kalafati,Lydia and Verginis, Panayotis and M', 'description' => '<p>The tuberculosis vaccine bacillus Calmette-Guérin (BCG) protects against some heterologous infections, probably via induction of non-specific innate immune memory in monocytes and natural killer (NK) cells, a process known as trained immunity. Recent studies have revealed that the induction of trained immunity is associated with a bias toward granulopoiesis in bone marrow hematopoietic progenitor cells, but it is unknown whether BCG vaccination also leads to functional reprogramming of mature neutrophils. Here, we show that BCG vaccination of healthy humans induces long-lasting changes in neutrophil phenotype, characterized by increased expression of activation markers and antimicrobial function. The enhanced function of human neutrophils persists for at least 3 months after vaccination and is associated with genome-wide epigenetic modifications in trimethylation at histone 3 lysine 4. Functional reprogramming of neutrophils by the induction of trained immunity might offer novel therapeutic strategies in clinical conditions that could benefit from modulation of neutrophil effector function.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33207187', 'doi' => '10.1016/j.celrep.2020.108387', 'modified' => '2021-03-15 17:07:29', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 60 => array( 'id' => '4086', 'name' => 'Macrophage Immune Memory Controls Endometriosis in Mice and Humans.', 'authors' => 'Jeljeli, Mohamed and Riccio, Luiza G C and Chouzenoux, Sandrine and Moresi,Fabiana and Toullec, Laurie and Doridot, Ludivine and Nicco, Carole andBourdon, Mathilde and Marcellin, Louis and Santulli, Pietro and Abrão,Mauricio S and Chapron, Charles and ', 'description' => '<p>Endometriosis is a frequent, chronic, inflammatory gynecological disease characterized by the presence of ectopic endometrial tissue causing pain and infertility. Macrophages have a central role in lesion establishment and maintenance by driving chronic inflammation and tissue remodeling. Macrophages can be reprogrammed to acquire memory-like characteristics after antigenic challenge to reinforce or inhibit a subsequent immune response, a phenomenon termed "trained immunity." Here, whereas bacille Calmette-Guérin (BCG) training enhances the lesion growth in a mice model of endometriosis, tolerization with repeated low doses of lipopolysaccharide (LPS) or adoptive transfer of LPS-tolerized macrophages elicits a suppressor effect. LPS-tolerized human macrophages mitigate the fibro-inflammatory phenotype of endometriotic cells in an interleukin-10 (IL-10)-dependent manner. A history of severe Gram-negative infection is associated with reduced infertility duration and alleviated symptoms, in contrast to patients with Gram-positive infection history. Thus, the manipulation of innate immune memory may be effective in dampening hyper-inflammatory conditions, opening the way to promising therapeutic approaches.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147452', 'doi' => '10.1016/j.celrep.2020.108325', 'modified' => '2021-03-15 17:14:08', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 61 => array( 'id' => '4050', 'name' => 'UTX/KDM6A suppresses AP-1 and a gliogenesis program during neuraldifferentiation of human pluripotent stem cells.', 'authors' => 'Xu, Beisi and Mulvey, Brett and Salie, Muneeb and Yang, Xiaoyang andMatsui, Yurika and Nityanandam, Anjana and Fan, Yiping and Peng, Jamy C', 'description' => '<p>BACKGROUND: UTX/KDM6A is known to interact and influence multiple different chromatin modifiers to promote an open chromatin environment to facilitate gene activation, but its molecular activities in developmental gene regulation remain unclear. RESULTS: We report that in human neural stem cells, UTX binding correlates with both promotion and suppression of gene expression. These activities enable UTX to modulate neural stem cell self-renewal, promote neurogenesis, and suppress gliogenesis. In neural stem cells, UTX has a less influence over histone H3 lysine 27 and lysine 4 methylation but more predominantly affects histone H3 lysine 27 acetylation and chromatin accessibility. Furthermore, UTX suppresses components of AP-1 and, in turn, a gliogenesis program. CONCLUSIONS: Our findings revealed that UTX coordinates dualistic gene regulation to govern neural stem cell properties and neurogenesis-gliogenesis switch.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32977832', 'doi' => '10.1186/s13072-020-00359-3', 'modified' => '2021-02-19 14:46:42', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 62 => array( 'id' => '4091', 'name' => 'Epigenetic regulation of the lineage specificity of primary human dermallymphatic and blood vascular endothelial cells.', 'authors' => 'Tacconi, Carlotta and He, Yuliang and Ducoli, Luca and Detmar, Michael', 'description' => '<p>Lymphatic and blood vascular endothelial cells (ECs) share several molecular and developmental features. However, these two cell types possess distinct phenotypic signatures, reflecting their different biological functions. Despite significant advances in elucidating how the specification of lymphatic and blood vascular ECs is regulated at the transcriptional level during development, the key molecular mechanisms governing their lineage identity under physiological or pathological conditions remain poorly understood. To explore the epigenomic signatures in the maintenance of EC lineage specificity, we compared the transcriptomic landscapes, histone composition (H3K4me3 and H3K27me3) and DNA methylomes of cultured matched human primary dermal lymphatic and blood vascular ECs. Our findings reveal that blood vascular lineage genes manifest a more 'repressed' histone composition in lymphatic ECs, whereas DNA methylation at promoters is less linked to the differential transcriptomes of lymphatic versus blood vascular ECs. Meta-analyses identified two transcriptional regulators, BCL6 and MEF2C, which potentially govern endothelial lineage specificity. Notably, the blood vascular endothelial lineage markers CD34, ESAM and FLT1 and the lymphatic endothelial lineage markers PROX1, PDPN and FLT4 exhibited highly differential epigenetic profiles and responded in distinct manners to epigenetic drug treatments. The perturbation of histone and DNA methylation selectively promoted the expression of blood vascular endothelial markers in lymphatic endothelial cells, but not vice versa. Overall, our study reveals that the fine regulation of lymphatic and blood vascular endothelial transcriptomes is maintained via several epigenetic mechanisms, which are crucial to the maintenance of endothelial cell identity.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32918672', 'doi' => '10.1007/s10456-020-09743-9', 'modified' => '2021-03-17 17:09:36', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 63 => array( 'id' => '4010', 'name' => 'Combined treatment with CBP and BET inhibitors reverses inadvertentactivation of detrimental super enhancer programs in DIPG cells.', 'authors' => 'Wiese, M and Hamdan, FH and Kubiak, K and Diederichs, C and Gielen, GHand Nussbaumer, G and Carcaboso, AM and Hulleman, E and Johnsen, SA andKramm, CM', 'description' => '<p>Diffuse intrinsic pontine gliomas (DIPG) are the most aggressive brain tumors in children with 5-year survival rates of only 2%. About 85% of all DIPG are characterized by a lysine-to-methionine substitution in histone 3, which leads to global H3K27 hypomethylation accompanied by H3K27 hyperacetylation. Hyperacetylation in DIPG favors the action of the Bromodomain and Extra-Terminal (BET) protein BRD4, and leads to the reprogramming of the enhancer landscape contributing to the activation of DIPG super enhancer-driven oncogenes. The activity of the acetyltransferase CREB-binding protein (CBP) is enhanced by BRD4 and associated with acetylation of nucleosomes at super enhancers (SE). In addition, CBP contributes to transcriptional activation through its function as a scaffold and protein bridge. Monotherapy with either a CBP (ICG-001) or BET inhibitor (JQ1) led to the reduction of tumor-related characteristics. Interestingly, combined treatment induced strong cytotoxic effects in H3.3K27M-mutated DIPG cell lines. RNA sequencing and chromatin immunoprecipitation revealed that these effects were caused by the inactivation of DIPG SE-controlled tumor-related genes. However, single treatment with ICG-001 or JQ1, respectively, led to activation of a subgroup of detrimental super enhancers. Combinatorial treatment reversed the inadvertent activation of these super enhancers and rescued the effect of ICG-001 and JQ1 single treatment on enhancer-driven oncogenes in H3K27M-mutated DIPG, but not in H3 wild-type pedHGG cells. In conclusion, combinatorial treatment with CBP and BET inhibitors is highly efficient in H3K27M-mutant DIPG due to reversal of inadvertent activation of detrimental SE programs in comparison with monotherapy.</p>', 'date' => '2020-08-21', 'pmid' => 'http://www.pubmed.gov/32826850', 'doi' => '10.1038/s41419-020-02800-7', 'modified' => '2020-12-18 13:25:09', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 64 => array( 'id' => '4028', 'name' => 'Methylation in pericytes after acute injury promotes chronic kidneydisease.', 'authors' => 'Chou, YH and Pan, SY and Shao, YH and Shih, HM and Wei, SY andLai, CF and Chiang, WC and Schrimpf, C and Yang, KC and Lai, LC andChen, YM and Chu, TS and Lin, SL', 'description' => '<p>The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury-induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-β1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD.</p>', 'date' => '2020-08-04', 'pmid' => 'http://www.pubmed.gov/32749240', 'doi' => '10.1172/JCI135773.', 'modified' => '2020-12-18 13:25:55', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 65 => array( 'id' => '4011', 'name' => 'Exploring the virulence gene interactome with CRISPR/dCas9 in the humanmalaria parasite.', 'authors' => 'Bryant, JM and Baumgarten, S and Dingli, F and Loew, D and Sinha, A andClaës, A and Preiser, PR and Dedon, PC and Scherf, A', 'description' => '<p>Mutually exclusive expression of the var multigene family is key to immune evasion and pathogenesis in Plasmodium falciparum, but few factors have been shown to play a direct role. We adapted a CRISPR-based proteomics approach to identify novel factors associated with var genes in their natural chromatin context. Catalytically inactive Cas9 ("dCas9") was targeted to var gene regulatory elements, immunoprecipitated, and analyzed with mass spectrometry. Known and novel factors were enriched including structural proteins, DNA helicases, and chromatin remodelers. Functional characterization of PfISWI, an evolutionarily divergent putative chromatin remodeler enriched at the var gene promoter, revealed a role in transcriptional activation. Proteomics of PfISWI identified several proteins enriched at the var gene promoter such as acetyl-CoA synthetase, a putative MORC protein, and an ApiAP2 transcription factor. These findings validate the CRISPR/dCas9 proteomics method and define a new var gene-associated chromatin complex. This study establishes a tool for targeted chromatin purification of unaltered genomic loci and identifies novel chromatin-associated factors potentially involved in transcriptional control and/or chromatin organization of virulence genes in the human malaria parasite.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32816370', 'doi' => 'https://dx.doi.org/10.15252%2Fmsb.20209569', 'modified' => '2020-12-18 13:26:33', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 66 => array( 'id' => '4019', 'name' => 'Targeted bisulfite sequencing for biomarker discovery.', 'authors' => 'Morselli, M and Farrell, C and Rubbi, L and Fehling, HL and Henkhaus, Rand Pellegrini, M', 'description' => '<p>Cytosine methylation is one of the best studied epigenetic modifications. In mammals, DNA methylation patterns vary among cells and is mainly found in the CpG context. DNA methylation is involved in important processes during development and differentiation and its dysregulation can lead to or is associated with diseases, such as cancer, loss-of-imprinting syndromes and neurological disorders. It has been also shown that DNA methylation at the cellular, tissue and organism level varies with age. To overcome the costs of Whole-Genome Bisulfite Sequencing, the gold standard method to detect 5-methylcytosines at a single base resolution, DNA methylation arrays have been developed and extensively used. This method allows one to assess the status of a fraction of the CpG sites present in the genome of an organism. In order to combine the relatively low cost of Methylation Arrays and digital signals of bisulfite sequencing, we developed a Targeted Bisulfite Sequencing method that can be applied to biomarker discovery for virtually any phenotype. Here we describe a comprehensive step-by-step protocol to build a DNA methylation-based epigenetic clock.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32755621', 'doi' => '10.1016/j.ymeth.2020.07.006', 'modified' => '2020-12-18 13:27:14', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 67 => array( 'id' => '4031', 'name' => 'Battle of the sex chromosomes: competition between X- and Y-chromosomeencoded proteins for partner interaction and chromatin occupancy drivesmulti-copy gene expression and evolution in muroid rodents.', 'authors' => 'Moretti, C and Blanco, M and Ialy-Radio, C and Serrentino, ME and Gobé,C and Friedman, R and Battail, C and Leduc, M and Ward, MA and Vaiman, Dand Tores, F and Cocquet, J', 'description' => '<p>Transmission distorters (TDs) are genetic elements that favor their own transmission to the detriments of others. Slx/Slxl1 (Sycp3-like-X-linked and Slx-like1) and Sly (Sycp3-like-Y-linked) are TDs which have been co-amplified on the X and Y chromosomes of Mus species. They are involved in an intragenomic conflict in which each favors its own transmission, resulting in sex ratio distortion of the progeny when Slx/Slxl1 vs. Sly copy number is unbalanced. They are specifically expressed in male postmeiotic gametes (spermatids) and have opposite effects on gene expression: Sly knockdown leads to the upregulation of hundreds of spermatid-expressed genes, while Slx/Slxl1-deficiency downregulates them. When both Slx/Slxl1 and Sly are knocked-down, sex ratio distortion and gene deregulation are corrected. Slx/Slxl1 and Sly are, therefore, in competition but the molecular mechanism remains unknown. By comparing their chromatin binding profiles and protein partners, we show that SLX/SLXL1 and SLY proteins compete for interaction with H3K4me3-reader SSTY1 (Spermiogenesis-specific-transcript-on-the-Y1) at the promoter of thousands of genes to drive their expression, and that the opposite effect they have on gene expression is mediated by different abilities to recruit SMRT/N-Cor transcriptional complex. Their target genes are predominantly spermatid-specific multicopy genes encoded by the sex chromosomes and the autosomal Speer/Takusan. Many of them have co-amplified with Slx/Slxl1/Sly but also Ssty during muroid rodent evolution. Overall, we identify Ssty as a key element of the X vs. Y intragenomic conflict, which may have influenced gene content and hybrid sterility beyond Mus lineage since Ssty amplification on the Y pre-dated that of Slx/Slxl1/Sly.</p>', 'date' => '2020-07-13', 'pmid' => 'http://www.pubmed.gov/32658962', 'doi' => '10.1093/molbev/msaa175/5870835', 'modified' => '2020-12-18 13:27:51', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 68 => array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ) ), 'Testimonial' => array(), 'Area' => array() ) $country = 'US' $countries_allowed = array( (int) 0 => 'CA', (int) 1 => 'US', (int) 2 => 'IE', (int) 3 => 'GB', (int) 4 => 'DK', (int) 5 => 'NO', (int) 6 => 'SE', (int) 7 => 'FI', (int) 8 => 'NL', (int) 9 => 'BE', (int) 10 => 'LU', (int) 11 => 'FR', (int) 12 => 'DE', (int) 13 => 'CH', (int) 14 => 'AT', (int) 15 => 'ES', (int) 16 => 'IT', (int) 17 => 'PT' ) $outsource = false $other_formats = array() $edit = '' $testimonials = '' $featured_testimonials = '' $related_products = '<li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201140</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-3047" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <form action="/en/carts/add/3047" id="CartAdd/3047Form" method="post" accept-charset="utf-8"><div style="display:none;"><input type="hidden" name="_method" value="POST"/></div><input type="hidden" name="data[Cart][product_id]" value="3047" id="CartProductId"/> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p>Add <input name="data[Cart][quantity]" placeholder="1" value="1" min="1" style="width:60px;display:inline" type="number" id="CartQuantity" required="required"/> <strong> Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico</strong> to my shopping cart.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="checkout" id="checkout" value="checkout" type="submit">Checkout</button> </div> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="keepshop" id="keepshop" type="submit">Keep shopping</button> </div> </div> </div> </div> </form><a class="close-reveal-modal" aria-label="Close">×</a></div><!-- END: ADD TO CART MODAL --><a href="#" id="1-5-ml-tube-holder-dock-for-bioruptor-pico" data-reveal-id="cartModal-3047" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 1.5 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201143</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: QUOTE MODAL --><div id="quoteModal-3048" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h3>Get a quote</h3><p class="lead">You are about to request a quote for <strong>Tube holder for 0.65 ml tubes - Bioruptor<sup>®</sup> Pico</strong>. 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Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201144</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-3049" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <form action="/en/carts/add/3049" id="CartAdd/3049Form" method="post" accept-charset="utf-8"><div style="display:none;"><input type="hidden" name="_method" value="POST"/></div><input type="hidden" name="data[Cart][product_id]" value="3049" id="CartProductId"/> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p>Add <input name="data[Cart][quantity]" placeholder="1" value="1" min="1" style="width:60px;display:inline" type="number" id="CartQuantity" required="required"/> <strong> Tube holder for 0.2 ml tubes - Bioruptor<sup>®</sup> Pico</strong> to my shopping cart.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 0.2 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201144', '1850', $('#CartQuantity').val());" name="checkout" id="checkout" value="checkout" type="submit">Checkout</button> </div> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 0.2 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201144', '1850', $('#CartQuantity').val());" name="keepshop" id="keepshop" type="submit">Keep shopping</button> </div> </div> </div> </div> </form><a class="close-reveal-modal" aria-label="Close">×</a></div><!-- END: ADD TO CART MODAL --><a href="#" id="0-2-ml-tube-holder-dock-for-bioruptor-pico" data-reveal-id="cartModal-3049" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 0.2 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack"><img src="/img/product/shearing_technologies/B01200016_tube_holder.jpg" alt="some alt" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01200016</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-1796" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <form action="/en/carts/add/1796" id="CartAdd/1796Form" method="post" accept-charset="utf-8"><div style="display:none;"><input type="hidden" name="_method" value="POST"/></div><input type="hidden" name="data[Cart][product_id]" value="1796" id="CartProductId"/> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p>Add <input name="data[Cart][quantity]" placeholder="1" value="1" min="1" style="width:60px;display:inline" type="number" id="CartQuantity" required="required"/> <strong> 15 ml sonication accessories for Bioruptor<sup>®</sup> Standard & Plus & Pico</strong> to my shopping cart.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('15 ml sonication accessories for Bioruptor<sup>®</sup> Standard & Plus & Pico', 'B01200016', '350', $('#CartQuantity').val());" name="checkout" id="checkout" value="checkout" type="submit">Checkout</button> </div> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('15 ml sonication accessories for Bioruptor<sup>®</sup> Standard & Plus & Pico', 'B01200016', '350', $('#CartQuantity').val());" name="keepshop" id="keepshop" type="submit">Keep shopping</button> </div> </div> </div> </div> </form><a class="close-reveal-modal" aria-label="Close">×</a></div><!-- END: ADD TO CART MODAL --><a href="#" id="15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack" data-reveal-id="cartModal-1796" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">15 ml sonication accessories for Bioruptor®...</h6> </div> </div> </li> ' $related = array( 'id' => '1796', 'antibody_id' => null, 'name' => '15 ml sonication accessories for Bioruptor<sup>®</sup> Standard & Plus & Pico', 'description' => '<p><span>This tube holder has been designed for being used in 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=> '1 pack', 'catalog_number' => 'B01200016', 'old_catalog_number' => 'O-ring-15', 'sf_code' => 'B01200016-', 'type' => 'ACC', 'search_order' => '01-Accessory', 'price_EUR' => '300', 'price_USD' => '350', 'price_GBP' => '250', 'price_JPY' => '46995', 'price_CNY' => '', 'price_AUD' => '875', 'country' => 'ALL', 'except_countries' => 'None', 'quote' => false, 'in_stock' => false, 'featured' => false, 'no_promo' => false, 'online' => true, 'master' => true, 'last_datasheet_update' => '0000-00-00', 'slug' => '15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack', 'meta_title' => '15 ml sonication accessories for Bioruptor® Standard & Plus & Pico', 'meta_keywords' => '', 'meta_description' => '15 ml sonication accessories for Bioruptor® Standard & Plus & Pico', 'modified' => '2022-01-25 04:00:28', 'created' => '2015-06-29 14:08:20', 'ProductsRelated' => array( 'id' => '4591', 'product_id' => '3046', 'related_id' => '1796' ), 'Image' => array( (int) 0 => array( 'id' => '116', 'name' => 'product/shearing_technologies/B01200016_tube_holder.jpg', 'alt' => 'some alt', 'modified' => '2015-06-10 17:28:55', 'created' => '2015-06-10 17:28:55', 'ProductsImage' => array( [maximum depth reached] ) ) ) ) $list = '<div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-1.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-2.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-3.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-4.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-5.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B010600010.jpg" /></div>' $img = array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => '2018-02-14 15:41:46', 'ProductsImage' => array( 'id' => '1093', 'product_id' => '3046', 'image_id' => '1772' ) ) $rrbs_service = array( (int) 0 => (int) 1894, (int) 1 => (int) 1895 ) $chipseq_service = array( (int) 0 => (int) 2683, (int) 1 => (int) 1835, (int) 2 => (int) 1836, (int) 3 => (int) 2684, (int) 4 => (int) 1838, (int) 5 => (int) 1839, (int) 6 => (int) 1856 ) $labelize = object(Closure) { } $old_catalog_number = '' $label = '<img src="/img/banners/banner-customizer-back.png" alt=""/>' $protocol = array( 'id' => '73', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:16:00', 'created' => '0000-00-00 00:00:00', 'ProductsProtocol' => array( 'id' => '241', 'product_id' => '3046', 'protocol_id' => '73' ) ) $document = array( 'id' => '1170', 'name' => 'Critical steps for Bioruptor® maintenance and efficient shearing', 'description' => '', 'image_id' => null, 'type' => 'Document', 'url' => 'files/products/shearing_technology/critical-steps-bioruptor-web.pdf', 'slug' => 'critical-steps-bioruptor-maintenance', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2023-08-31 14:27:41', 'created' => '2023-08-31 14:27:41', 'ProductsDocument' => array( 'id' => '3264', 'product_id' => '3046', 'document_id' => '1170' ) ) $publication = array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( 'id' => '6424', 'product_id' => '3046', 'publication_id' => '4549' ) ) $externalLink = ' <a href="https://www.researchsquare.com/article/rs-1832996/v1" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755 View::_evaluate() - CORE/Cake/View/View.php, line 971 View::_render() - CORE/Cake/View/View.php, line 933 View::render() - CORE/Cake/View/View.php, line 473 Controller::render() - CORE/Cake/Controller/Controller.php, line 963 Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 200 Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167 [main] - APP/webroot/index.php, line 118
Notice (8): Undefined variable: message [APP/View/Products/view.ctp, line 755]Code Context<!-- BEGIN: REQUEST_FORM MODAL --><div id="request_formModal" class="reveal-modal medium" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"><?= $this->element('Forms/simple_form', array('solution_of_interest' => $solution_of_interest, 'header' => $header, 'message' => $message, 'campaign_id' => $campaign_id)) ?>$viewFile = '/home/website-server/www/app/View/Products/view.ctp' $dataForView = array( 'language' => 'en', 'noindex' => 'noindex', 'meta_keywords' => '', 'meta_description' => 'Bioruptor® Pico sonication device', 'meta_title' => 'Bioruptor® Pico sonication device', 'product' => array( 'Product' => array( 'id' => '3046', 'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa fa-arrow-circle-right"></i> <a href="https://www.diagenode.com/pages/chromatin-prep-easyshear-kit-guide">Read more</a></h3> </div> <p> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> </p> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <script src="chrome-extension://hhojmcideegachlhfgfdhailpfhgknjm/web_accessible_resources/index.js"></script> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'format' => '1 unit', 'catalog_number' => 'B01080010', 'old_catalog_number' => '', 'sf_code' => 'B01080010-', 'type' => 'ACC', 'search_order' => '00-Machine', 'price_EUR' => '27000', 'price_USD' => '30000', 'price_GBP' => '23500', 'price_JPY' => '4229550', 'price_CNY' => '/', 'price_AUD' => '75000', 'country' => 'ALL', 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'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa 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Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>®</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>®</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>®</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div> <div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 µl volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.1 ml Bioruptor® Microtubes (Cat. No. B01200041). <strong>Panel B, 100 µl volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.65 ml Bioruptor® Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 µl volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016). Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37°C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 µl of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div> <div class="small-12 medium-12 large-12 columns"><br /><br /></div> <div class="small-12 medium-12 large-12 columns"> <p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p> </div> <div class="small-12 medium-12 large-12 columns"> <div class="page" title="Page 7"> <table> <tbody> <tr valign="middle"> <td></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>SDS concentration</strong></p> </td> <td style="text-align: center;"> <p>< 0.1%</p> </td> <td style="text-align: center;"> <p>0.2%</p> </td> <td style="text-align: center;"> <p>1%</p> </td> <td style="text-align: center;"> <p>0.5%</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Nuclei isolation</strong></p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>No</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Allows for shearing of... cells/tissue</strong></p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>up to 25 g of tissue</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Corresponding to shearing buffers from</strong></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p> <p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p> </td> </tr> </tbody> </table> <p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor® Pico</span></a></em></p> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'chromatin-shearing', 'meta_keywords' => 'Chromatin shearing,Chromatin Immunoprecipitation,Bioruptor,Sonication,Sonicator', 'meta_description' => 'Diagenode's Bioruptor® is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.', 'meta_title' => 'Chromatin shearing using Bioruptor® sonication device | Diagenode', 'modified' => '2017-11-15 10:14:02', 'created' => '2015-03-05 15:56:30', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3', 'position' => '10', 'parent_id' => null, 'name' => '次世代シーケンシング', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2 style="font-size: 22px;">DNA断片化、ライブラリー調製、自動化：NGSのワンストップショップ</h2> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-12 medium-12 large-12 columns"> <h4>1. 断片化装置を選択してください：150 bp〜75 kbの範囲でDNAを断片化します。</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-pico-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/bioruptor_pico.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/megaruptor2-1-unit"><img src="https://www.diagenode.com/img/product/shearing_technologies/B06010001_megaruptor2.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-one-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/br-one-profil.png" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns">5μlまで断片化：150 bp〜2 kb<br />NGS DNAライブラリー調製およびFFPE核酸抽出に最適で、</td> <td class="small-4 medium-4 large-4 columns">2 kb〜75 kbの範囲をできます。<br />メイトペアライブラリー調製および長いフラグメントDNAシーケンシングに最適で、この軽量デスクトップデバイスで</td> <td class="small-4 medium-4 large-4 columns">20または50μlの断片化が可能です。</td> </tr> </tbody> </table> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-8 medium-8 large-8 columns"> <h4>2. 最適化されたライブラリー調整キットを選択してください。</h4> </th> <th class="small-4 medium-4 large-4 columns"> <h4>3. ライブラリー前処理自動化を選択して、比類のないデータ再現性を実感</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><img src="https://www.diagenode.com/img/product/kits/microPlex_library_preparation.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns"><img src="https://www.diagenode.com/img/product/kits/box_kit.jpg" style="display: block; margin-left: auto; margin-right: auto;" height="173" width="250" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/sx-8g-ip-star-compact-automated-system-1-unit"><img src="https://www.diagenode.com/img/product/automation/B03000002%20_ipstar_compact.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">50pgの低入力：MicroPlex Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">5ng以上：iDeal Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">Achieve great NGS data easily</td> </tr> </tbody> </table> </div> </div> <blockquote> <div class="row"> <div class="small-12 medium-12 large-12 columns"><span class="label" style="margin-bottom: 16px; margin-left: -22px; font-size: 15px;">DiagenodeがNGS研究にぴったりなプロバイダーである理由</span> <p>Diagenodeは15年以上もエピジェネティクス研究に専念、専門としています。 ChIP研究クロマチン用のユニークな断片化システムの開発から始まり、 専門知識を活かし、5μlのせん断体積まで可能で、NGS DNAライブラリーの調製に最適な最先端DNA断片化装置の開発にたどり着きました。 我々は以来、ChIP-seq、Methyl-seq、NGSライブラリー調製用キットを研究開発し、業界をリードする免疫沈降研究と同様に、ライブラリー調製を自動化および完結させる独自の自動化システムを開発にも成功しました。</p> <ul> <li>信頼されるせん断装置</li> <li>様々なインプットからのライブラリ作成キット</li> <li>独自の自動化デバイス</li> </ul> </div> </div> </blockquote> <div class="row"> <div class="small-12 columns"> <ul class="accordion" data-accordion=""> <li class="accordion-navigation"><a href="#panel1a">次世代シーケンシングへの理解とその専門知識</a> <div id="panel1a" class="content"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p><strong>次世代シーケンシング (NGS)</strong> ）は、著しいスケールとハイスループットでシーケンシングを行い、1日に数十億もの塩基生成を可能にします。 NGSのハイスループットは迅速でありながら正確で、再現性のあるデータセットを実現し、さらにシーケンシング費用を削減します。 NGSは、ゲノムシーケンシング、ゲノム再シーケンシング、デノボシーケンシング、トランスクリプトームシーケンシング、その他にDNA-タンパク質相互作用の検出やエピゲノムなどを示します。 指数関数的に増加するシーケンシングデータの需要は、計算分析の障害や解釈、データストレージなどの課題を解決します。</p> <p>アプリケーションおよび出発物質に応じて、数百万から数十億の鋳型DNA分子を大規模に並行してシーケンシングすることが可能です。その為に、異なる化学物質を使用するいくつかの市販のNGSプラットフォームを利用することができます。 NGSプラットフォームの種類によっては、事前準備とライブラリー作成が必要です。</p> <p>NGSにとっても、特にデータ処理と分析に関した大きな課題はあります。第3世代技術はゲノミクス研究にさらに革命を起こすであろうと大きく期待されています。</p> </div> </div> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <p><strong>NGS アプリケーション</strong></p> <ul> <li>全ゲノム配列決定</li> <li>デノボシーケンシング</li> <li>標的配列</li> <li>Exomeシーケンシング</li> <li>トランスクリプトーム配列決定</li> <li>ゲノム配列決定</li> <li>ミトコンドリア配列決定</li> <li>DNA-タンパク質相互作用（ChIP-seq</li> <li>バリアント検出</li> <li>ゲノム仕上げ</li> </ul> </div> <div class="small-6 medium-6 large-6 columns"> <p><strong>研究分野におけるNGS:</strong></p> <ul> <li>腫瘍学</li> <li>リプロダクティブ・ヘルス</li> <li>法医学ゲノミクス</li> <li>アグリゲノミックス</li> <li>複雑な病気</li> <li>微生物ゲノミクス</li> <li>食品・環境ゲノミクス</li> <li>創薬ゲノミクス - パーソナライズド・メディカル</li> </ul> </div> <div class="small-12 medium-12 large-12 columns"> <p><strong>NGSの用語</strong></p> <dl> <dt>リード（読み取り）</dt> <dd>この装置から得られた連続した単一のストレッチ</dd> <dt>断片リード</dt> <dd>フラグメントライブラリからの読み込み。 シーケンシングプラットフォームに応じて、読み取りは通常約100〜300bp。</dd> <dt>断片ペアエンドリード</dt> <dd>断片ライブラリーからDNA断片の各末端2つの読み取り。</dd> <dt>メイトペアリード</dt> <dd>大きなDNA断片（通常は予め定義されたサイズ範囲）の各末端から2つの読み取り。</dd> <dt>カバレッジ（例）</dt> <dd>30×適用範囲とは、参照ゲノム中の各塩基対が平均30回の読み取りを示す。</dd> </dl> </div> </div> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2>NGSプラットフォーム</h2> <h3><a href="http://www.illumina.com" target="_blank">イルミナ</a></h3> <p>イルミナは、クローン的に増幅された鋳型DNA（クラスター）上に位置する、蛍光標識された可逆的鎖ターミネーターヌクレオチドを用いた配列別合成技術を使用。 DNAクラスターは、ガラスフローセルの表面上に固定化され、 ワークフローは、4つのヌクレオチド（それぞれ異なる蛍光色素で標識された）の組み込み、4色イメージング、色素や末端基の切断、取り込み、イメージングなどを繰り返します。フローセルは大規模な並列配列決定を受ける。 この方法により、単一蛍光標識されたヌクレオチドの制御添加によるモノヌクレオチドのエラーを回避する可能性があります。 読み取りの長さは、通常約100〜150 bpです。</p> <h3><a href="http://www.lifetechnologies.com" target="_blank">イオン トレント</a></h3> <p>イオントレントは、半導体技術チップを用いて、合成中にヌクレオチドを取り込む際に放出されたプロトンを検出します。 これは、イオン球粒子と呼ばれるビーズの表面にエマルションPCR（emPCR）を使用し、リンクされた特定のアダプターを用いてDNA断片を増幅します。 各ビーズは1種類のDNA断片で覆われていて、異なるDNA断片を有するビーズは次いで、チップの陽子感知ウェル内に配置されます。 チップには一度に4つのヌクレオチドのうちの1つが浸水し、このプロセスは異なるヌクレオチドで15秒ごとに繰り返されます。 配列決定の間に4つの塩基の各々が1つずつ導入されます、組み込みの場合はプロトンが放出され、電圧信号が取り込みに比例して検出されます。.</p> <h3><a href="http://www.pacificbiosciences.com" target="_blank">パシフィック バイオサイエンス</a></h3> <p>パシフィックバイオサイエンスでは、20kbを超える塩基対の読み取りも、単一分子リアルタイム（SMRT）シーケンシングによる構造および細胞タイプの変化を観察することができます。 このプラットフォームでは、超長鎖二本鎖DNA（dsDNA）断片が、Megaruptor（登録商標）のようなDiagenode装置を用いたランダムシアリングまたは目的の標的領域の増幅によって生成されます。 SMRTbellライブラリーは、ユニバーサルヘアピンアダプターをDNA断片の各末端に連結することによって生成します。 サイズ選択条件による洗浄ステップの後、配列決定プライマーをSMRTbellテンプレートにアニーリングし、鋳型DNAに結合したDNAポリメラーゼを含む配列決定を、蛍光標識ヌクレオチドの存在下で開始。 各塩基が取り込まれると、異なる蛍光のパルスをリアルタイムで検出します。</p> <h3><a href="https://nanoporetech.com" target="_blank">オックスフォード ナノポア</a></h3> <p>Oxford Nanoporeは、単一のDNA分子配列決定に基づく技術を開発します。その技術により生物学的分子、すなわちDNAが一群の電気抵抗性高分子膜として位置するナノスケールの孔（ナノ細孔）またはその近くを通過し、イオン電流が変化します。 この変化に関する情報は、例えば4つのヌクレオチド（AまたはG r CまたはT）ならびに修飾されたヌクレオチドすべてを区別することによって分子情報に訳されます。 シーケンシングミニオンデバイスのフローセルは、数百個のナノポアチャネルのセンサアレイを含みます。 DNAサンプルは、Diagenode社のMegaruptor（登録商標）を用いてランダムシアリングによって生成され得る超長鎖DNAフラグメントが必要です。</p> <h3><a href="http://www.lifetechnologies.com/be/en/home/life-science/sequencing/next-generation-sequencing/solid-next-generation-sequencing.html" target="_blank">SOLiD</a></h3> <p>SOLiDは、ユニークな化学作用により、何千という個々のDNA分子の同時配列決定を可能にします。 それは、アダプター対ライブラリーのフラグメントが適切で、せん断されたゲノムDNAへのアダプターのライゲーションによるライブラリー作製から始まります。 次のステップでは、エマルジョンPCR（emPCR）を実施して、ビーズの表面上の個々の鋳型DNA分子をクローン的に増幅。 emPCRでは、個々の鋳型DNAをPCR試薬と混合し、水中油型エマルジョン内の疎水性シェルで囲まれた水性液滴内のプライマーコートビーズを、配列決定のためにロードするスライドガラスの表面にランダムに付着。 この技術は、シークエンシングプライマーへのライゲーションで競合する4つの蛍光標識されたジ塩基プローブのセットを使用します。</p> <h3><a href="http://454.com/products/technology.asp" target="_blank">454</a></h3> <p>454は、大規模並列パイロシーケンシングを利用しています。 始めに全ゲノムDNAまたは標的遺伝子断片の300〜800bp断片のライブラリー調製します。 次に、DNAフラグメントへのアダプターの付着および単一のDNA鎖の分離。 その後アダプターに連結されたDNAフラグメントをエマルジョンベースのクローン増幅（emPCR）で処理し、DNAライブラリーフラグメントをミクロンサイズのビーズ上に配置します。 各DNA結合ビーズを光ファイバーチップ上のウェルに入れ、器具に挿入します。 4つのDNAヌクレオチドは、配列決定操作中に固定された順序で連続して加えられ、並行して配列決定されます。</p> </div> </div> </div> </li> </ul> </div> </div>', 'in_footer' => true, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'next-generation-sequencing', 'meta_keywords' => 'Next-generation sequencing,NGS,Whole genome sequencing,NGS platforms,DNA/RNA shearing', 'meta_description' => 'Diagenode offers kits and DNA/RNA shearing technology prior to next-generation sequencing, many Next-generation sequencing platforms require preparation of the DNA.', 'meta_title' => 'Next-generation sequencing (NGS) Applications and Methods | Diagenode', 'modified' => '2018-07-26 05:24:29', 'created' => '2015-04-01 22:47:04', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '13', 'position' => '10', 'parent_id' => '3', 'name' => 'DNA/RNA shearing', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns">In recent years, advances in Next-Generation Sequencing (NGS) have revolutionized genomics and biology. This growth has fueled demands on upstream techniques for optimal sample preparation and genomic library construction. One of the most critical aspects of optimal library preparation is the quality of the DNA to be sequenced. The DNA must first be effectively and consistently sheared into the appropriate fragment size (depending on the sequencing platform) to enable sensitive and reliable NGS results. The <strong>Bioruptor</strong><sup>®</sup> <strong>Pico</strong> and the <strong>Megaruptor</strong><sup>®</sup> provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows. Follow our guidelines and find the good parameters for your expected DNA size: <a href="https://pybrevet.typeform.com/to/o8cQfM">DNA shearing with the Bioruptor<sup>®</sup></a>.</div> </div> <p></p> <div class="row"> <div class="small-7 medium-7 large-7 columns text-center"><img src="https://www.diagenode.com/img/applications/true-flexibility-with-br-ngs.jpg" /></div> <div class="small-5 medium-5 large-5 columns"><small><strong>Programmable DNA size distribution and high reproducibility with Bioruptor<sup>®</sup> Pico using 0.65 (panel A) or 0.1 ml (panel B) microtubes</strong>. <b>Panel A:</b> 200 bp after 13 cycles (13 sec ON/OFF) using 100 µl volume. Average size: 204; CV%:1.89%). <b>Panel B:</b> 200 bp after 20 cycles (30 sec ON/OFF) using 10 µl volume. (Average size: 215 bp; CV%: 6.6%). <b>Panel A & B:</b> peak electropherogram view. <b>Panel C & D:</b> virtual gel view.</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-10 medium-10 large-10 columns text-center end small-offset-1"><img src="https://www.diagenode.com/img/applications/megaruptor-short-frag.jpg" /></div> <div class="small-12 medium-12 large-12 columns"><small><strong> Reproducible and narrow DNA size distribution with Megaruptor® using short fragment size Hydropores Validation using two different DNA sources and two different methods of analysis. A:</strong> Shearing of lambda phage genomic DNA (20 ng/μl; 150 μl/sample) sheared at different speed settings and analyzed on 1% agarose gel. <strong>B:</strong> Bioanalyzer profiles of human genomic DNA (20 ng/μl; 150 μl/sample) sheared at different software settings of 2 and 5 kb. Three independent experiments were run for each setting. (Agilent DNA 12000 kit was used for separation and fragment sizing).</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-4 medium-4 large-4 columns text-center"><img src="https://www.diagenode.com/img/applications/megaruptor-long-frag.jpg" /></div> <div class="small-8 medium-8 large-8 columns"><small><strong> Demonstrated shearing to fragment sizes between 15 kb and 75 kb with Megaruptor® using long fragment size Hydropores. </strong>Image shows DNA size distribution of human genomic DNA sheared with long fragment Hydropores. DNA was analyzed by pulsed field gel electrophoresis (PFGE) in 1% agarose gel and a mean size of smears was estimated using Image Lab 4.1 software.<br /> * indicates unsheared DNA </small></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'dna-rna-shearing', 'meta_keywords' => 'DNA/RNA shearing,Bioruptor® Pico,Megaruptor®,Next-Generation Sequencing ', 'meta_description' => 'Bioruptor® Pico and the Megaruptor® provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows.', 'meta_title' => 'DNA shearing & RNA shearing for Next-Generation Sequencing (NGS) | Diagenode', 'modified' => '2017-12-08 14:44:11', 'created' => '2014-10-29 12:45:41', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '17', 'position' => '10', 'parent_id' => '4', 'name' => 'Protein extraction', 'description' => '<div class="row"> <div class="large-12 columns">Various biochemical and analytical techniques require the extraction of protein from tissues or mammalian, yeast and bacterial cells. Obtaining high quality and yields of proteins is important for further downstream protein characterization such as in PAGE, western blotting, mass spectrometry or protein purification. The efficient disruption and homogenization of tissues and cultured cells obtained in just one step using <strong>Diagenode's Bioruptor</strong><sup>®</sup> deliver high quality protein.</div> </div> <p></p> <div class="row"> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_standard_plus.png" /> <p><small>Western blot analysis of GAPDH and HSP90 proteins in tissues (various mouse tissues) and cultured cell extracts (HeLA).</small></p> </div> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_pico.png" /> <p><small>Western blot analysis of GAPDH and ß-tubulin proteins in tissues (mouse liver) and cultured cell extracts (HeLA).</small></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'protein-extraction', 'meta_keywords' => 'Protein extraction,Bioruptor,Sonication,Protein Analysis', 'meta_description' => 'Diagenode provides efficient disruption and homogenization of tissues and cultured cells obtained in just one step using Bioruptor® deliver high quality protein.', 'meta_title' => 'Protein extraction using Bioruptor® Sonication device | Diagenode', 'modified' => '2017-10-16 14:39:42', 'created' => '2014-07-02 04:41:03', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '6', 'position' => '10', 'parent_id' => '1', 'name' => 'メチル化DNA結合タンパク質', 'description' => '<div class="row"> <div class="large-12 columns">MBD方法は、メチル化DNAに対するH6-GST-MBD融合タンパク質の非常に高い親和性に基づいています。 このタンパク質は、N末端His6タグを含むグルタチオン-S-トランスフェラーゼ（GST）とのC末端融合物として、ヒトMeCP2のメチル結合ドメイン（MBD）を含有します。 このH6-GST-MBD融合タンパク質を用いて、メチル化CpGを含むDNAを特異的に単離する事が可能です。<br /><br />DiagenodeのMethylCap®キットは、二本鎖DNAの高濃縮と、メチル化CpG密度の関数における微分分画を可能にします。 分画はサンプルの複雑さを軽減し、次世代のシーケンシングを容易にします。 MethylCapアッセイに先立ち、DNAを最初に抽出し、Picoruptorソニケーターを用いて断片化します。<br /> <h3>概要</h3> <p class="text-center"><br /><img src="https://www.diagenode.com/img/applications/methyl_binding_domain_overview.jpg" /></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'methylbinding-domain-protein', 'meta_keywords' => 'Epigenetic,Methylbinding Domain Protein,MBD,DNA methylation,DNA replication,MethylCap,MethylCap assay,', 'meta_description' => 'Methylbinding Domain Protein(MBD) approach is based on the very high affinity of a H6-GST-MBD fusion protein for methylated DNA. This protein consists of the methyl binding domain (MBD) of human MeCP2, as a C-terminal fusion with Glutathione-S-transferase', 'meta_title' => 'Epigenetic Methylbinding Domain Protein(MBD) - DNA methylation | Diagenode', 'modified' => '2019-03-22 12:32:12', 'created' => '2015-06-02 17:05:42', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '9', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-seq', 'description' => '<div class="row"> <div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div> <div class="large-12 columns"></div> <h5 class="large-12 columns"><strong></strong></h5> <h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div> <div class="large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by sonication to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with <strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: Reverse cross-links, elute, and purify </li> <li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify IP'd material</li> <li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chromatin-immunoprecipitation-sequencing', 'meta_keywords' => 'Chromatin Immunoprecipitation Sequencing,ChIP-Seq,ChIP-seq grade antibodies,DNA purification,qPCR,Shearing of chromatin', 'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing', 'meta_title' => 'Chromatin Immunoprecipitation - ChIP-seq Kits - Dna methylation | Diagenode', 'modified' => '2017-11-14 09:57:16', 'created' => '2015-04-12 18:08:46', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '11', 'position' => '10', 'parent_id' => '3', 'name' => 'FFPE DNA extraction', 'description' => '<div class="row"> <div class="large-12 columns">Diagenode's high yields FFPE DNA extraction using Bioruptor<sup><span>®</span></sup> is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no toxic reagents, digest tissues, and purify DNA with high yields and low sample degradation. The DNA can then be analyzed by traditional methods or can be sheared with the Bioruptor<sup>®</sup> Pico ultrasonicator for downstream NGS library prep using the MicroPlex Library Preparation Kit.</div> <div class="small-12 medium-12 large-12 columns text-center"><img src="https://www.diagenode.com/img/applications/ffpe_workflow.png" /></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'ffpe-dna-extraction', 'meta_keywords' => 'FFPE DNA extraction,Next-Gen Sequencing,Bioruptor® ultrasonicator', 'meta_description' => 'Diagenode's high yields FFPE DNA extraction using Bioruptor is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no tox', 'meta_title' => 'FFPE DNA extraction using Bioruptor® ultrasonicator | Diagenode', 'modified' => '2017-10-16 14:34:57', 'created' => '2014-10-01 01:24:40', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '10', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-qPCR', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns text-justify"> <p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p> <p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p> </div> <div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div> <div class="small-12 medium-12 large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li> <li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chip-qpcr', 'meta_keywords' => 'Chromatin immunoprecipitation,ChIP Quantitative PCR,polymerase chain reaction (PCR)', 'meta_description' => 'Diagenode's ChIP qPCR kits can be used to quantify enriched DNA after chromatin immunoprecipitation. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of', 'meta_title' => 'ChIP Quantitative PCR (ChIP-qPCR) | Diagenode', 'modified' => '2018-01-09 16:46:56', 'created' => '2014-12-11 00:22:08', 'ProductsApplication' => array( [maximum depth reached] ) ) ), 'Category' => array( (int) 0 => array( 'id' => '6', 'position' => '1', 'parent_id' => '1', 'name' => 'Bioruptor<sup>®</sup>', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"><br /> <p><span>Diagenode focuses on state-of-the-art preparation of high quality biological and chemical samples by developing the industry’s most advanced water bath sonicators and hydrodynamic devices. Our instruments are ideal for a number of applications in various fields of studies including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</span></p> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor/TAB-BR-comparaison.pdf" target="_blank"><img src="https://www.diagenode.com/img/bouton-comparaison.png" /></a></p> </div> <!-- <center> <div class="small-12 medium-4 large-4 columns"> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </div> </center></div> <p><span></span></p> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;"></h2> <h2 style="text-align: center;">Technology explained</h2> <div class="container-wrapper-genially" style="position: relative; min-height: 400px; max-width: 80%; margin: 0 auto;"><video width="300" height="150" style="position: absolute; top: 45%; left: 50%; transform: translate(-50%, -50%); width: 80px; height: 80px; margin-bottom: 10%;" class="loader-genially" autoplay="autoplay" loop="loop" playsinline="playsInline" muted="muted"><source src="https://static.genial.ly/resources/panel-loader-low.mp4" type="video/mp4" />Your browser does not support the video tag.</video> <div id="601970a2edea170d2af29118" class="genially-embed" style="margin: 0px auto; position: relative; height: auto; width: 100%;"></div> </div> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script>// <![CDATA[ (function (d) { var js, id = "genially-embed-js", ref = d.getElementsByTagName("script")[0]; if (d.getElementById(id)) { return; } js = d.createElement("script"); js.id = id; js.async = true; js.src = "https://view.genial.ly/static/embed/embed.js"; ref.parentNode.insertBefore(js, ref); }(document)); // ]]></script> </div> </div>--> <p><span> <br /></span></p> <div class="spacer"></div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">Reproductibility is our priority</h2> </div> </div> <div><img src="https://www.diagenode.com/img/shearing/reproductibility.png" alt="reproductibility" /> <p class="bottom_note"></p> </div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">An affordable instrument for wide range of applications</h2> </div> </div> <p style="text-align: center;">Designed for any researchers, the Bioruptor gives the user the right level of flexibility.</p> <table style="width: 972px;"> <tbody> <tr style="height: 56px;"> <th style="width: 380px; height: 56px;"></th> <th class="text-center" style="width: 126px; height: 56px;">Bioruptor</th> <th class="text-center" style="width: 141px; height: 56px;">Cup Horn Sonicators</th> <th class="text-center" style="width: 156px; height: 56px;">Focused <br />ultra-sonicators</th> <th class="text-center" style="width: 155px; height: 56px;">Multi Sample Sonicator</th> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Instrument pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Consumables pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Range of applications</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Scalable and sample volume flexibility</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Throughput</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> </tbody> </table> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;"></h2> <h2 style="text-align: center;">Bioruptor ultrasonication for best results in:</h2> <p><b><span>✓ Chromatin shearing</span><span> </span><span style="font-weight: 400;">- Industry leader in accurate and tight fragment ranges</span></b></p> <p><b><span>✓ DNA shearing</span><span> </span><span style="font-weight: 400;">- Excellent results for optimal fragment lengths in NGS library prep</span></b></p> <p><b><span>✓<span> </span></span>Protein aggregation studies </b><span style="font-weight: 400;">- Standardizing seeding with the robust Bioruptor.<br /></span><i><span style="font-weight: 400;">Read the app note by Dr. Kelvin Luk at the University of Pennsylvania </span></i><a href="https://www.diagenode.com/en/documents/standardizing-seeding-experiments-for-the-understanding-of-parkinson-disease" style="color: #13b29c;"><i><span style="font-weight: 400;">“Standardizing seeding experiments using the Bioruptor® for the understanding of the neuronal alpha-synuclein pathology”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>3D genome analysis with Hi-C</b><span style="font-weight: 400;"> - Preparing chromatin libraries with high-quality sonication.<br /></span><i><span style="font-weight: 400;">Read the app note, “</span></i><a href="https://www.diagenode.com/en/documents/applicationnote-arima-low-input" style="color: #13b29c;"><i><span style="font-weight: 400;">Unlock Low-Input 3D Genome Analysis with the Arima-HiC Kit”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>Mass spectrometry</b> <b>and increasing protein identification</b><span style="font-weight: 400;">- Sample preparation using Preomics iST and Bioruptor sonication.<br /></span><i><span style="font-weight: 400;">Read the app note “</span></i><a href="https://www.diagenode.com/en/documents/wp-ist-adaptators" style="color: #13b29c;"><i><span style="font-weight: 400;">Increase your iST ultrasonication throughput with the new Bioruptor® Pico cartridge holder”</span></i></a></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>Cell lysis, liposome prep, protein extraction, RNA extraction and more</b></span></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>CUT&RUN –Sonication of input DNA (for enrichment comparison) for NGS</b></span></p> </div> </div> <p><a href="https://www.diagenode.com/en/categories/bioruptor-maintenance"><img src="https://www.diagenode.com/img/banners/maintenance-banner-br.png" /></a></p> <p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> </div>', 'no_promo' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'hide' => false, 'all_format' => false, 'is_antibody' => false, 'slug' => 'bioruptor-shearing-device', 'cookies_tag_id' => null, 'meta_keywords' => 'Bioruptor,ultrasonicator devices,probe sonicator,Next-Generation Sequencing', 'meta_description' => 'Bioruptor Sonication is ideal for Chromatin Shearing for Chromatin Immunoprecipitation (ChIP), Genomic DNA Shearing for next Generation Sequencing, RNA Shearing, Cell and Tissue Disruption', 'meta_title' => 'Bioruptor Sonication for Chromatin, DNA / RNA Shearing, Cell and Tissue Disruption | Diagenode', 'modified' => '2024-08-28 14:03:21', 'created' => '2014-12-18 22:08:39', 'ProductsCategory' => array( [maximum depth reached] ), 'CookiesTag' => array([maximum depth reached]) ) ), 'Document' => array( (int) 0 => array( 'id' => '1067', 'name' => 'Chromatin Shearing Guide', 'description' => '<p>Guide for successful chromatin preparation using the 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=> null, 'type' => 'Document', 'url' => 'files/products/shearing_technology/bioruptor/org-tubes-pico-01_20.pdf', 'slug' => 'org-tubes-pico-01-20', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-02-10 11:16:30', 'created' => '2020-02-10 10:55:30', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1127', 'name' => 'Unlock Low-Input 3D Genome Analysis with the Arima-HiC Kit', 'description' => '<p><span>By combining the optimized chemistry of the Arima-HiC kit along with new low input protocols, the potential applications of powerful Hi-C technology are unlocked. When studying samples that are difficult to obtain or grow, low input solutions can help you understand genome structure across a new range of low input samples. In addition, the Diagenode Bioruptor Pico assures that chromatin is sheared to optimal fragment lengths.</span></p>', 'image_id' => '247', 'type' => 'Application Note', 'url' => 'files/application_notes/ApplicationNote-Arima-Low-Input.pdf', 'slug' => 'applicationnote-arima-low-input', 'meta_keywords' => 'application note arima low input', 'meta_description' => 'application note arima low input', 'modified' => '2021-02-09 09:55:59', 'created' => '2021-02-09 09:55:59', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1074', 'name' => 'Datasheet of Bioruptor tubes', 'description' => '<p>Datasheet of Diagenode tubes for Bioruptor Pico and Bioruptor Plus.</p>', 'image_id' => null, 'type' => 'Datasheet', 'url' => 'files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf', 'slug' => 'tds-bioruptor-tubes', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2022-02-23 12:21:44', 'created' => '2020-03-23 10:41:46', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '1170', 'name' => 'Critical steps for Bioruptor® maintenance and efficient shearing', 'description' => '', 'image_id' => null, 'type' => 'Document', 'url' => 'files/products/shearing_technology/critical-steps-bioruptor-web.pdf', 'slug' => 'critical-steps-bioruptor-maintenance', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2023-08-31 14:27:41', 'created' => '2023-08-31 14:27:41', 'ProductsDocument' => array( [maximum depth reached] ) ) ), 'Feature' => array( (int) 0 => array( 'id' => '6', 'name' => 'All-in-one solution', 'slug' => '', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2015-07-24 11:50:41', 'created' => '2014-06-21 12:07:09', 'ProductsFeature' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '16', 'name' => 'Highly reproducible', 'slug' => '', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2015-11-09 14:21:15', 'created' => '2015-05-11 05:24:25', 'ProductsFeature' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '7', 'name' => 'Processing of 6-16 samples', 'slug' => '', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2018-03-13 11:10:21', 'created' => '2014-11-09 09:21:21', 'ProductsFeature' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1', 'name' => 'User friendly software', 'slug' => '', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2015-07-24 17:39:16', 'created' => '2014-06-27 10:32:35', 'ProductsFeature' => array( [maximum depth reached] ) ) ), 'Image' => array( (int) 0 => array( 'id' => '1803', 'name' => 'product/shearing_technologies/B01080000-1.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:55:07', 'created' => '2020-01-10 10:52:54', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '1804', 'name' => 'product/shearing_technologies/B01080000-2.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:08', 'created' => '2020-01-10 10:53:08', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '1805', 'name' => 'product/shearing_technologies/B01080000-3.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:46', 'created' => '2020-01-10 10:53:46', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1806', 'name' => 'product/shearing_technologies/B01080000-4.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:56', 'created' => '2020-01-10 10:53:56', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1807', 'name' => 'product/shearing_technologies/B01080000-5.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:54:06', 'created' => '2020-01-10 10:54:06', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => '2018-02-14 15:41:46', 'ProductsImage' => array( [maximum depth reached] ) ) ), 'Promotion' => array(), 'Protocol' => array( (int) 0 => array( 'id' => '73', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:16:00', 'created' => '0000-00-00 00:00:00', 'ProductsProtocol' => array( [maximum depth reached] ) ) ), 'Publication' => array( (int) 0 => array( 'id' => '4881', 'name' => 'LEO1 Is Required for Efficient Entry into Quiescence, Control of H3K9 Methylation and Gene Expression in Human Fibroblasts', 'authors' => 'Laurent M. et al.', 'description' => '<p><span>(1) Background: The LEO1 (Left open reading frame 1) protein is a conserved subunit of the PAF1C complex (RNA polymerase II-associated factor 1 complex). PAF1C has well-established mechanistic functions in elongation of transcription and RNA processing. We previously showed, in fission yeast, that LEO1 controls histone H3K9 methylation levels by affecting the turnover of histone H3 in chromatin, and that it is essential for the proper regulation of gene expression during cellular quiescence. Human fibroblasts enter a reversible quiescence state upon serum deprivation in the growth media. Here we investigate the function of LEO1 in human fibroblasts. (2) Methods: We knocked out the </span><span class="html-italic">LEO1</span><span><span> </span>gene using CRISPR/Cas9 methodology in human fibroblasts and verified that the LEO1 protein was undetectable by Western blot. We characterized the phenotype of the<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout cells with FACS analysis and cell growth assays. We used RNA-sequencing using spike-in controls to measure gene expression and spike-in controlled ChIP-sequencing experiments to measure the histone modification H3K9me2 genome-wide. (3) Results: Gene expression levels are altered in quiescent cells, however factors controlling chromatin and gene expression changes in quiescent human cells are largely unknown. The<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout fibroblasts are viable but have reduced metabolic activity compared to wild-type cells.<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells showed a slower entry into quiescence and a different morphology compared to wild-type cells. Gene expression was generally reduced in quiescent wild-type cells. The downregulated genes included genes involved in cell proliferation. A small number of genes were upregulated in quiescent wild-type cells including several genes involved in ERK1/ERK2 and Wnt signaling. In quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells, many genes were mis-regulated compared to wild-type cells. This included genes involved in Calcium ion transport and cell morphogenesis. Finally, spike-in controlled ChIP-sequencing experiments demonstrated that the histone modification H3K9me2 levels are globally increased in quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells. (4) Conclusions: Thus, LEO1 is important for proper entry into cellular quiescence, control of H3K9me2 levels, and gene expression in human fibroblasts.</span></p>', 'date' => '2023-11-17', 'pmid' => 'https://www.mdpi.com/2218-273X/13/11/1662', 'doi' => 'https://doi.org/10.3390/biom13111662', 'modified' => '2023-11-21 12:01:53', 'created' => '2023-11-21 12:01:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '4845', 'name' => 'DeSUMOylation of chromatin-bound proteins limits the rapidtranscriptional reprogramming induced by daunorubicin in acute myeloidleukemias.', 'authors' => 'Boulanger M. et al.', 'description' => '<p>Genotoxicants have been used for decades as front-line therapies against cancer on the basis of their DNA-damaging actions. However, some of their non-DNA-damaging effects are also instrumental for killing dividing cells. We report here that the anthracycline Daunorubicin (DNR), one of the main drugs used to treat Acute Myeloid Leukemia (AML), induces rapid (3 h) and broad transcriptional changes in AML cells. The regulated genes are particularly enriched in genes controlling cell proliferation and death, as well as inflammation and immunity. These transcriptional changes are preceded by DNR-dependent deSUMOylation of chromatin proteins, in particular at active promoters and enhancers. Surprisingly, inhibition of SUMOylation with ML-792 (SUMO E1 inhibitor), dampens DNR-induced transcriptional reprogramming. Quantitative proteomics shows that the proteins deSUMOylated in response to DNR are mostly transcription factors, transcriptional co-regulators and chromatin organizers. Among them, the CCCTC-binding factor CTCF is highly enriched at SUMO-binding sites found in cis-regulatory regions. This is notably the case at the promoter of the DNR-induced NFKB2 gene. DNR leads to a reconfiguration of chromatin loops engaging CTCF- and SUMO-bound NFKB2 promoter with a distal cis-regulatory region and inhibition of SUMOylation with ML-792 prevents these changes.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37462077', 'doi' => '10.1093/nar/gkad581', 'modified' => '2023-08-01 14:16:43', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '4846', 'name' => 'RNA polymerase II CTD is dispensable for transcription and requiredfor termination in human cells.', 'authors' => 'Yahia Y. et al.', 'description' => '<p>The largest subunit of RNA polymerase (Pol) II harbors an evolutionarily conserved C-terminal domain (CTD), composed of heptapeptide repeats, central to the transcriptional process. Here, we analyze the transcriptional phenotypes of a CTD-Δ5 mutant that carries a large CTD truncation in human cells. Our data show that this mutant can transcribe genes in living cells but displays a pervasive phenotype with impaired termination, similar to but more severe than previously characterized mutations of CTD tyrosine residues. The CTD-Δ5 mutant does not interact with the Mediator and Integrator complexes involved in the activation of transcription and processing of RNAs. Examination of long-distance interactions and CTCF-binding patterns in CTD-Δ5 mutant cells reveals no changes in TAD domains or borders. Our data demonstrate that the CTD is largely dispensable for the act of transcription in living cells. We propose a model in which CTD-depleted Pol II has a lower entry rate onto DNA but becomes pervasive once engaged in transcription, resulting in a defect in termination.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37424514', 'doi' => '10.15252/embr.202256150', 'modified' => '2023-08-01 14:17:54', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '4793', 'name' => 'Targeting lymphoid-derived IL-17 signaling to delay skin aging.', 'authors' => 'Paloma S. et al.', 'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, γδ T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-κB in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218', 'doi' => '10.1038/s43587-023-00431-z', 'modified' => '2023-06-14 15:56:56', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '4796', 'name' => 'Nicotinamide N-methyltransferase sustains a core epigenetic programthat promotes metastatic colonization in breast cancer.', 'authors' => 'Couto J.P. et al.', 'description' => '<p><span>Metastatic colonization of distant organs accounts for over 90% of deaths related to solid cancers, yet the molecular determinants of metastasis remain poorly understood. Here, we unveil a mechanism of colonization in the aggressive basal-like subtype of breast cancer that is driven by the NAD</span><sup>+</sup><span><span> </span>metabolic enzyme nicotinamide N-methyltransferase (NNMT). We demonstrate that NNMT imprints a basal genetic program into cancer cells, enhancing their plasticity. In line, NNMT expression is associated with poor clinical outcomes in patients with breast cancer. Accordingly, ablation of NNMT dramatically suppresses metastasis formation in pre-clinical mouse models. Mechanistically, NNMT depletion results in a methyl overflow that increases histone H3K9 trimethylation (H3K9me3) and DNA methylation at the promoters of PR/SET Domain-5 (PRDM5) and extracellular matrix-related genes. PRDM5 emerged in this study as a pro-metastatic gene acting via induction of cancer-cell intrinsic transcription of collagens. Depletion of PRDM5 in tumor cells decreases COL1A1 deposition and impairs metastatic colonization of the lungs. These findings reveal a critical activity of the NNMT-PRDM5-COL1A1 axis for cancer cell plasticity and metastasis in basal-like breast cancer.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37259596', 'doi' => '10.15252/embj.2022112559', 'modified' => '2023-06-15 08:35:19', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '4812', 'name' => 'SOX expression in prostate cancer drives resistance to nuclear hormonereceptor signaling inhibition through the WEE1/CDK1 signaling axis.', 'authors' => 'Williams A. et al.', 'description' => '<p><span>The development of androgen receptor signaling inhibitor (ARSI) drug resistance in prostate cancer (PC) remains therapeutically challenging. Our group has described the role of sex determining region Y-box 2 (SOX2) overexpression in ARSI-resistant PC. Continuing this work, we report that NR3C1, the gene encoding glucocorticoid receptor (GR), is a novel SOX2 target in PC, positively regulating its expression. Similar to ARSI treatment, SOX2-positive PC cells are insensitive to GR signaling inhibition using a GR modulating therapy. To understand SOX2-mediated nuclear hormone receptor signaling inhibitor (NHRSI) insensitivity, we performed RNA-seq in SOX2-positive and -negative PC cells following NHRSI treatment. RNA-seq prioritized differentially regulated genes mediating the cell cycle, including G2 checkpoint WEE1 Kinase (WEE1) and cyclin-dependent kinase 1 (CDK1). Additionally, WEE1 and CDK1 were differentially expressed in PC patient tumors dichotomized by high vs low SOX2 gene expression. Importantly, pharmacological targeting of WEE1 (WEE1i) in combination with an ARSI or GR modulator re-sensitizes SOX2-positive PC cells to nuclear hormone receptor signaling inhibition in vitro, and WEE1i combined with ARSI significantly slowed tumor growth in vivo. Collectively, our data suggest SOX2 predicts NHRSI resistance, and simultaneously indicates the addition of WEE1i to improve therapeutic efficacy of NHRSIs in SOX2-positive PC.</span></p>', 'date' => '2023-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37169162', 'doi' => '10.1016/j.canlet.2023.216209', 'modified' => '2023-06-15 08:58:59', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '4787', 'name' => 'The Effect of Metformin and Carbohydrate-Controlled Diet onDNA Methylation and Gene Expression in the Endometrium of Womenwith Polycystic Ovary Syndrome.', 'authors' => 'Garcia-Gomez E. et al.', 'description' => '<p>Polycystic ovary syndrome (PCOS) is an endocrine disease associated with infertility and metabolic disorders in reproductive-aged women. In this study, we evaluated the expression of eight genes related to endometrial function and their DNA methylation levels in the endometrium of PCOS patients and women without the disease (control group). In addition, eight of the PCOS patients underwent intervention with metformin (1500 mg/day) and a carbohydrate-controlled diet (type and quantity) for three months. Clinical and metabolic parameters were determined, and RT-qPCR and MeDIP-qPCR were used to evaluate gene expression and DNA methylation levels, respectively. Decreased expression levels of , , and genes and increased DNA methylation levels of the promoter were found in the endometrium of PCOS patients compared to controls. After metformin and nutritional intervention, some metabolic and clinical variables improved in PCOS patients. This intervention was associated with increased expression of , , and genes and reduced DNA methylation levels of the promoter in the endometrium of PCOS women. Our preliminary findings suggest that metformin and a carbohydrate-controlled diet improve endometrial function in PCOS patients, partly by modulating DNA methylation of the gene promoter and the expression of genes implicated in endometrial receptivity and insulin signaling.</p>', 'date' => '2023-04-01', 'pmid' => 'https://doi.org/10.3390%2Fijms24076857', 'doi' => '10.3390/ijms24076857', 'modified' => '2023-06-12 08:58:33', 'created' => '2023-05-05 12:34:24', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '4763', 'name' => 'Chromatin profiling identifies transcriptional readthrough as a conservedmechanism for piRNA biogenesis in mosquitoes.', 'authors' => 'Qu J. et al.', 'description' => '<p>The piRNA pathway in mosquitoes differs substantially from other model organisms, with an expanded PIWI gene family and functions in antiviral defense. Here, we define core piRNA clusters as genomic loci that show ubiquitous piRNA expression in both somatic and germline tissues. These core piRNA clusters are enriched for non-retroviral endogenous viral elements (nrEVEs) in antisense orientation and depend on key biogenesis factors, Veneno, Tejas, Yb, and Shutdown. Combined transcriptome and chromatin state analyses identify transcriptional readthrough as a conserved mechanism for cluster-derived piRNA biogenesis in the vector mosquitoes Aedes aegypti, Aedes albopictus, Culex quinquefasciatus, and Anopheles gambiae. Comparative analyses between the two Aedes species suggest that piRNA clusters function as traps for nrEVEs, allowing adaptation to environmental challenges such as virus infection. Our systematic transcriptome and chromatin state analyses lay the foundation for studies of gene regulation, genome evolution, and piRNA function in these important vector species.</p>', 'date' => '2023-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36930642', 'doi' => '10.1016/j.celrep.2023.112257', 'modified' => '2023-04-17 09:12:37', 'created' => '2023-04-14 13:41:22', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 8 => array( 'id' => '4720', 'name' => 'Activation of AKT induces EZH2-mediated β-catenin trimethylation incolorectal cancer.', 'authors' => 'Ghobashi A. H. et al.', 'description' => '<p>Colorectal cancer (CRC) develops in part through the deregulation of different signaling pathways, including activation of the WNT/β-catenin and PI3K/AKT pathways. Enhancer of zeste homolog 2 (EZH2) is a lysine methyltransferase that is involved in regulating stem cell development and differentiation and is overexpressed in CRC. However, depending on the study EZH2 has been found to be both positively and negatively correlated with the survival of CRC patients suggesting that EZH2's role in CRC may be context specific. In this study, we explored how PI3K/AKT activation alters EZH2's role in CRC. We found that activation of AKT by PTEN knockdown or by hydrogen peroxide treatment induced EZH2 phosphorylation at serine 21. Phosphorylation of EZH2 resulted in EZH2-mediated methylation of β-catenin and an associated increased interaction between β-catenin, TCF1, and RNA polymerase II. AKT activation increased β-catenin's enrichment across the genome and EZH2 inhibition reduced this enrichment by reducing the methylation of β-catenin. Furthermore, PTEN knockdown increased the expression of epithelial-mesenchymal transition (EMT)-related genes, and somewhat unexpectedly EZH2 inhibition further increased the expression of these genes. Consistent with these findings, EZH2 inhibition enhanced the migratory phenotype of PTEN knockdown cells. Overall, we demonstrated that EZH2 modulates AKT-induced changes in gene expression through the AKT/EZH2/ β-catenin axis in CRC with active PI3K/AKT signaling. Therefore, it is important to consider the use of EZH2 inhibitors in CRC with caution as these inhibitors will inhibit EZH2-mediated methylation of histone and non-histone targets such as β-catenin, which can have tumor-promoting effects.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1101%2F2023.01.31.526429', 'doi' => '10.1101/2023.01.31.526429', 'modified' => '2023-03-28 09:13:16', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 9 => array( 'id' => '4667', 'name' => 'Detailed molecular and epigenetic characterization of the Pig IPECJ2and Chicken SL-29 cell lines', 'authors' => 'de Vos J. et al.', 'description' => '<p>The pig IPECJ2 and chicken SL-29 cell lines are of interest because of their untransformed nature and wide use in functional studies. Molecular characterization of these cell lines is important to gain insight into possible molecular aberrations. The aims of this paper are providing a molecular and epigenetic characterization of the IPEC-J2 and SL-29 cell lines and providing a cell-line reference for the FAANG community, and future biomedical research. Whole genome sequencing , gene expression, DNA methylation , chromatin accessibility and ChIP-seq of four histone marks (H3K4me1, H3K4me3, H3K27ac, H3K27me3) and an insulator (CTCF) are used to achieve these aims. Heteroploidy (aneuploidy) of various chromosomes was observed from whole genome sequencing analysis in both cell lines. Furthermore, higher gene expression for genes located on chromosomes with aneuploidy in comparison to diploid chromosomes was observed. Regulatory complexity of gene expression, DNA methylation and chromatin accessibility was investigated through an integrative approach.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.isci.2023.106252', 'doi' => '10.1016/j.isci.2023.106252', 'modified' => '2023-04-07 16:52:26', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 10 => array( 'id' => '4673', 'name' => 'Signal-induced enhancer activation requires Ku70 to readtopoisomerase1-DNA covalent complexes.', 'authors' => 'Tan Y. et al.', 'description' => '<p>Enhancer activation serves as the main mechanism regulating signal-dependent transcriptional programs, ensuring cellular plasticity, yet central questions persist regarding their mechanism of activation. Here, by successfully mapping topoisomerase I-DNA covalent complexes genome-wide, we find that most, if not all, acutely activated enhancers, including those induced by 17β-estradiol, dihydrotestosterone, tumor necrosis factor alpha and neuronal depolarization, are hotspots for topoisomerase I-DNA covalent complexes, functioning as epigenomic signatures read by the classic DNA damage sensor protein, Ku70. Ku70 in turn nucleates a heterochromatin protein 1 gamma (HP1γ)-mediator subunit Med26 complex to facilitate acute, but not chronic, transcriptional activation programs. Together, our data uncover a broad, unappreciated transcriptional code, required for most, if not all, acute signal-dependent enhancer activation events in both mitotic and postmitotic cells.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36747093', 'doi' => '10.1038/s41594-022-00883-8', 'modified' => '2023-04-14 09:24:10', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 11 => array( 'id' => '4668', 'name' => 'Cotranscriptional demethylation induces global loss of H3K4me2 fromactive genes in Arabidopsis', 'authors' => 'Mori S. et al.', 'description' => '<p>Based on studies of animals and yeasts, methylation of histone H3 lysine 4 (H3K4me1/2/3, for mono-, di-, and tri-methylation, respectively) is regarded as the key epigenetic modification of transcriptionally active genes. In plants, however, H3K4me2 correlates negatively with transcription, and the regulatory mechanisms of this counterintuitive H3K4me2 distribution in plants remain largely unexplored. A previous genetic screen for factors regulating plant regeneration identified Arabidopsis LYSINE-SPECIFIC DEMETHYLASE 1-LIKE 3 (LDL3), which is a major H3K4me2 demethylase. Here, we show that LDL3-mediated H3K4me2 demethylation depends on the transcription elongation factor Paf1C and phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII). In addition, LDL3 binds to phosphorylated RNAPII. These results suggest that LDL3 is recruited to transcribed genes by binding to elongating RNAPII and demethylates H3K4me2 cotranscriptionally. Importantly, the negative correlation between H3K4me2 and transcription is disrupted in the ldl3 mutant, demonstrating the genome-wide impacts of the transcription-driven LDL3 pathway to control H3K4me2 in plants. Our findings implicate H3K4me2 in plants as chromatin memory for transcriptionally repressive states, which ensures robust gene control.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.02.17.528985v1', 'doi' => '10.1101/2023.02.17.528985', 'modified' => '2023-04-14 09:31:55', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 12 => array( 'id' => '4670', 'name' => 'Epigenetic regulation of plastin 3 expression by the macrosatelliteDXZ4 and the transcriptional regulator CHD4.', 'authors' => 'Strathmann E. A. et al.', 'description' => '<p>Dysregulated Plastin 3 (PLS3) levels associate with a wide range of skeletal and neuromuscular disorders and the most common types of solid and hematopoietic cancer. Most importantly, PLS3 overexpression protects against spinal muscular atrophy. Despite its crucial role in F-actin dynamics in healthy cells and its involvement in many diseases, the mechanisms that regulate PLS3 expression are unknown. Interestingly, PLS3 is an X-linked gene and all asymptomatic SMN1-deleted individuals in SMA-discordant families who exhibit PLS3 upregulation are female, suggesting that PLS3 may escape X chromosome inactivation. To elucidate mechanisms contributing to PLS3 regulation, we performed a multi-omics analysis in two SMA-discordant families using lymphoblastoid cell lines and iPSC-derived spinal motor neurons originated from fibroblasts. We show that PLS3 tissue-specifically escapes X-inactivation. PLS3 is located ∼500 kb proximal to the DXZ4 macrosatellite, which is essential for X chromosome inactivation. By applying molecular combing in a total of 25 lymphoblastoid cell lines (asymptomatic individuals, individuals with SMA, control subjects) with variable PLS3 expression, we found a significant correlation between the copy number of DXZ4 monomers and PLS3 levels. Additionally, we identified chromodomain helicase DNA binding protein 4 (CHD4) as an epigenetic transcriptional regulator of PLS3 and validated co-regulation of the two genes by siRNA-mediated knock-down and overexpression of CHD4. We show that CHD4 binds the PLS3 promoter by performing chromatin immunoprecipitation and that CHD4/NuRD activates the transcription of PLS3 by dual-luciferase promoter assays. Thus, we provide evidence for a multilevel epigenetic regulation of PLS3 that may help to understand the protective or disease-associated PLS3 dysregulation.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.ajhg.2023.02.004', 'doi' => '10.1016/j.ajhg.2023.02.004', 'modified' => '2023-04-14 09:36:04', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 13 => array( 'id' => '4672', 'name' => 'A dataset of definitive endoderm and hepatocyte differentiations fromhuman induced pluripotent stem cells.', 'authors' => 'Tanaka Y. et al.', 'description' => '<p>Hepatocytes are a major parenchymal cell type in the liver and play an essential role in liver function. Hepatocyte-like cells can be differentiated in vitro from induced pluripotent stem cells (iPSCs) via definitive endoderm (DE)-like cells and hepatoblast-like cells. Here, we explored the in vitro differentiation time-course of hepatocyte-like cells. We performed methylome and transcriptome analyses for hepatocyte-like cell differentiation. We also analyzed DE-like cell differentiation by methylome, transcriptome, chromatin accessibility, and GATA6 binding profiles, using finer time-course samples. In this manuscript, we provide a detailed description of the dataset and the technical validations. Our data may be valuable for the analysis of the molecular mechanisms underlying hepatocyte and DE differentiations.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36788249', 'doi' => '10.1038/s41597-023-02001-9', 'modified' => '2023-04-14 09:41:29', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 14 => array( 'id' => '4643', 'name' => 'The mineralocorticoid receptor modulates timing and location of genomicbinding by glucocorticoid receptor in response to synthetic glucocorticoidsin keratinocytes.', 'authors' => 'Carceller-Zazo E. et al.', 'description' => '<p>Glucocorticoids (GCs) exert potent antiproliferative and anti-inflammatory properties, explaining their therapeutic efficacy for skin diseases. GCs act by binding to the GC receptor (GR) and the mineralocorticoid receptor (MR), co-expressed in classical and non-classical targets including keratinocytes. Using knockout mice, we previously demonstrated that GR and MR exert essential nonoverlapping functions in skin homeostasis. These closely related receptors may homo- or heterodimerize to regulate transcription, and theoretically bind identical GC-response elements (GRE). We assessed the contribution of MR to GR genomic binding and the transcriptional response to the synthetic GC dexamethasone (Dex) using control (CO) and MR knockout (MR ) keratinocytes. GR chromatin immunoprecipitation (ChIP)-seq identified peaks common and unique to both genotypes upon Dex treatment (1 h). GREs, AP-1, TEAD, and p53 motifs were enriched in CO and MR peaks. However, GR genomic binding was 35\% reduced in MR , with significantly decreased GRE enrichment, and reduced nuclear GR. Surface plasmon resonance determined steady state affinity constants, suggesting preferred dimer formation as MR-MR > GR-MR ~ GR-GR; however, kinetic studies demonstrated that GR-containing dimers had the longest lifetimes. Despite GR-binding differences, RNA-seq identified largely similar subsets of differentially expressed genes in both genotypes upon Dex treatment (3 h). However, time-course experiments showed gene-dependent differences in the magnitude of expression, which correlated with earlier and more pronounced GR binding to GRE sites unique to CO including near Nr3c1. Our data show that endogenous MR has an impact on the kinetics and differential genomic binding of GR, affecting the time-course, specificity, and magnitude of GC transcriptional responses in keratinocytes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36527388', 'doi' => '10.1096/fj.202201199RR', 'modified' => '2023-03-28 08:55:08', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 15 => array( 'id' => '4605', 'name' => 'Gene Regulatory Interactions at Lamina-Associated Domains', 'authors' => 'Madsen-Østerbye J. et al.', 'description' => '<p>The nuclear lamina provides a repressive chromatin environment at the nuclear periphery. However, whereas most genes in lamina-associated domains (LADs) are inactive, over ten percent reside in local euchromatic contexts and are expressed. How these genes are regulated and whether they are able to interact with regulatory elements remain unclear. Here, we integrate publicly available enhancer-capture Hi-C data with our own chromatin state and transcriptomic datasets to show that inferred enhancers of active genes in LADs are able to form connections with other enhancers within LADs and outside LADs. Fluorescence in situ hybridization analyses show proximity changes between differentially expressed genes in LADs and distant enhancers upon the induction of adipogenic differentiation. We also provide evidence of involvement of lamin A/C, but not lamin B1, in repressing genes at the border of an in-LAD active region within a topological domain. Our data favor a model where the spatial topology of chromatin at the nuclear lamina is compatible with gene expression in this dynamic nuclear compartment.</p>', 'date' => '2023-01-01', 'pmid' => 'https://doi.org/10.3390%2Fgenes14020334', 'doi' => '10.3390/genes14020334', 'modified' => '2023-04-04 08:57:32', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 16 => array( 'id' => '4578', 'name' => 'The aryl hydrocarbon receptor cell intrinsically promotes resident memoryCD8 T cell differentiation and function.', 'authors' => 'Dean J. W. et al.', 'description' => '<p>The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4 T cells; however, its cell-intrinsic role in CD8 T cells remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8 T cell (T) differentiation and function. Genetic ablation of Ahr in mouse CD8 T cells leads to increased CD127KLRG1 short-lived effector cells and CD44CD62L T central memory cells but reduced granzyme-B-producing CD69CD103 T cells. Genome-wide analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8 T cell population, revealed by single-cell RNA-seq, is diminished upon Ahr deletion, compromising anti-tumor immunity. Human intestinal intraepithelial CD8 T cells also highly express AHR that regulates in vitro T differentiation and granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8 T cell immunity.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36640340', 'doi' => '10.1016/j.celrep.2022.111963', 'modified' => '2023-04-11 10:14:26', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 17 => array( 'id' => '4577', 'name' => 'Impact of Fetal Exposure to Endocrine Disrupting ChemicalMixtures on FOXA3 Gene and Protein Expression in Adult RatTestes.', 'authors' => 'Walker C. et al.', 'description' => '<p>Perinatal exposure to endocrine disrupting chemicals (EDCs) has been shown to affect male reproductive functions. However, the effects on male reproduction of exposure to EDC mixtures at doses relevant to humans have not been fully characterized. In previous studies, we found that in utero exposure to mixtures of the plasticizer di(2-ethylhexyl) phthalate (DEHP) and the soy-based phytoestrogen genistein (Gen) induced abnormal testis development in rats. In the present study, we investigated the molecular basis of these effects in adult testes from the offspring of pregnant SD rats gavaged with corn oil or Gen + DEHP mixtures at 0.1 or 10 mg/kg/day. Testicular transcriptomes were determined by microarray and RNA-seq analyses. A protein analysis was performed on paraffin and frozen testis sections, mainly by immunofluorescence. The transcription factor forkhead box protein 3 (FOXA3), a key regulator of Leydig cell function, was identified as the most significantly downregulated gene in testes from rats exposed in utero to Gen + DEHP mixtures. FOXA3 protein levels were decreased in testicular interstitium at a dose previously found to reduce testosterone levels, suggesting a primary effect of fetal exposure to Gen + DEHP on adult Leydig cells, rather than on spermatids and Sertoli cells, also expressing FOXA3. Thus, FOXA3 downregulation in adult testes following fetal exposure to Gen + DEHP may contribute to adverse male reproductive outcomes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36674726', 'doi' => '10.3390/ijms24021211', 'modified' => '2023-04-11 10:18:58', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 18 => array( 'id' => '4721', 'name' => 'Transfer of blocker-based qPCR reactions for DNA methylation analysisinto a microfluidic LoC system using thermal modeling.', 'authors' => 'Kärcher J.et al.', 'description' => '<p>Changes in the DNA methylation landscape are associated with many diseases like cancer. Therefore, DNA methylation analysis is of great interest for molecular diagnostics and can be applied, e.g., for minimally invasive diagnostics in liquid biopsy samples like blood plasma. Sensitive detection of local methylation, which occurs in various cancer types, can be achieved with quantitative HeavyMethyl-PCR using oligonucleotides that block the amplification of unmethylated DNA. A transfer of these quantitative PCRs (qPCRs) into point-of-care (PoC) devices like microfluidic Lab-on-Chip (LoC) cartridges can be challenging as LoC systems show significantly different thermal properties than qPCR cyclers. We demonstrate how an adequate thermal model of the specific LoC system can help us to identify a suitable thermal profile, even for complex HeavyMethyl qPCRs, with reduced experimental effort. Using a simulation-based approach, we demonstrate a proof-of-principle for the successful LoC transfer of colorectal /-qPCR from Epi Procolon® colorectal carcinoma test, by avoidance of oligonucleotide interactions.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36506005', 'doi' => '10.1063/5.0108374', 'modified' => '2023-03-28 09:15:30', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 19 => array( 'id' => '4575', 'name' => 'Intranasal administration of Acinetobacter lwoffii in a murine model ofasthma induces IL-6-mediated protection associated with cecal microbiotachanges.', 'authors' => 'Alashkar A. B. et al.', 'description' => '<p>BACKGROUND: Early-life exposure to certain environmental bacteria including Acinetobacter lwoffii (AL) has been implicated in protection from chronic inflammatory diseases including asthma later in life. However, the underlying mechanisms at the immune-microbe interface remain largely unknown. METHODS: The effects of repeated intranasal AL exposure on local and systemic innate immune responses were investigated in wild-type and Il6 , Il10 , and Il17 mice exposed to ovalbumin-induced allergic airway inflammation. Those investigations were expanded by microbiome analyses. To assess for AL-associated changes in gene expression, the picture arising from animal data was supplemented by in vitro experiments of macrophage and T-cell responses, yielding expression and epigenetic data. RESULTS: The asthma preventive effect of AL was confirmed in the lung. Repeated intranasal AL administration triggered a proinflammatory immune response particularly characterized by elevated levels of IL-6, and consequently, IL-6 induced IL-10 production in CD4 T-cells. Both IL-6 and IL-10, but not IL-17, were required for asthma protection. AL had a profound impact on the gene regulatory landscape of CD4 T-cells which could be largely recapitulated by recombinant IL-6. AL administration also induced marked changes in the gastrointestinal microbiome but not in the lung microbiome. By comparing the effects on the microbiota according to mouse genotype and AL-treatment status, we have identified microbial taxa that were associated with either disease protection or activity. CONCLUSION: These experiments provide a novel mechanism of Acinetobacter lwoffii-induced asthma protection operating through IL-6-mediated epigenetic activation of IL-10 production and with associated effects on the intestinal microbiome.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36458896', 'doi' => '10.1111/all.15606', 'modified' => '2023-04-11 10:23:07', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 20 => array( 'id' => '4574', 'name' => 'Trichoderma root colonization triggers epigenetic changes in jasmonic andsalicylic acid pathway-related genes.', 'authors' => 'Agostini R. B. et al.', 'description' => '<p>Beneficial interactions between plant-roots and Trichoderma spp. lead to a local and systemic enhancement of the plant immune system through a mechanism known as priming of defenses. In recent reports, we outlined a repertoire of genes and proteins differentially regulated in distant tissues of maize plants previously inoculated with Trichoderma atroviride. To further investigate the mechanisms involved in the systemic activation of plant responses, we continued evaluating the regulatory aspects of a selected group of genes when priming is triggered in maize plants. We conducted a time-course expression experiment from the beginning of the interaction between T. atroviride and maize roots, along plant vegetative growth and during Colletotrichum graminicola leaf infection. In addition to gene expression studies, the levels of jasmonic and salicylic acid were determined in the same samples for a comprehensive understanding of the gene expression results. Lastly, chromatin structure and modification assays were designed to evaluate the role of epigenetic marks during the long-lasting activation of the primed state of maize plants. The overall analysis of the results allowed us to shed some light on the interplay between the phytohormones and epigenetic regulatory events in the systemic and long-lasting regulation of maize plant defenses after Trichoderma inoculation.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36575905', 'doi' => '10.1093/jxb/erac518', 'modified' => '2023-04-14 09:08:14', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 21 => array( 'id' => '4474', 'name' => 'DNA sequence and chromatin modifiers cooperate to confer epigeneticbistability at imprinting control regions.', 'authors' => 'Butz S. et al.', 'description' => '<p>Genomic imprinting is regulated by parental-specific DNA methylation of imprinting control regions (ICRs). Despite an identical DNA sequence, ICRs can exist in two distinct epigenetic states that are memorized throughout unlimited cell divisions and reset during germline formation. Here, we systematically study the genetic and epigenetic determinants of this epigenetic bistability. By iterative integration of ICRs and related DNA sequences to an ectopic location in the mouse genome, we first identify the DNA sequence features required for maintenance of epigenetic states in embryonic stem cells. The autonomous regulatory properties of ICRs further enabled us to create DNA-methylation-sensitive reporters and to screen for key components involved in regulating their epigenetic memory. Besides DNMT1, UHRF1 and ZFP57, we identify factors that prevent switching from methylated to unmethylated states and show that two of these candidates, ATF7IP and ZMYM2, are important for the stability of DNA and H3K9 methylation at ICRs in embryonic stem cells.</p>', 'date' => '2022-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36333500', 'doi' => '10.1038/s41588-022-01210-z', 'modified' => '2022-11-18 12:20:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 22 => array( 'id' => '4493', 'name' => 'Smc5/6 silences episomal transcription by a three-step function.', 'authors' => 'Abdul F. et al.', 'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36097294', 'doi' => '10.1038/s41594-022-00829-0', 'modified' => '2022-11-18 12:41:42', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 23 => array( 'id' => '4495', 'name' => 'Exploration of nuclear body-enhanced sumoylation reveals that PMLrepresses 2-cell features of embryonic stem cells.', 'authors' => 'Tessier S. et al.', 'description' => '<p>Membrane-less organelles are condensates formed by phase separation whose functions often remain enigmatic. Upon oxidative stress, PML scaffolds Nuclear Bodies (NBs) to regulate senescence or metabolic adaptation. PML NBs recruit many partner proteins, but the actual biochemical mechanism underlying their pleiotropic functions remains elusive. Similarly, PML role in embryonic stem cell (ESC) and retro-element biology is unsettled. Here we demonstrate that PML is essential for oxidative stress-driven partner SUMO2/3 conjugation in mouse ESCs (mESCs) or leukemia, a process often followed by their poly-ubiquitination and degradation. Functionally, PML is required for stress responses in mESCs. Differential proteomics unravel the KAP1 complex as a PML NB-dependent SUMO2-target in arsenic-treated APL mice or mESCs. PML-driven KAP1 sumoylation enables activation of this key epigenetic repressor implicated in retro-element silencing. Accordingly, Pml mESCs re-express transposable elements and display 2-Cell-Like features, the latter enforced by PML-controlled SUMO2-conjugation of DPPA2. Thus, PML orchestrates mESC state by coordinating SUMO2-conjugation of different transcriptional regulators, raising new hypotheses about PML roles in cancer.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36175410', 'doi' => '10.1038/s41467-022-33147-6', 'modified' => '2022-11-21 10:21:48', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 24 => array( 'id' => '4502', 'name' => 'Loss of epigenetic regulation disrupts lineage integrity, inducesaberrant alveogenesis and promotes breast cancer.', 'authors' => 'Langille E. et al.', 'description' => '<p>Systematically investigating the scores of genes mutated in cancer and discerning disease drivers from inconsequential bystanders is a prerequisite for Precision Medicine but remains challenging. Here, we developed a somatic CRISPR/Cas9 mutagenesis screen to study 215 recurrent 'long-tail' breast cancer genes, which revealed epigenetic regulation as a major tumor suppressive mechanism. We report that components of the BAP1 and the COMPASS-like complexes, including KMT2C/D, KDM6A, BAP1 and ASXL1/2 ("EpiDrivers"), cooperate with PIK3CAH1047R to transform mouse and human breast epithelial cells. Mechanistically, we find that activation of PIK3CAH1047R and concomitant EpiDriver loss triggered an alveolar-like lineage conversion of basal mammary epithelial cells and accelerated formation of luminal-like tumors, suggesting a basal origin for luminal tumors. EpiDrivers mutations are found in ~39\% of human breast cancers and ~50\% of ductal-carcinoma-in-situ express casein suggesting that lineage infidelity and alveogenic mimicry may significantly contribute to early steps of breast cancer etiology.</p>', 'date' => '2022-09-01', 'pmid' => 'https://aacrjournals.org/cancerdiscovery/article-abstract/doi/10.1158/2159-8290.CD-21-0865/709222/Loss-of-epigenetic-regulation-disrupts-lineage?redirectedFrom=fulltext', 'doi' => '10.1158/2159-8290.CD-21-0865', 'modified' => '2022-11-21 10:34:24', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 25 => array( 'id' => '4449', 'name' => 'RAD51 protects human cells from transcription-replication conflicts.', 'authors' => 'Bhowmick R. et al.', 'description' => '<p>Oncogene activation during tumorigenesis promotes DNA replication stress (RS), which subsequently drives the formation of cancer-associated chromosomal rearrangements. Many episodes of physiological RS likely arise due to conflicts between the DNA replication and transcription machineries operating simultaneously at the same loci. One role of the RAD51 recombinase in human cells is to protect replication forks undergoing RS. Here, we have identified a key role for RAD51 in preventing transcription-replication conflicts (TRCs) from triggering replication fork breakage. The genomic regions most affected by RAD51 deficiency are characterized by being replicated and transcribed in early S-phase and show significant overlap with loci prone to cancer-associated amplification. Consistent with a role for RAD51 in protecting against transcription-replication conflicts, many of the adverse effects of RAD51 depletion are ameliorated by inhibiting early S-phase transcription. We propose a model whereby RAD51 suppresses fork breakage and subsequent inadvertent amplification of genomic loci prone to experiencing TRCs.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36002000', 'doi' => '10.1016/j.molcel.2022.07.010', 'modified' => '2022-10-14 16:44:54', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 26 => array( 'id' => '4511', 'name' => 'The Arabidopsis APOLO and human UPAT sequence-unrelated longnoncoding RNAs can modulate DNA and histone methylation machineries inplants.', 'authors' => 'Fonouni-Farde C. et al.', 'description' => '<p>BACKGROUND: RNA-DNA hybrid (R-loop)-associated long noncoding RNAs (lncRNAs), including the Arabidopsis lncRNA AUXIN-REGULATED PROMOTER LOOP (APOLO), are emerging as important regulators of three-dimensional chromatin conformation and gene transcriptional activity. RESULTS: Here, we show that in addition to the PRC1-component LIKE HETEROCHROMATIN PROTEIN 1 (LHP1), APOLO interacts with the methylcytosine-binding protein VARIANT IN METHYLATION 1 (VIM1), a conserved homolog of the mammalian DNA methylation regulator UBIQUITIN-LIKE CONTAINING PHD AND RING FINGER DOMAINS 1 (UHRF1). The APOLO-VIM1-LHP1 complex directly regulates the transcription of the auxin biosynthesis gene YUCCA2 by dynamically determining DNA methylation and H3K27me3 deposition over its promoter during the plant thermomorphogenic response. Strikingly, we demonstrate that the lncRNA UHRF1 Protein Associated Transcript (UPAT), a direct interactor of UHRF1 in humans, can be recognized by VIM1 and LHP1 in plant cells, despite the lack of sequence homology between UPAT and APOLO. In addition, we show that increased levels of APOLO or UPAT hamper VIM1 and LHP1 binding to YUCCA2 promoter and globally alter the Arabidopsis transcriptome in a similar manner. CONCLUSIONS: Collectively, our results uncover a new mechanism in which a plant lncRNA coordinates Polycomb action and DNA methylation through the interaction with VIM1, and indicates that evolutionary unrelated lncRNAs with potentially conserved structures may exert similar functions by interacting with homolog partners.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36038910', 'doi' => '10.1186/s13059-022-02750-7', 'modified' => '2022-11-21 10:43:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 27 => array( 'id' => '4552', 'name' => 'Prolonged FOS activity disrupts a global myogenic transcriptionalprogram by altering 3D chromatin architecture in primary muscleprogenitor cells.', 'authors' => 'Barutcu A Rasim et al.', 'description' => '<p>BACKGROUND: The AP-1 transcription factor, FBJ osteosarcoma oncogene (FOS), is induced in adult muscle satellite cells (SCs) within hours following muscle damage and is required for effective stem cell activation and muscle repair. However, why FOS is rapidly downregulated before SCs enter cell cycle as progenitor cells (i.e., transiently expressed) remains unclear. Further, whether boosting FOS levels in the proliferating progeny of SCs can enhance their myogenic properties needs further evaluation. METHODS: We established an inducible, FOS expression system to evaluate the impact of persistent FOS activity in muscle progenitor cells ex vivo. We performed various assays to measure cellular proliferation and differentiation, as well as uncover changes in RNA levels and three-dimensional (3D) chromatin interactions. RESULTS: Persistent FOS activity in primary muscle progenitor cells severely antagonizes their ability to differentiate and form myotubes within the first 2 weeks in culture. RNA-seq analysis revealed that ectopic FOS activity in muscle progenitor cells suppressed a global pro-myogenic transcriptional program, while activating a stress-induced, mitogen-activated protein kinase (MAPK) transcriptional signature. Additionally, we observed various FOS-dependent, chromosomal re-organization events in A/B compartments, topologically associated domains (TADs), and genomic loops near FOS-regulated genes. CONCLUSIONS: Our results suggest that elevated FOS activity in recently activated muscle progenitor cells perturbs cellular differentiation by altering the 3D chromosome organization near critical pro-myogenic genes. This work highlights the crucial importance of tightly controlling FOS expression in the muscle lineage and suggests that in states of chronic stress or disease, persistent FOS activity in muscle precursor cells may disrupt the muscle-forming process.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35971133', 'doi' => '10.1186/s13395-022-00303-x', 'modified' => '2022-11-24 10:11:55', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 28 => array( 'id' => '4452', 'name' => 'Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.', 'authors' => 'Schomann T. et al.', 'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>', 'date' => '2022-07-01', 'pmid' => 'https://doi.org/10.3390%2Fbiom12081048', 'doi' => '10.3390/biom12081048', 'modified' => '2022-10-21 09:33:25', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 29 => array( 'id' => '4446', 'name' => 'Variation in PU.1 binding and chromatin looping at neutrophil enhancersinfluences autoimmune disease susceptibility', 'authors' => 'Watt S. et al. ', 'description' => '<p>Neutrophils play fundamental roles in innate inflammatory response, shape adaptive immunity1, and have been identified as a potentially causal cell type underpinning genetic associations with immune system traits and diseases2,3 The majority of these variants are non-coding and the underlying mechanisms are not fully understood. Here, we profiled the binding of one of the principal myeloid transcriptional regulators, PU.1, in primary neutrophils across nearly a hundred volunteers, and elucidate the coordinated genetic effects of PU.1 binding variation, local chromatin state, promoter-enhancer interactions and gene expression. We show that PU.1 binding and the associated chain of molecular changes underlie genetically-driven differences in cell count and autoimmune disease susceptibility. Our results advance interpretation for genetic loci associated with neutrophil biology and immune disease.</p>', 'date' => '2022-05-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/620260v1.abstract', 'doi' => '10.1101/620260', 'modified' => '2022-10-14 16:39:03', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 30 => array( 'id' => '4217', 'name' => 'CREBBP/EP300 acetyltransferase inhibition disrupts FOXA1-bound enhancers to inhibit the proliferation of ER+ breast cancer cells.', 'authors' => 'Bommi-Reddy A. et al.', 'description' => '<p><span>Therapeutic targeting of the estrogen receptor (ER) is a clinically validated approach for estrogen receptor positive breast cancer (ER+ BC), but sustained response is limited by acquired resistance. Targeting the transcriptional coactivators required for estrogen receptor activity represents an alternative approach that is not subject to the same limitations as targeting estrogen receptor itself. In this report we demonstrate that the acetyltransferase activity of coactivator paralogs CREBBP/EP300 represents a promising therapeutic target in ER+ BC. Using the potent and selective inhibitor CPI-1612, we show that CREBBP/EP300 acetyltransferase inhibition potently suppresses in vitro and in vivo growth of breast cancer cell line models and acts in a manner orthogonal to directly targeting ER. CREBBP/EP300 acetyltransferase inhibition suppresses ER-dependent transcription by targeting lineage-specific enhancers defined by the pioneer transcription factor FOXA1. These results validate CREBBP/EP300 acetyltransferase activity as a viable target for clinical development in ER+ breast cancer.</span></p>', 'date' => '2022-03-30', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/35353838/', 'doi' => '10.1371/journal.pone.0262378', 'modified' => '2022-04-12 10:56:54', 'created' => '2022-04-12 10:56:54', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 31 => array( 'id' => '4407', 'name' => 'Transient regulation of focal adhesion via Tensin3 is required fornascent oligodendrocyte differentiation', 'authors' => 'Merour E. et al.', 'description' => '<p>The differentiation of oligodendroglia from oligodendrocyte precursor cells (OPCs) to complex and extensive myelinating oligodendrocytes (OLs) is a multistep process that involves largescale morphological changes with significant strain on the cytoskeleton. While key chromatin and transcriptional regulators of differentiation have been identified, their target genes responsible for the morphological changes occurring during OL myelination are still largely unknown. Here, we show that the regulator of focal adhesion, Tensin3 (Tns3), is a direct target gene of Olig2, Chd7, and Chd8, transcriptional regulators of OL differentiation. Tns3 is transiently upregulated and localized to cell processes of immature OLs, together with integrin-β1, a key mediator of survival at this transient stage. Constitutive Tns3 loss-of-function leads to reduced viability in mouse and humans, with surviving knockout mice still expressing Tns3 in oligodendroglia. Acute deletion of Tns3 in vivo, either in postnatal neural stem cells (NSCs) or in OPCs, leads to a two-fold reduction in OL numbers. We find that the transient upregulation of Tns3 is required to protect differentiating OPCs and immature OLs from cell death by preventing the upregulation of p53, a key regulator of apoptosis. Altogether, our findings reveal a specific time window during which transcriptional upregulation of Tns3 in immature OLs is required for OL differentiation likely by mediating integrin-β1 survival signaling to the actin cytoskeleton as OL undergo the large morphological changes required for their terminal differentiation.</p>', 'date' => '2022-02-01', 'pmid' => 'https://doi.org/10.1101%2F2022.02.25.481980', 'doi' => '10.1101/2022.02.25.481980', 'modified' => '2022-08-11 15:05:41', 'created' => '2022-08-11 12:14:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 32 => array( 'id' => '4238', 'name' => 'The long noncoding RNA H19 regulates tumor plasticity inneuroendocrine prostate cancer', 'authors' => 'Singh N. et al.', 'description' => '<p>Neuroendocrine (NE) prostate cancer (NEPC) is a lethal subtype of castration-resistant prostate cancer (PCa) arising either de novo or from transdifferentiated prostate adenocarcinoma following androgen deprivation therapy (ADT). Extensive computational analysis has identified a high degree of association between the long noncoding RNA (lncRNA) H19 and NEPC, with the longest isoform highly expressed in NEPC. H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown). It contributes to treatment resistance, with the knockdown of H19 re-sensitizing PCa to ADT. It is also essential for the proliferation and invasion of NEPC. H19 levels are negatively regulated by androgen signaling via androgen receptor (AR). When androgen is absent SOX2 levels increase, driving H19 transcription and facilitating transdifferentiation. H19 facilitates the PRC2 complex in regulating methylation changes at H3K27me3/H3K4me3 histone sites of AR-driven and NEPC-related genes. Additionally, this lncRNA induces alterations in genome-wide DNA methylation on CpG sites, further regulating genes associated with the NEPC phenotype. Our clinical data identify H19 as a candidate diagnostic marker and predictive marker of NEPC with elevated H19 levels associated with an increased probability of biochemical recurrence and metastatic disease in patients receiving ADT. Here we report H19 as an early upstream regulator of cell fate, plasticity, and treatment resistance in NEPC that can reverse/transform cells to a treatable form of PCa once therapeutically deactivated.</p>', 'date' => '2021-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34934057', 'doi' => '10.1038/s41467-021-26901-9', 'modified' => '2022-05-19 17:06:50', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 33 => array( 'id' => '4239', 'name' => 'Epromoters function as a hub to recruit key transcription factorsrequired for the inflammatory response', 'authors' => 'Santiago-Algarra D. et al. ', 'description' => '<p>Gene expression is controlled by the involvement of gene-proximal (promoters) and distal (enhancers) regulatory elements. Our previous results demonstrated that a subset of gene promoters, termed Epromoters, work as bona fide enhancers and regulate distal gene expression. Here, we hypothesized that Epromoters play a key role in the coordination of rapid gene induction during the inflammatory response. Using a high-throughput reporter assay we explored the function of Epromoters in response to type I interferon. We find that clusters of IFNa-induced genes are frequently associated with Epromoters and that these regulatory elements preferentially recruit the STAT1/2 and IRF transcription factors and distally regulate the activation of interferon-response genes. Consistently, we identified and validated the involvement of Epromoter-containing clusters in the regulation of LPS-stimulated macrophages. Our findings suggest that Epromoters function as a local hub recruiting the key TFs required for coordinated regulation of gene clusters during the inflammatory response.</p>', 'date' => '2021-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34795220', 'doi' => '10.1038/s41467-021-26861-0', 'modified' => '2022-05-19 17:10:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 34 => array( 'id' => '4231', 'name' => 'Differential contribution to gene expression prediction of histonemodifications at enhancers or promoters.', 'authors' => 'González-Ramírez M. et al.', 'description' => '<p>The ChIP-seq signal of histone modifications at promoters is a good predictor of gene expression in different cellular contexts, but whether this is also true at enhancers is not clear. To address this issue, we develop quantitative models to characterize the relationship of gene expression with histone modifications at enhancers or promoters. We use embryonic stem cells (ESCs), which contain a full spectrum of active and repressed (poised) enhancers, to train predictive models. As many poised enhancers in ESCs switch towards an active state during differentiation, predictive models can also be trained on poised enhancers throughout differentiation and in development. Remarkably, we determine that histone modifications at enhancers, as well as promoters, are predictive of gene expression in ESCs and throughout differentiation and development. Importantly, we demonstrate that their contribution to the predictive models varies depending on their location in enhancers or promoters. Moreover, we use a local regression (LOESS) to normalize sequencing data from different sources, which allows us to apply predictive models trained in a specific cellular context to a different one. We conclude that the relationship between gene expression and histone modifications at enhancers is universal and different from promoters. Our study provides new insight into how histone modifications relate to gene expression based on their location in enhancers or promoters.</p>', 'date' => '2021-09-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473698/', 'doi' => '10.1371/journal.pcbi.1009368', 'modified' => '2022-05-19 16:50:59', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 35 => array( 'id' => '4315', 'name' => 'Atg7 deficiency in microglia drives an altered transcriptomic profileassociated with an impaired neuroinflammatory response', 'authors' => 'Friess L. et al.', 'description' => '<p>Microglia, resident immunocompetent cells of the central nervous system, can display a range of reaction states and thereby exhibit distinct biological functions across development, adulthood and under disease conditions. Distinct gene expression profiles are reported to define each of these microglial reaction states. Hence, the identification of modulators of selective microglial transcriptomic signature, which have the potential to regulate unique microglial function has gained interest. Here, we report the identification of ATG7 (Autophagy-related 7) as a selective modulator of an NF-κB-dependent transcriptional program controlling the pro-inflammatory response of microglia. We also uncover that microglial Atg7-deficiency was associated with reduced microglia-mediated neurotoxicity, and thus a loss of biological function associated with the pro-inflammatory microglial reactive state. Further, we show that Atg7-deficiency in microglia did not impact on their ability to respond to alternative stimulus, such as one driving them towards an anti-inflammatory/tumor supportive phenotype. The identification of distinct regulators, such as Atg7, controlling specific microglial transcriptional programs could lead to developing novel therapeutic strategies aiming to manipulate selected microglial phenotypes, instead of the whole microglial population with is associated with several pitfalls. Supplementary Information The online version contains supplementary material available at 10.1186/s13041-021-00794-7.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34082793', 'doi' => '10.1186/s13041-021-00794-7', 'modified' => '2022-08-02 16:47:13', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 36 => array( 'id' => '4349', 'name' => 'Lasp1 regulates adherens junction dynamics and fibroblast transformationin destructive arthritis', 'authors' => 'Beckmann D. et al.', 'description' => '<p>The LIM and SH3 domain protein 1 (Lasp1) was originally cloned from metastatic breast cancer and characterised as an adaptor molecule associated with tumourigenesis and cancer cell invasion. However, the regulation of Lasp1 and its function in the aggressive transformation of cells is unclear. Here we use integrative epigenomic profiling of invasive fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA) and from mouse models of the disease, to identify Lasp1 as an epigenomically co-modified region in chronic inflammatory arthritis and a functionally important binding partner of the Cadherin-11/β-Catenin complex in zipper-like cell-to-cell contacts. In vitro, loss or blocking of Lasp1 alters pathological tissue formation, migratory behaviour and platelet-derived growth factor response of arthritic FLS. In arthritic human TNF transgenic mice, deletion of Lasp1 reduces arthritic joint destruction. Therefore, we show a function of Lasp1 in cellular junction formation and inflammatory tissue remodelling and identify Lasp1 as a potential target for treating inflammatory joint disorders associated with aggressive cellular transformation.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34131132', 'doi' => '10.1038/s41467-021-23706-8', 'modified' => '2022-08-03 17:02:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 37 => array( 'id' => '4136', 'name' => 'The lncRNA and the transcription factor WRKY42 target common cell wallEXTENSIN encoding genes to trigger root hair cell elongation.', 'authors' => 'Pacheco, J. M. et al.', 'description' => '<p>Plant long noncoding RNAs (lncRNAs) are key chromatin dynamics regulators, directing the transcriptional programs driving a wide variety of developmental outputs. Recently, we uncovered how the lncRNA () directly recognizes the locus encoding the root hair (RH) master regulator () modulating its transcriptional activation and leading to low temperature-induced RH elongation. We further demonstrated that interacts with the transcription factor WRKY42 in a novel ribonucleoprotein complex shaping epigenetic environment and integrating signals governing RH growth and development. In this work, we expand this model showing that is able to bind and positively control the expression of several cell wall EXTENSIN (EXT) encoding genes, including , a key regulator for RH growth. Interestingly, emerged as a novel common target of and WRKY42. Furthermore, we showed that the ROS homeostasis-related gene is deregulated upon overexpression, likely through the RHD6-RSL4 pathway, and that is required for low temperature-dependent enhancement of RH growth. Collectively, our results uncover an intricate regulatory network involving the /WRKY42 hub in the control of master and effector genes during RH development.</p>', 'date' => '2021-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33944666', 'doi' => '10.1080/15592324.2021.1920191', 'modified' => '2021-12-13 09:06:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 38 => array( 'id' => '4143', 'name' => 'Placental uptake and metabolism of 25(OH)Vitamin D determines itsactivity within the fetoplacental unit', 'authors' => 'Ashley, B. et al.', 'description' => '<p>Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes, but the underlying mechanisms have not been elucidated. Using physiological human placental perfusion approaches and intact villous explants we demonstrate a role for the placenta in regulating the relationships between maternal 25(OH)D concentrations and fetal physiology. Here, we demonstrate active placental uptake of 25(OH)D3 by endocytosis and placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the fetal and maternal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than solely the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer, including transcriptional activation and inflammatory responses. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta; with widespread effects on the placenta itself. These data show complex and synergistic interplay between vitamin D and the placenta, and inform possible interventions to optimise placental function to better support fetal growth and the maternal adaptations to pregnancy.</p>', 'date' => '2021-05-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.01.431439', 'doi' => '10.1101/2021.03.01.431439', 'modified' => '2021-12-13 09:29:25', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 39 => array( 'id' => '4147', 'name' => 'Waves of sumoylation support transcription dynamics during adipocytedifferentiation', 'authors' => 'Zhao, X. et al.', 'description' => '<p>Tight control of gene expression networks required for adipose tissue formation and plasticity is essential for adaptation to energy needs and environmental cues. However, little is known about the mechanisms that orchestrate the dramatic transcriptional changes leading to adipocyte differentiation. We investigated the regulation of nascent transcription by the sumoylation pathway during adipocyte differentiation using SLAMseq and ChIPseq. We discovered that the sumoylation pathway has a dual function in differentiation; it supports the initial downregulation of pre-adipocyte-specific genes, while it promotes the establishment of the mature adipocyte transcriptional program. By characterizing sumoylome dynamics in differentiating adipocytes by mass spectrometry, we found that sumoylation of specific transcription factors like Pparγ/RXR and their co-factors is associated with the transcription of adipogenic genes. Our data demonstrate that the sumoylation pathway coordinates the rewiring of transcriptional networks required for formation of functional adipocytes. This study also provides an in-depth resource of gene transcription dynamics, SUMO-regulated genes and sumoylation sites during adipogenesis.</p>', 'date' => '2021-04-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.20.432084', 'doi' => '10.1101/2021.02.20.432084', 'modified' => '2021-12-14 09:23:28', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 40 => array( 'id' => '4171', 'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.', 'authors' => 'Ryan, Genevieve E. et al.', 'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse LβT2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733', 'doi' => '10.1016/j.mce.2021.111286', 'modified' => '2021-12-21 15:57:35', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 41 => array( 'id' => '4181', 'name' => 'Genetic perturbation of PU.1 binding and chromatin looping at neutrophilenhancers associates with autoimmune disease.', 'authors' => 'Watt, Stephen et al.', 'description' => '<p>Neutrophils play fundamental roles in innate immune response, shape adaptive immunity, and are a potentially causal cell type underpinning genetic associations with immune system traits and diseases. Here, we profile the binding of myeloid master regulator PU.1 in primary neutrophils across nearly a hundred volunteers. We show that variants associated with differential PU.1 binding underlie genetically-driven differences in cell count and susceptibility to autoimmune and inflammatory diseases. We integrate these results with other multi-individual genomic readouts, revealing coordinated effects of PU.1 binding variants on the local chromatin state, enhancer-promoter contacts and downstream gene expression, and providing a functional interpretation for 27 genes underlying immune traits. Collectively, these results demonstrate the functional role of PU.1 and its target enhancers in neutrophil transcriptional control and immune disease susceptibility.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863903', 'doi' => '10.1038/s41467-021-22548-8', 'modified' => '2021-12-21 16:50:30', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 42 => array( 'id' => '4126', 'name' => 'Fra-1 regulates its target genes via binding to remote enhancers withoutexerting major control on chromatin architecture in triple negative breastcancers.', 'authors' => 'Bejjani, Fabienne and Tolza, Claire and Boulanger, Mathias and Downes,Damien and Romero, Raphaël and Maqbool, Muhammad Ahmad and Zine ElAabidine, Amal and Andrau, Jean-Christophe and Lebre, Sophie and Brehelin,Laurent and Parrinello, Hughes and Rohmer,', 'description' => '<p>The ubiquitous family of dimeric transcription factors AP-1 is made up of Fos and Jun family proteins. It has long been thought to operate principally at gene promoters and how it controls transcription is still ill-understood. The Fos family protein Fra-1 is overexpressed in triple negative breast cancers (TNBCs) where it contributes to tumor aggressiveness. To address its transcriptional actions in TNBCs, we combined transcriptomics, ChIP-seqs, machine learning and NG Capture-C. Additionally, we studied its Fos family kin Fra-2 also expressed in TNBCs, albeit much less. Consistently with their pleiotropic effects, Fra-1 and Fra-2 up- and downregulate individually, together or redundantly many genes associated with a wide range of biological processes. Target gene regulation is principally due to binding of Fra-1 and Fra-2 at regulatory elements located distantly from cognate promoters where Fra-1 modulates the recruitment of the transcriptional co-regulator p300/CBP and where differences in AP-1 variant motif recognition can underlie preferential Fra-1- or Fra-2 bindings. Our work also shows no major role for Fra-1 in chromatin architecture control at target gene loci, but suggests collaboration between Fra-1-bound and -unbound enhancers within chromatin hubs sometimes including promoters for other Fra-1-regulated genes. Our work impacts our view of AP-1.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33533919', 'doi' => '10.1093/nar/gkab053', 'modified' => '2021-12-07 10:09:23', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 43 => array( 'id' => '4139', 'name' => 'Cell-specific alterations inPitx1regulatory landscape activation caused bythe loss of a single enhancer', 'authors' => 'Rouco, R. et al.', 'description' => '<p>Most developmental genes rely on multiple transcriptional enhancers for their accurate expression during embryogenesis. Because enhancers may have partially redundant activities, the loss of one of them often leads to a partial loss of gene expression and concurrent moderate phenotypic outcome, if any. While such a phenomenon has been observed in many instances, the nature of the underlying mechanisms remains elusive. We used the Pitx1 testbed locus to characterize in detail the regulatory and cellular identity alterations following the deletion in vivo of one of its enhancers (Pen), which normally accounts for 30 percent of Pitx1 expression in hindlimb buds. By combining single cell transcriptomics and a novel in embryo cell tracing approach, we observed that this global decrease in Pitx1 expression results from both an increase in the number of non- or low-expressing cells, and a decrease in the number of high-expressing cells. We found that the over-representation of Pitx1 non/low-expressing cells originates from a failure of the Pitx1 locus to coordinate enhancer activities and 3D chromatin changes. The resulting increase in Pitx1 non/low-expressing cells eventually affects the proximal limb more severely than the distal limb, leading to a clubfoot phenotype likely produced through a localized heterochrony and concurrent loss of irregular connective tissue. This data suggests that, in some cases, redundant enhancers may be used to locally enforce a robust activation of their host regulatory landscapes.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.10.434611', 'doi' => '10.1101/2021.03.10.434611', 'modified' => '2021-12-13 09:18:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 44 => array( 'id' => '4141', 'name' => 'Transgenic mice for in vivo epigenome editing with CRISPR-based systems', 'authors' => 'Gemberling, M. et al.', 'description' => '<p>The discovery, characterization, and adaptation of the RNA-guided clustered regularly interspersed short palindromic repeat (CRISPR)-Cas9 system has greatly increased the ease with which genome and epigenome editing can be performed. Fusion of chromatin-modifying domains to the nuclease-deactivated form of Cas9 (dCas9) has enabled targeted gene activation or repression in both cultured cells and in vivo in animal models. However, delivery of the large dCas9 fusion proteins to target cell types and tissues is an obstacle to widespread adoption of these tools for in vivo studies. Here we describe the generation and validation of two conditional transgenic mouse lines for targeted gene regulation, Rosa26:LSL-dCas9-p300 for gene activation and Rosa26:LSL-dCas9-KRAB for gene repression. Using the dCas9p300 and dCas9KRAB transgenic mice we demonstrate activation or repression of genes in both the brain and liver in vivo, and T cells and fibroblasts ex vivo. We show gene regulation and targeted epigenetic modification with gRNAs targeting either transcriptional start sites (TSS) or distal enhancer elements, as well as corresponding changes to downstream phenotypes. These mouse lines are convenient and valuable tools for facile, temporally controlled, and tissue-restricted epigenome editing and manipulation of gene expression in vivo.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.08.434430', 'doi' => '10.1101/2021.03.08.434430', 'modified' => '2021-12-13 09:23:10', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 45 => array( 'id' => '4163', 'name' => 'Transcriptional programming drives Ibrutinib-resistance evolution in mantlecell lymphoma.', 'authors' => 'Zhao, Xiaohong et al.', 'description' => '<p>Ibrutinib, a bruton's tyrosine kinase (BTK) inhibitor, provokes robust clinical responses in aggressive mantle cell lymphoma (MCL), yet many patients relapse with lethal Ibrutinib-resistant (IR) disease. Here, using genomic, chemical proteomic, and drug screen profiling, we report that enhancer remodeling-mediated transcriptional activation and adaptive signaling changes drive the aggressive phenotypes of IR. Accordingly, IR MCL cells are vulnerable to inhibitors of the transcriptional machinery and especially so to inhibitors of cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the positive transcription elongation factor b (P-TEFb) of RNA polymerase II (RNAPII). Further, CDK9 inhibition disables reprogrammed signaling circuits and prevents the emergence of IR in MCL. Finally, and importantly, we find that a robust and facile ex vivo image-based functional drug screening platform can predict clinical therapeutic responses of IR MCL and identify vulnerabilities that can be targeted to disable the evolution of IR.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33730585', 'doi' => '10.1016/j.celrep.2021.108870', 'modified' => '2021-12-21 15:28:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 46 => array( 'id' => '4119', 'name' => 'Coordinated changes in gene expression, H1 variant distribution and genome3D conformation in response to H1 depletion', 'authors' => 'Serna-Pujol, Nuria and Salinas-Pena, Monica and Mugianesi, Francesca and LeDily, François and Marti-Renom, Marc A. and Jordan, Albert', 'description' => '<p>Up to seven members of the histone H1 family may contribute to chromatin compaction and its regulation in human somatic cells. In breast cancer cells, knock-down of multiple H1 variants deregulates many genes, promotes the appearance of genome-wide accessibility sites and triggers an interferon response via activation of heterochromatic repeats. However, how these changes in the expression profile relate to the re-distribution of H1 variants as well as to genome conformational changes have not been yet studied. Here, we combined ChIP-seq of five endogenous H1 variants with Chromosome Conformation Capture analysis in wild-type and H1 knock-down T47D cells. The results indicate that H1 variants coexist in the genome in two large groups depending on the local DNA GC content and that their distribution is robust with respect to multiple H1 depletion. Despite the small changes in H1 variants distribution, knock-down of H1 translated into more isolated but de-compacted chromatin structures at the scale of Topologically Associating Domains or TADs. Such changes in TAD structure correlated with a coordinated gene expression response of their resident genes. This is the first report describing simultaneous profiling of five endogenous H1 variants within a cell line and giving functional evidence of genome topology alterations upon H1 depletion in human cancer cells.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.12.429879', 'doi' => '10.1101/2021.02.12.429879', 'modified' => '2021-12-07 09:43:11', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 47 => array( 'id' => '4144', 'name' => 'REPROGRAMMING CBX8-PRC1 FUNCTION WITH A POSITIVE ALLOSTERICMODULATOR', 'authors' => 'Suh, J. L. et al.', 'description' => '<p>Canonical targeting of Polycomb Repressive Complex 1 (PRC1) to repress developmental genes is mediated by cell type-specific, paralogous chromobox (CBX) proteins (CBX2, 4, 6, 7 and 8). Based on their central role in silencing and their misregulation associated with human disease including cancer, CBX proteins are attractive targets for small molecule chemical probe development. Here, we have used a quantitative and target-specific cellular assay to discover a potent positive allosteric modulator (PAM) of CBX8. The PAM activity of UNC7040 antagonizes H3K27me3 binding by CBX8 while increasing interactions with nucleic acids and participation in variant PRC1. We show that treatment with UNC7040 leads to efficient PRC1 chromatin eviction, loss of silencing and reduced proliferation across different cancer cell lines. Our discovery and characterization of UNC7040 not only revealed the most cellularly potent CBX8-specific chemical probe to date, but also corroborates a mechanism of polycomb regulation by non-histone lysine methylated interaction partners.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.23.432388', 'doi' => '10.1101/2021.02.23.432388', 'modified' => '2021-12-13 09:35:04', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 48 => array( 'id' => '4145', 'name' => 'Germline activity of the heat shock factor HSF-1 programs theinsulin-receptor daf-2 in C. elegans', 'authors' => 'Das, S. et al.', 'description' => '<p>The mechanisms by which maternal stress alters offspring phenotypes remain poorly understood. Here we report that the heat shock transcription factor HSF-1, activated in the C. elegans maternal germline upon stress, epigenetically programs the insulin-like receptor daf-2 by increasing repressive H3K9me2 levels throughout the daf-2 gene. This increase occurs by the recruitment of the C. elegans SETDB1 homolog MET-2 by HSF-1. Increased H3K9me2 levels at daf-2 persist in offspring to downregulate daf-2, activate the C. elegans FOXO ortholog DAF-16 and enhance offspring stress resilience. Thus, HSF-1 activity in the mother promotes the early life programming of the insulin/IGF-1 signaling (IIS) pathway and determines the strategy of stress resilience in progeny.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.22.432344', 'doi' => '10.1101/2021.02.22.432344', 'modified' => '2021-12-14 09:13:54', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 49 => array( 'id' => '4151', 'name' => 'The epigenetic landscape in purified myonuclei from fast and slow muscles', 'authors' => 'Bengtsen, M. et al.', 'description' => '<p>Muscle cells have different phenotypes adapted to different usage and can be grossly divided into fast/glycolytic and slow/oxidative types. While most muscles contain a mixture of such fiber types, we aimed at providing a genome-wide analysis of chromatin environment by ChIP-Seq in two muscle extremes, the almost completely fast/glycolytic extensor digitorum longus (EDL) and slow/oxidative soleus muscles. Muscle is a heterogeneous tissue where less than 60\% of the nuclei are inside muscle fibers. Since cellular homogeneity is critical in epigenome-wide association studies we devised a new method for purifying skeletal muscle nuclei from whole tissue based on the nuclear envelope protein Pericentriolar material 1 (PCM1) being a specific marker for myonuclei. Using antibody labeling and a magnetic-assisted sorting approach we were able to sort out myonuclei with 95\% purity. The sorting eliminated influence from other cell types in the tissue and improved the myo-specific signal. A genome-wide comparison of the epigenetic landscape in EDL and soleus reflected the functional properties of the two muscles each with a distinct regulatory program involving distal enhancers, including a glycolytic super-enhancer in the EDL. The two muscles are also regulated by different sets of transcription factors; e.g. in soleus binding sites for MEF2C, NFATC2 and PPARA were enriched, while in EDL MYOD1 and SOX1 binding sites were found to be overrepresented. In addition, novel factors for muscle regulation such as MAF, ZFX and ZBTB14 were identified.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.04.429545', 'doi' => '10.1101/2021.02.04.429545', 'modified' => '2021-12-14 09:40:02', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 50 => array( 'id' => '4166', 'name' => 'The glucocorticoid receptor recruits the COMPASS complex to regulateinflammatory transcription at macrophage enhancers.', 'authors' => 'Greulich, Franziska et al.', 'description' => '<p>Glucocorticoids (GCs) are effective anti-inflammatory drugs; yet, their mechanisms of action are poorly understood. GCs bind to the glucocorticoid receptor (GR), a ligand-gated transcription factor controlling gene expression in numerous cell types. Here, we characterize GR's protein interactome and find the SETD1A (SET domain containing 1A)/COMPASS (complex of proteins associated with Set1) histone H3 lysine 4 (H3K4) methyltransferase complex highly enriched in activated mouse macrophages. We show that SETD1A/COMPASS is recruited by GR to specific cis-regulatory elements, coinciding with H3K4 methylation dynamics at subsets of sites, upon treatment with lipopolysaccharide (LPS) and GCs. By chromatin immunoprecipitation sequencing (ChIP-seq) and RNA-seq, we identify subsets of GR target loci that display SETD1A occupancy, H3K4 mono-, di-, or tri-methylation patterns, and transcriptional changes. However, our data on methylation status and COMPASS recruitment suggest that SETD1A has additional transcriptional functions. Setd1a loss-of-function studies reveal that SETD1A/COMPASS is required for GR-controlled transcription of subsets of macrophage target genes. We demonstrate that the SETD1A/COMPASS complex cooperates with GR to mediate anti-inflammatory effects.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33567280', 'doi' => '10.1016/j.celrep.2021.108742', 'modified' => '2021-12-21 15:42:49', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 51 => array( 'id' => '4185', 'name' => 'A distinct metabolic response characterizes sensitivity to EZH2inhibition in multiple myeloma.', 'authors' => 'Nylund P. et al.', 'description' => '<p>Multiple myeloma (MM) is a heterogeneous haematological disease that remains clinically challenging. Increased activity of the epigenetic silencer EZH2 is a common feature in patients with poor prognosis. Previous findings have demonstrated that metabolic profiles can be sensitive markers for response to treatment in cancer. While EZH2 inhibition (EZH2i) has proven efficient in inducing cell death in a number of human MM cell lines, we hereby identified a subset of cell lines that despite a global loss of H3K27me3, remains viable after EZH2i. By coupling liquid chromatography-mass spectrometry with gene and miRNA expression profiling, we found that sensitivity to EZH2i correlated with distinct metabolic signatures resulting from a dysregulation of genes involved in methionine cycling. Specifically, EZH2i resulted in a miRNA-mediated downregulation of methionine cycling-associated genes in responsive cells. This induced metabolite accumulation and DNA damage, leading to G2 arrest and apoptosis. Altogether, we unveiled that sensitivity to EZH2i in human MM cell lines is associated with a specific metabolic and gene expression profile post-treatment.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33579905', 'doi' => '10.1038/s41419-021-03447-8', 'modified' => '2022-01-05 14:59:39', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 52 => array( 'id' => '4108', 'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma', 'authors' => 'Laubscher et. al.', 'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that </span><em>SMARCA4</em><span><span> </span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span> </span></span><em>de novo</em><span><span> </span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>', 'date' => '2021-01-07', 'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1', 'doi' => ' 10.21203/rs.3.rs-131009/v1', 'modified' => '2021-07-07 11:52:23', 'created' => '2021-07-07 06:38:34', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 53 => array( 'id' => '4098', 'name' => 'A Tumor Suppressor Enhancer of PTEN in T-cell development and leukemia', 'authors' => 'L. Tottone at al.', 'description' => '<p>Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss of expression of PTEN is associated with the pathogenesis of various cancers, including T-cell leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts with the <em>PTEN</em> promoter in multiple hematopoietic populations, including T-cells, and acts as a hub of relevant transcription factors in T-ALL. Consistently, loss of PE leads to reduced <em>PTEN</em> levels in T-ALL cells. Moreover, PE-null mice show reduced <em>Pten</em> levels in thymocytes and accelerated development of NOTCH1-induced T-ALL. Furthermore, secondary loss of PE in established leukemias leads to accelerated progression and a gene expression signature driven by <em>Pten</em> loss. Finally, we uncovered recurrent deletions encompassing PE in T-ALL, which are associated with decreased <em>PTEN</em> levels. Altogether, our results identify PE as the first long-range tumor suppressor enhancer directly implicated in cancer.</p>', 'date' => '2021-01-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33458694/', 'doi' => '10.1158/2643-3230.BCD-20-0201 ', 'modified' => '2021-05-04 09:51:10', 'created' => '2021-05-04 09:51:10', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 54 => array( 'id' => '4157', 'name' => 'Stronger induction of trained immunity by mucosal BCG or MTBVAC vaccination compared to standard intradermal vaccination.', 'authors' => 'Vierboom, M.P.M. et al. ', 'description' => '<p>BCG vaccination can strengthen protection against pathogens through the induction of epigenetic and metabolic reprogramming of innate immune cells, a process called trained immunity. We and others recently demonstrated that mucosal or intravenous BCG better protects rhesus macaques from infection and TB disease than standard intradermal vaccination, correlating with local adaptive immune signatures. In line with prior mouse data, here, we show in rhesus macaques that intravenous BCG enhances innate cytokine production associated with changes in H3K27 acetylation typical of trained immunity. Alternative delivery of BCG does not alter the cytokine production of unfractionated bronchial lavage cells. However, mucosal but not intradermal vaccination, either with BCG or the -derived candidate MTBVAC, enhances innate cytokine production by blood- and bone marrow-derived monocytes associated with metabolic rewiring, typical of trained immunity. These results provide support to strategies for improving TB vaccination and, more broadly, modulating innate immunity via mucosal surfaces.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33521699', 'doi' => '10.1016/j.xcrm.2020.100185', 'modified' => '2021-12-16 10:50:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 55 => array( 'id' => '4193', 'name' => 'Postoperative abdominal sepsis induces selective and persistent changes inCTCF binding within the MHC-II region of human monocytes.', 'authors' => 'Siegler B. et al.', 'description' => '<p>BACKGROUND: Postoperative abdominal infections belong to the most common triggers of sepsis and septic shock in intensive care units worldwide. While monocytes play a central role in mediating the initial host response to infections, sepsis-induced immune dysregulation is characterized by a defective antigen presentation to T-cells via loss of Major Histocompatibility Complex Class II DR (HLA-DR) surface expression. Here, we hypothesized a sepsis-induced differential occupancy of the CCCTC-Binding Factor (CTCF), an architectural protein and superordinate regulator of transcription, inside the Major Histocompatibility Complex Class II (MHC-II) region in patients with postoperative sepsis, contributing to an altered monocytic transcriptional response during critical illness. RESULTS: Compared to a matched surgical control cohort, postoperative sepsis was associated with selective and enduring increase in CTCF binding within the MHC-II. In detail, increased CTCF binding was detected at four sites adjacent to classical HLA class II genes coding for proteins expressed on monocyte surface. Gene expression analysis revealed a sepsis-associated decreased transcription of (i) the classical HLA genes HLA-DRA, HLA-DRB1, HLA-DPA1 and HLA-DPB1 and (ii) the gene of the MHC-II master regulator, CIITA (Class II Major Histocompatibility Complex Transactivator). Increased CTCF binding persisted in all sepsis patients, while transcriptional recovery CIITA was exclusively found in long-term survivors. CONCLUSION: Our experiments demonstrate differential and persisting alterations of CTCF occupancy within the MHC-II, accompanied by selective changes in the expression of spatially related HLA class II genes, indicating an important role of CTCF in modulating the transcriptional response of immunocompromised human monocytes during critical illness.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33939725', 'doi' => '10.1371/journal.pone.0250818', 'modified' => '2022-01-06 14:22:15', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 56 => array( 'id' => '4204', 'name' => 'S-adenosyl-l-homocysteine hydrolase links methionine metabolism to thecircadian clock and chromatin remodeling.', 'authors' => 'Greco C. M. et al. ', 'description' => '<p>Circadian gene expression driven by transcription activators CLOCK and BMAL1 is intimately associated with dynamic chromatin remodeling. However, how cellular metabolism directs circadian chromatin remodeling is virtually unexplored. We report that the S-adenosylhomocysteine (SAH) hydrolyzing enzyme adenosylhomocysteinase (AHCY) cyclically associates to CLOCK-BMAL1 at chromatin sites and promotes circadian transcriptional activity. SAH is a potent feedback inhibitor of S-adenosylmethionine (SAM)-dependent methyltransferases, and timely hydrolysis of SAH by AHCY is critical to sustain methylation reactions. We show that AHCY is essential for cyclic H3K4 trimethylation, genome-wide recruitment of BMAL1 to chromatin, and subsequent circadian transcription. Depletion or targeted pharmacological inhibition of AHCY in mammalian cells markedly decreases the amplitude of circadian gene expression. In mice, pharmacological inhibition of AHCY in the hypothalamus alters circadian locomotor activity and rhythmic transcription within the suprachiasmatic nucleus. These results reveal a previously unappreciated connection between cellular metabolism, chromatin dynamics, and circadian regulation.</p>', 'date' => '2020-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33328229', 'doi' => '10.1126/sciadv.abc5629', 'modified' => '2022-01-06 14:59:48', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 57 => array( 'id' => '4040', 'name' => 'Genomic profiling of T-cell activation suggests increased sensitivity ofmemory T cells to CD28 costimulation.', 'authors' => 'Glinos, Dafni A and Soskic, Blagoje and Williams, Cayman and Kennedy, Alanand Jostins, Luke and Sansom, David M and Trynka, Gosia', 'description' => '<p>T-cell activation is a critical driver of immune responses. The CD28 costimulation is an essential regulator of CD4 T-cell responses, however, its relative importance in naive and memory T cells is not fully understood. Using different model systems, we observe that human memory T cells are more sensitive to CD28 costimulation than naive T cells. To deconvolute how the T-cell receptor (TCR) and CD28 orchestrate activation of human T cells, we stimulate cells using varying intensities of TCR and CD28 and profiled gene expression. We show that genes involved in cell cycle progression and division are CD28-driven in memory cells, but under TCR control in naive cells. We further demonstrate that T-helper differentiation and cytokine expression are controlled by CD28. Using chromatin accessibility profiling, we observe that AP1 transcriptional regulation is enriched when both TCR and CD28 are engaged, whereas open chromatin near CD28-sensitive genes is enriched for NF-kB motifs. Lastly, we show that CD28-sensitive genes are enriched in GWAS regions associated with immune diseases, implicating a role for CD28 in disease development. Our study provides important insights into the differential role of costimulation in naive and memory T-cell responses and disease susceptibility.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33223527', 'doi' => '10.1038/s41435-020-00118-0', 'modified' => '2021-02-19 12:08:04', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 58 => array( 'id' => '4060', 'name' => 'A genetic variant controls interferon-β gene expression in human myeloidcells by preventing C/EBP-β binding on a conserved enhancer.', 'authors' => 'Assouvie, Anaïs and Rotival, Maxime and Hamroune, Juliette and Busso,Didier and Romeo, Paul-Henri and Quintana-Murci, Lluis and Rousselet,Germain', 'description' => '<p>Interferon β (IFN-β) is a cytokine that induces a global antiviral proteome, and regulates the adaptive immune response to infections and tumors. Its effects strongly depend on its level and timing of expression. Therefore, the transcription of its coding gene IFNB1 is strictly controlled. We have previously shown that in mice, the TRIM33 protein restrains Ifnb1 transcription in activated myeloid cells through an upstream inhibitory sequence called ICE. Here, we show that the deregulation of Ifnb1 expression observed in murine Trim33-/- macrophages correlates with abnormal looping of both ICE and the Ifnb1 gene to a 100 kb downstream region overlapping the Ptplad2/Hacd4 gene. This region is a predicted myeloid super-enhancer in which we could characterize 3 myeloid-specific active enhancers, one of which (E5) increases the response of the Ifnb1 promoter to activation. In humans, the orthologous region contains several single nucleotide polymorphisms (SNPs) known to be associated with decreased expression of IFNB1 in activated monocytes, and loops to the IFNB1 gene. The strongest association is found for the rs12553564 SNP, located in the E5 orthologous region. The minor allele of rs12553564 disrupts a conserved C/EBP-β binding motif, prevents binding of C/EBP-β, and abolishes the activation-induced enhancer activity of E5. Altogether, these results establish a link between a genetic variant preventing binding of a transcription factor and a higher order phenotype, and suggest that the frequent minor allele (around 30\% worldwide) might be associated with phenotypes regulated by IFN-β expression in myeloid cells.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147208', 'doi' => '10.1371/journal.pgen.1009090', 'modified' => '2021-02-19 17:29:34', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 59 => array( 'id' => '4084', 'name' => 'BCG Vaccination Induces Long-Term Functional Reprogramming of HumanNeutrophils.', 'authors' => 'Moorlag, Simone J C F M and Rodriguez-Rosales, Yessica Alina and Gillard,Joshua and Fanucchi, Stephanie and Theunissen, Kate and Novakovic, Borisand de Bont, Cynthia M and Negishi, Yutaka and Fok, Ezio T and Kalafati,Lydia and Verginis, Panayotis and M', 'description' => '<p>The tuberculosis vaccine bacillus Calmette-Guérin (BCG) protects against some heterologous infections, probably via induction of non-specific innate immune memory in monocytes and natural killer (NK) cells, a process known as trained immunity. Recent studies have revealed that the induction of trained immunity is associated with a bias toward granulopoiesis in bone marrow hematopoietic progenitor cells, but it is unknown whether BCG vaccination also leads to functional reprogramming of mature neutrophils. Here, we show that BCG vaccination of healthy humans induces long-lasting changes in neutrophil phenotype, characterized by increased expression of activation markers and antimicrobial function. The enhanced function of human neutrophils persists for at least 3 months after vaccination and is associated with genome-wide epigenetic modifications in trimethylation at histone 3 lysine 4. Functional reprogramming of neutrophils by the induction of trained immunity might offer novel therapeutic strategies in clinical conditions that could benefit from modulation of neutrophil effector function.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33207187', 'doi' => '10.1016/j.celrep.2020.108387', 'modified' => '2021-03-15 17:07:29', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 60 => array( 'id' => '4086', 'name' => 'Macrophage Immune Memory Controls Endometriosis in Mice and Humans.', 'authors' => 'Jeljeli, Mohamed and Riccio, Luiza G C and Chouzenoux, Sandrine and Moresi,Fabiana and Toullec, Laurie and Doridot, Ludivine and Nicco, Carole andBourdon, Mathilde and Marcellin, Louis and Santulli, Pietro and Abrão,Mauricio S and Chapron, Charles and ', 'description' => '<p>Endometriosis is a frequent, chronic, inflammatory gynecological disease characterized by the presence of ectopic endometrial tissue causing pain and infertility. Macrophages have a central role in lesion establishment and maintenance by driving chronic inflammation and tissue remodeling. Macrophages can be reprogrammed to acquire memory-like characteristics after antigenic challenge to reinforce or inhibit a subsequent immune response, a phenomenon termed "trained immunity." Here, whereas bacille Calmette-Guérin (BCG) training enhances the lesion growth in a mice model of endometriosis, tolerization with repeated low doses of lipopolysaccharide (LPS) or adoptive transfer of LPS-tolerized macrophages elicits a suppressor effect. LPS-tolerized human macrophages mitigate the fibro-inflammatory phenotype of endometriotic cells in an interleukin-10 (IL-10)-dependent manner. A history of severe Gram-negative infection is associated with reduced infertility duration and alleviated symptoms, in contrast to patients with Gram-positive infection history. Thus, the manipulation of innate immune memory may be effective in dampening hyper-inflammatory conditions, opening the way to promising therapeutic approaches.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147452', 'doi' => '10.1016/j.celrep.2020.108325', 'modified' => '2021-03-15 17:14:08', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 61 => array( 'id' => '4050', 'name' => 'UTX/KDM6A suppresses AP-1 and a gliogenesis program during neuraldifferentiation of human pluripotent stem cells.', 'authors' => 'Xu, Beisi and Mulvey, Brett and Salie, Muneeb and Yang, Xiaoyang andMatsui, Yurika and Nityanandam, Anjana and Fan, Yiping and Peng, Jamy C', 'description' => '<p>BACKGROUND: UTX/KDM6A is known to interact and influence multiple different chromatin modifiers to promote an open chromatin environment to facilitate gene activation, but its molecular activities in developmental gene regulation remain unclear. RESULTS: We report that in human neural stem cells, UTX binding correlates with both promotion and suppression of gene expression. These activities enable UTX to modulate neural stem cell self-renewal, promote neurogenesis, and suppress gliogenesis. In neural stem cells, UTX has a less influence over histone H3 lysine 27 and lysine 4 methylation but more predominantly affects histone H3 lysine 27 acetylation and chromatin accessibility. Furthermore, UTX suppresses components of AP-1 and, in turn, a gliogenesis program. CONCLUSIONS: Our findings revealed that UTX coordinates dualistic gene regulation to govern neural stem cell properties and neurogenesis-gliogenesis switch.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32977832', 'doi' => '10.1186/s13072-020-00359-3', 'modified' => '2021-02-19 14:46:42', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 62 => array( 'id' => '4091', 'name' => 'Epigenetic regulation of the lineage specificity of primary human dermallymphatic and blood vascular endothelial cells.', 'authors' => 'Tacconi, Carlotta and He, Yuliang and Ducoli, Luca and Detmar, Michael', 'description' => '<p>Lymphatic and blood vascular endothelial cells (ECs) share several molecular and developmental features. However, these two cell types possess distinct phenotypic signatures, reflecting their different biological functions. Despite significant advances in elucidating how the specification of lymphatic and blood vascular ECs is regulated at the transcriptional level during development, the key molecular mechanisms governing their lineage identity under physiological or pathological conditions remain poorly understood. To explore the epigenomic signatures in the maintenance of EC lineage specificity, we compared the transcriptomic landscapes, histone composition (H3K4me3 and H3K27me3) and DNA methylomes of cultured matched human primary dermal lymphatic and blood vascular ECs. Our findings reveal that blood vascular lineage genes manifest a more 'repressed' histone composition in lymphatic ECs, whereas DNA methylation at promoters is less linked to the differential transcriptomes of lymphatic versus blood vascular ECs. Meta-analyses identified two transcriptional regulators, BCL6 and MEF2C, which potentially govern endothelial lineage specificity. Notably, the blood vascular endothelial lineage markers CD34, ESAM and FLT1 and the lymphatic endothelial lineage markers PROX1, PDPN and FLT4 exhibited highly differential epigenetic profiles and responded in distinct manners to epigenetic drug treatments. The perturbation of histone and DNA methylation selectively promoted the expression of blood vascular endothelial markers in lymphatic endothelial cells, but not vice versa. Overall, our study reveals that the fine regulation of lymphatic and blood vascular endothelial transcriptomes is maintained via several epigenetic mechanisms, which are crucial to the maintenance of endothelial cell identity.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32918672', 'doi' => '10.1007/s10456-020-09743-9', 'modified' => '2021-03-17 17:09:36', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 63 => array( 'id' => '4010', 'name' => 'Combined treatment with CBP and BET inhibitors reverses inadvertentactivation of detrimental super enhancer programs in DIPG cells.', 'authors' => 'Wiese, M and Hamdan, FH and Kubiak, K and Diederichs, C and Gielen, GHand Nussbaumer, G and Carcaboso, AM and Hulleman, E and Johnsen, SA andKramm, CM', 'description' => '<p>Diffuse intrinsic pontine gliomas (DIPG) are the most aggressive brain tumors in children with 5-year survival rates of only 2%. About 85% of all DIPG are characterized by a lysine-to-methionine substitution in histone 3, which leads to global H3K27 hypomethylation accompanied by H3K27 hyperacetylation. Hyperacetylation in DIPG favors the action of the Bromodomain and Extra-Terminal (BET) protein BRD4, and leads to the reprogramming of the enhancer landscape contributing to the activation of DIPG super enhancer-driven oncogenes. The activity of the acetyltransferase CREB-binding protein (CBP) is enhanced by BRD4 and associated with acetylation of nucleosomes at super enhancers (SE). In addition, CBP contributes to transcriptional activation through its function as a scaffold and protein bridge. Monotherapy with either a CBP (ICG-001) or BET inhibitor (JQ1) led to the reduction of tumor-related characteristics. Interestingly, combined treatment induced strong cytotoxic effects in H3.3K27M-mutated DIPG cell lines. RNA sequencing and chromatin immunoprecipitation revealed that these effects were caused by the inactivation of DIPG SE-controlled tumor-related genes. However, single treatment with ICG-001 or JQ1, respectively, led to activation of a subgroup of detrimental super enhancers. Combinatorial treatment reversed the inadvertent activation of these super enhancers and rescued the effect of ICG-001 and JQ1 single treatment on enhancer-driven oncogenes in H3K27M-mutated DIPG, but not in H3 wild-type pedHGG cells. In conclusion, combinatorial treatment with CBP and BET inhibitors is highly efficient in H3K27M-mutant DIPG due to reversal of inadvertent activation of detrimental SE programs in comparison with monotherapy.</p>', 'date' => '2020-08-21', 'pmid' => 'http://www.pubmed.gov/32826850', 'doi' => '10.1038/s41419-020-02800-7', 'modified' => '2020-12-18 13:25:09', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 64 => array( 'id' => '4028', 'name' => 'Methylation in pericytes after acute injury promotes chronic kidneydisease.', 'authors' => 'Chou, YH and Pan, SY and Shao, YH and Shih, HM and Wei, SY andLai, CF and Chiang, WC and Schrimpf, C and Yang, KC and Lai, LC andChen, YM and Chu, TS and Lin, SL', 'description' => '<p>The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury-induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-β1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD.</p>', 'date' => '2020-08-04', 'pmid' => 'http://www.pubmed.gov/32749240', 'doi' => '10.1172/JCI135773.', 'modified' => '2020-12-18 13:25:55', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 65 => array( 'id' => '4011', 'name' => 'Exploring the virulence gene interactome with CRISPR/dCas9 in the humanmalaria parasite.', 'authors' => 'Bryant, JM and Baumgarten, S and Dingli, F and Loew, D and Sinha, A andClaës, A and Preiser, PR and Dedon, PC and Scherf, A', 'description' => '<p>Mutually exclusive expression of the var multigene family is key to immune evasion and pathogenesis in Plasmodium falciparum, but few factors have been shown to play a direct role. We adapted a CRISPR-based proteomics approach to identify novel factors associated with var genes in their natural chromatin context. Catalytically inactive Cas9 ("dCas9") was targeted to var gene regulatory elements, immunoprecipitated, and analyzed with mass spectrometry. Known and novel factors were enriched including structural proteins, DNA helicases, and chromatin remodelers. Functional characterization of PfISWI, an evolutionarily divergent putative chromatin remodeler enriched at the var gene promoter, revealed a role in transcriptional activation. Proteomics of PfISWI identified several proteins enriched at the var gene promoter such as acetyl-CoA synthetase, a putative MORC protein, and an ApiAP2 transcription factor. These findings validate the CRISPR/dCas9 proteomics method and define a new var gene-associated chromatin complex. This study establishes a tool for targeted chromatin purification of unaltered genomic loci and identifies novel chromatin-associated factors potentially involved in transcriptional control and/or chromatin organization of virulence genes in the human malaria parasite.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32816370', 'doi' => 'https://dx.doi.org/10.15252%2Fmsb.20209569', 'modified' => '2020-12-18 13:26:33', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 66 => array( 'id' => '4019', 'name' => 'Targeted bisulfite sequencing for biomarker discovery.', 'authors' => 'Morselli, M and Farrell, C and Rubbi, L and Fehling, HL and Henkhaus, Rand Pellegrini, M', 'description' => '<p>Cytosine methylation is one of the best studied epigenetic modifications. In mammals, DNA methylation patterns vary among cells and is mainly found in the CpG context. DNA methylation is involved in important processes during development and differentiation and its dysregulation can lead to or is associated with diseases, such as cancer, loss-of-imprinting syndromes and neurological disorders. It has been also shown that DNA methylation at the cellular, tissue and organism level varies with age. To overcome the costs of Whole-Genome Bisulfite Sequencing, the gold standard method to detect 5-methylcytosines at a single base resolution, DNA methylation arrays have been developed and extensively used. This method allows one to assess the status of a fraction of the CpG sites present in the genome of an organism. In order to combine the relatively low cost of Methylation Arrays and digital signals of bisulfite sequencing, we developed a Targeted Bisulfite Sequencing method that can be applied to biomarker discovery for virtually any phenotype. Here we describe a comprehensive step-by-step protocol to build a DNA methylation-based epigenetic clock.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32755621', 'doi' => '10.1016/j.ymeth.2020.07.006', 'modified' => '2020-12-18 13:27:14', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 67 => array( 'id' => '4031', 'name' => 'Battle of the sex chromosomes: competition between X- and Y-chromosomeencoded proteins for partner interaction and chromatin occupancy drivesmulti-copy gene expression and evolution in muroid rodents.', 'authors' => 'Moretti, C and Blanco, M and Ialy-Radio, C and Serrentino, ME and Gobé,C and Friedman, R and Battail, C and Leduc, M and Ward, MA and Vaiman, Dand Tores, F and Cocquet, J', 'description' => '<p>Transmission distorters (TDs) are genetic elements that favor their own transmission to the detriments of others. Slx/Slxl1 (Sycp3-like-X-linked and Slx-like1) and Sly (Sycp3-like-Y-linked) are TDs which have been co-amplified on the X and Y chromosomes of Mus species. They are involved in an intragenomic conflict in which each favors its own transmission, resulting in sex ratio distortion of the progeny when Slx/Slxl1 vs. Sly copy number is unbalanced. They are specifically expressed in male postmeiotic gametes (spermatids) and have opposite effects on gene expression: Sly knockdown leads to the upregulation of hundreds of spermatid-expressed genes, while Slx/Slxl1-deficiency downregulates them. When both Slx/Slxl1 and Sly are knocked-down, sex ratio distortion and gene deregulation are corrected. Slx/Slxl1 and Sly are, therefore, in competition but the molecular mechanism remains unknown. By comparing their chromatin binding profiles and protein partners, we show that SLX/SLXL1 and SLY proteins compete for interaction with H3K4me3-reader SSTY1 (Spermiogenesis-specific-transcript-on-the-Y1) at the promoter of thousands of genes to drive their expression, and that the opposite effect they have on gene expression is mediated by different abilities to recruit SMRT/N-Cor transcriptional complex. Their target genes are predominantly spermatid-specific multicopy genes encoded by the sex chromosomes and the autosomal Speer/Takusan. Many of them have co-amplified with Slx/Slxl1/Sly but also Ssty during muroid rodent evolution. Overall, we identify Ssty as a key element of the X vs. Y intragenomic conflict, which may have influenced gene content and hybrid sterility beyond Mus lineage since Ssty amplification on the Y pre-dated that of Slx/Slxl1/Sly.</p>', 'date' => '2020-07-13', 'pmid' => 'http://www.pubmed.gov/32658962', 'doi' => '10.1093/molbev/msaa175/5870835', 'modified' => '2020-12-18 13:27:51', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 68 => array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ) ), 'Testimonial' => array(), 'Area' => array() ) $country = 'US' $countries_allowed = array( (int) 0 => 'CA', (int) 1 => 'US', (int) 2 => 'IE', (int) 3 => 'GB', (int) 4 => 'DK', (int) 5 => 'NO', (int) 6 => 'SE', (int) 7 => 'FI', (int) 8 => 'NL', (int) 9 => 'BE', (int) 10 => 'LU', (int) 11 => 'FR', (int) 12 => 'DE', (int) 13 => 'CH', (int) 14 => 'AT', (int) 15 => 'ES', (int) 16 => 'IT', (int) 17 => 'PT' ) $outsource = false $other_formats = array() $edit = '' $testimonials = '' $featured_testimonials = '' $related_products = '<li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201140</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-3047" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <form action="/en/carts/add/3047" id="CartAdd/3047Form" method="post" accept-charset="utf-8"><div style="display:none;"><input type="hidden" name="_method" value="POST"/></div><input type="hidden" name="data[Cart][product_id]" value="3047" id="CartProductId"/> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p>Add <input name="data[Cart][quantity]" placeholder="1" value="1" min="1" style="width:60px;display:inline" type="number" id="CartQuantity" required="required"/> <strong> Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico</strong> to my shopping cart.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="checkout" id="checkout" value="checkout" type="submit">Checkout</button> </div> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="keepshop" id="keepshop" type="submit">Keep shopping</button> </div> </div> </div> </div> </form><a class="close-reveal-modal" aria-label="Close">×</a></div><!-- END: ADD TO CART MODAL --><a href="#" id="1-5-ml-tube-holder-dock-for-bioruptor-pico" data-reveal-id="cartModal-3047" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 1.5 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201143</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: QUOTE MODAL --><div id="quoteModal-3048" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h3>Get a quote</h3><p class="lead">You are about to request a quote for <strong>Tube holder for 0.65 ml tubes - Bioruptor<sup>®</sup> Pico</strong>. 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data-reveal-id="cartModal-3049" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 0.2 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack"><img src="/img/product/shearing_technologies/B01200016_tube_holder.jpg" alt="some alt" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01200016</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-1796" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <form action="/en/carts/add/1796" id="CartAdd/1796Form" method="post" accept-charset="utf-8"><div style="display:none;"><input type="hidden" name="_method" value="POST"/></div><input type="hidden" name="data[Cart][product_id]" value="1796" id="CartProductId"/> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p>Add <input name="data[Cart][quantity]" placeholder="1" value="1" min="1" style="width:60px;display:inline" type="number" id="CartQuantity" required="required"/> <strong> 15 ml sonication accessories for Bioruptor<sup>®</sup> Standard & Plus & Pico</strong> to my shopping cart.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('15 ml sonication accessories for Bioruptor<sup>®</sup> Standard & Plus & Pico', 'B01200016', '350', $('#CartQuantity').val());" name="checkout" id="checkout" value="checkout" type="submit">Checkout</button> </div> 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=> '1 pack', 'catalog_number' => 'B01200016', 'old_catalog_number' => 'O-ring-15', 'sf_code' => 'B01200016-', 'type' => 'ACC', 'search_order' => '01-Accessory', 'price_EUR' => '300', 'price_USD' => '350', 'price_GBP' => '250', 'price_JPY' => '46995', 'price_CNY' => '', 'price_AUD' => '875', 'country' => 'ALL', 'except_countries' => 'None', 'quote' => false, 'in_stock' => false, 'featured' => false, 'no_promo' => false, 'online' => true, 'master' => true, 'last_datasheet_update' => '0000-00-00', 'slug' => '15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack', 'meta_title' => '15 ml sonication accessories for Bioruptor® Standard & Plus & Pico', 'meta_keywords' => '', 'meta_description' => '15 ml sonication accessories for Bioruptor® Standard & Plus & Pico', 'modified' => '2022-01-25 04:00:28', 'created' => '2015-06-29 14:08:20', 'ProductsRelated' => array( 'id' => '4591', 'product_id' => '3046', 'related_id' => '1796' ), 'Image' => array( (int) 0 => array( 'id' => '116', 'name' => 'product/shearing_technologies/B01200016_tube_holder.jpg', 'alt' => 'some alt', 'modified' => '2015-06-10 17:28:55', 'created' => '2015-06-10 17:28:55', 'ProductsImage' => array( [maximum depth reached] ) ) ) ) $list = '<div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-1.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-2.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-3.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-4.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-5.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B010600010.jpg" /></div>' $img = array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => '2018-02-14 15:41:46', 'ProductsImage' => array( 'id' => '1093', 'product_id' => '3046', 'image_id' => '1772' ) ) $rrbs_service = array( (int) 0 => (int) 1894, (int) 1 => (int) 1895 ) $chipseq_service = array( (int) 0 => (int) 2683, (int) 1 => (int) 1835, (int) 2 => (int) 1836, (int) 3 => (int) 2684, (int) 4 => (int) 1838, (int) 5 => (int) 1839, (int) 6 => (int) 1856 ) $labelize = object(Closure) { } $old_catalog_number = '' $label = '<img src="/img/banners/banner-customizer-back.png" alt=""/>' $protocol = array( 'id' => '73', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:16:00', 'created' => '0000-00-00 00:00:00', 'ProductsProtocol' => array( 'id' => '241', 'product_id' => '3046', 'protocol_id' => '73' ) ) $document = array( 'id' => '1170', 'name' => 'Critical steps for Bioruptor® maintenance and efficient shearing', 'description' => '', 'image_id' => null, 'type' => 'Document', 'url' => 'files/products/shearing_technology/critical-steps-bioruptor-web.pdf', 'slug' => 'critical-steps-bioruptor-maintenance', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2023-08-31 14:27:41', 'created' => '2023-08-31 14:27:41', 'ProductsDocument' => array( 'id' => '3264', 'product_id' => '3046', 'document_id' => '1170' ) ) $publication = array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( 'id' => '6424', 'product_id' => '3046', 'publication_id' => '4549' ) ) $externalLink = ' <a href="https://www.researchsquare.com/article/rs-1832996/v1" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755 View::_evaluate() - CORE/Cake/View/View.php, line 971 View::_render() - CORE/Cake/View/View.php, line 933 View::render() - CORE/Cake/View/View.php, line 473 Controller::render() - CORE/Cake/Controller/Controller.php, line 963 Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 200 Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167 [main] - APP/webroot/index.php, line 118
Notice (8): Undefined variable: campaign_id [APP/View/Products/view.ctp, line 755]Code Context<!-- BEGIN: REQUEST_FORM MODAL --><div id="request_formModal" class="reveal-modal medium" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"><?= $this->element('Forms/simple_form', array('solution_of_interest' => $solution_of_interest, 'header' => $header, 'message' => $message, 'campaign_id' => $campaign_id)) ?>$viewFile = '/home/website-server/www/app/View/Products/view.ctp' $dataForView = array( 'language' => 'en', 'noindex' => 'noindex', 'meta_keywords' => '', 'meta_description' => 'Bioruptor® Pico sonication device', 'meta_title' => 'Bioruptor® Pico sonication device', 'product' => array( 'Product' => array( 'id' => '3046', 'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa 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53 => array( [maximum depth reached] ), (int) 54 => array( [maximum depth reached] ), (int) 55 => array( [maximum depth reached] ), (int) 56 => array( [maximum depth reached] ), (int) 57 => array( [maximum depth reached] ), (int) 58 => array( [maximum depth reached] ), (int) 59 => array( [maximum depth reached] ), (int) 60 => array( [maximum depth reached] ), (int) 61 => array( [maximum depth reached] ), (int) 62 => array( [maximum depth reached] ), (int) 63 => array( [maximum depth reached] ), (int) 64 => array( [maximum depth reached] ), (int) 65 => array( [maximum depth reached] ), (int) 66 => array( [maximum depth reached] ), (int) 67 => array( [maximum depth reached] ), (int) 68 => array( [maximum depth reached] ) ), 'Testimonial' => array(), 'Area' => array() ) ) $language = 'en' $noindex = 'noindex' $meta_keywords = '' $meta_description = 'Bioruptor® Pico sonication device' $meta_title = 'Bioruptor® Pico sonication device' $product = array( 'Product' => array( 'id' => '3046', 'antibody_id' => null, 'name' => 'Bioruptor<sup>®</sup> Pico sonication device', 'description' => '<p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" /></a></p> <div class="row"> <div class="small-12 medium-8 large-8 columns"><br /> <p><span>The Bioruptor® Pico is the latest innovation in shearing and represents a new breakthrough as an all-in-one shearing system capable of shearing samples from 150 bp to 1 kb. </span>Since 2004, Diagenode has accumulated <strong>shearing expertise</strong> to design the Bioruptor® Pico and guarantee the best experience with the <strong>sample preparation</strong> for <strong>number of applications -- in various fields of studies</strong> including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</p> </div> <div class="small-12 medium-4 large-4 columns"><center> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img src="https://www.diagenode.com/img/epicafe-OFF.png"></a>'); } // ]]></script> </center></div> </div> <p>The Bioruptor Pico shearing accessories and consumables have been developed to allow <strong>flexibility in sample volumes</strong> (20 µl - 2 ml) and a <strong>fast parallel processing of samples</strong> (up to 16 samples simultaneously). <span>The built-in cooling system (Bioruptor® Cooler) ensures high precision <strong>temperature control</strong>. The <strong>user-friendly interface</strong> has been designed for any researcher, providing an easy and advanced modes that give both beginners and experienced users the right level of control. </span></p> <p>In addition, Diagenode provides fully-validated tubes that remain <strong>budget-friendly with low operating cost</strong> (< 1€/$/DNA sample) and shearing kits for best sample quality. <span></span></p> <p><strong>Application versatility</strong>:</p> <ul> <li>DNA shearing for Next-Generation-Sequencing</li> <li>Chromatin shearing</li> <li>RNA shearing</li> <li>Protein extraction from tissues and cells (also for mass spectrometry)</li> <li>FFPE DNA extraction</li> <li>Protein aggregation studies</li> <li>CUT&RUN - shearing of input DNA for NGS</li> </ul> <div style="background-color: #f1f3f4; margin: 10px; padding: 50px;"> <p><strong>Bioruptor Pico: Recommended for CUT&RUN sequencing for input DNA</strong><br /><br /> By combining antibody-targeted controlled cleavage by MNase and NGS, <strong>CUT&RUN sequencing</strong> can be used to identify protein-DNA binding sites genome-wide. CUT&RUN works by using the DNA cleaving activity of a Protein A-fused MNase to isolate DNA that is bound by a protein of interest. This targeted digestion is controlled by the addition of calcium, which MNase requires for its nuclease activity. After MNase digestion, short DNA fragments are released and can then be purified for subsequent library preparation and high-throughput sequencing. While CUT&RUN does not require mechanical shearing chromatin given the enzymatic approach, sonication is highly recommended for the fragmentation of the input DNA (used to compare the enriched sample) in order to be compatible with downstream NGS. The Bioruptor Pico is the ideal instrument of choice for generating optimal DNA fragments with a tight distribution, assuring excellent library prep and excellent sequencing results for your CUT&RUN assay.<br /><br /> <strong>Explore the Bioruptor Pico now.</strong></p> </div> <div class="extra-spaced"><center><img alt="Bioruptor Sonication for Chromatin shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-reproducibility-is-priority.jpg" /></center></div> <div class="extra-spaced"><center><a href="https://www.diagenode.com/en/pages/form-demo"> <img alt="Bioruptor Sonication for RNA shearing" src="https://www.diagenode.com/img/product/shearing_technologies/pico-request-demo.jpg" /></a></center></div> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label1' => 'Specifications', 'info1' => '<center><img alt="Ultrasonic Sonicator" src="https://www.diagenode.com/img/product/shearing_technologies/pico-table.jpg" /></center> <div id="ConnectiveDocSignExtentionInstalled" data-extension-version="1.0.4"></div>', 'label2' => 'View accessories & consumables for Bioruptor<sup>®</sup> Pico', 'info2' => '<h3>Shearing Accessories</h3> <table style="width: 641px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 300px; height: 37px;"><strong>Name</strong></td> <td style="width: 171px; text-align: center; height: 37px;">Catalog number</td> <td style="width: 160px; text-align: center; height: 37px;">Throughput</td> </tr> </thead> <tbody> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-2-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.2 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201144</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">16 samples</span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 0.65 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201143</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">12 samples<br /></span></td> </tr> <tr style="height: 38px;"> <td style="width: 300px; height: 38px;"><a href="https://www.diagenode.com/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico">Tube holder for 1.5 ml tubes</a></td> <td style="width: 171px; text-align: center; height: 38px;"><span style="font-weight: 400;">B01201140</span></td> <td style="width: 160px; text-align: center; height: 38px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> <tr style="height: 37px;"> <td style="width: 300px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack">15 ml sonication accessories</a></td> <td style="width: 171px; text-align: center; height: 37px;"><span style="font-weight: 400;">B01200016</span></td> <td style="width: 160px; text-align: center; height: 37px;"><span style="font-weight: 400;">6 samples<br /></span></td> </tr> </tbody> </table> <h3>Shearing Consumables</h3> <table style="width: 646px;"> <thead> <tr style="background-color: #dddddd; height: 37px;"> <td style="width: 286px; height: 37px;"><strong>Name</strong></td> <td style="width: 76px; height: 37px; text-align: center;">Catalog Number</td> </tr> </thead> <tbody> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/02ml-microtubes-for-bioruptor-pico">0.2 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010020</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/0-65-ml-bioruptor-microtubes-500-tubes">0.65 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010011</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/1-5-ml-bioruptor-microtubes-with-caps-300-tubes">1.5 ml Pico Microtubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010016</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-50-pc">15 ml Pico Tubes</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C30010017</span></td> </tr> <tr style="height: 37px;"> <td style="width: 286px; height: 37px;"><a href="https://www.diagenode.com/en/p/15-ml-bioruptor-tubes-sonication-beads-50-rxns">15 ml Pico Tubes & sonication beads</a></td> <td style="width: 76px; height: 37px; text-align: center;"><span style="font-weight: 400;">C01020031</span></td> </tr> </tbody> </table> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf">Find datasheet for Diagenode tubes here</a></p> <p><a href="../documents/bioruptor-organigram-tubes">Which tubes for which Bioruptor®?</a></p>', 'label3' => 'Available shearing Kits', 'info3' => '<p>Diagenode has optimized a range of solutions for <strong>successful chromatin preparation</strong>. Chromatin EasyShear Kits together with the Pico ultrasonicator combine the benefits of efficient cell lysis and chromatin shearing, while keeping epitopes accessible to the antibody, critical for efficient chromatin immunoprecipitation. Each Chromatin EasyShear Kit provides optimized reagents and a thoroughly validated protocol according to your specific experimental needs. SDS concentration is adapted to each workflow taking into account target-specific requirements.</p> <p>For best results, choose your desired ChIP kit followed by the corresponding Chromatin EasyShear Kit (to optimize chromatin shearing ). The Chromatin EasyShear Kits can be used independently of Diagenode’s ChIP kits for chromatin preparation prior to any chromatin immunoprecipitation protocol. Choose an appropriate kit for your specific experimental needs.</p> <h2>Kit choice guide</h2> <table style="border: 0;" valign="center"> <tbody> <tr style="background: #fff;"> <th class="text-center"></th> <th class="text-center" style="font-size: 17px;">SAMPLE TYPE</th> <th class="text-center" style="font-size: 17px;">SAMPLE INPUT</th> <th class="text-center" style="font-size: 17px;">KIT</th> <th class="text-center" style="font-size: 17px;">SDS<br /> CONCENTRATION</th> <th class="text-center" style="font-size: 17px;">NUCLEI<br /> ISOLATION</th> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="5"><img src="https://www.diagenode.com/img/label-histones.png" /></td> <td class="text-center" style="border-bottom: 1px solid #dedede;"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">< 100,000</td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin EasyShear Kit<br />High SDS</a></td> <td class="text-center" style="font-size: 17px; border-bottom: 1px solid #dedede;">1%</td> <td class="text-center" style="border-bottom: 1px solid #dedede;"><img src="https://www.diagenode.com/img/cross-unvalid-green.jpg" width="18" height="20" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center" style="font-size: 17px;">> 100,000</td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-ultra-low-sds">Chromatin EasyShear Kit<br />Ultra Low SDS</a></td> <td class="text-center" style="font-size: 17px;">< 0.1%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff; border-bottom: 1px solid #dedede;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">PLANT TISSUE</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-shearing-plant-chip-seq-kit">Chromatin EasyShear Kit<br />for Plant</a></td> <td class="text-center" style="font-size: 17px;">0.5%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> <td class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td class="text-center" style="font-size: 17px;">0.2%</td> <td class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td colspan="7"></td> </tr> <tr style="background: #fff;"> <td rowspan="6"><img src="https://www.diagenode.com/img/label-tf.png" /></td> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">CELLS</div> </td> <td class="text-center"></td> <td rowspan="3" class="text-center" style="font-size: 17px;"><a href="https://www.diagenode.com/en/p/chromatin-easyshear-kit-low-sds">Chromatin EasyShear Kit<br />Low SDS</a></td> <td rowspan="3" class="text-center" style="font-size: 17px;">0.2%</td> <td rowspan="3" class="text-center"><img src="https://www.diagenode.com/img/valid.png" width="20" height="16" /></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">TISSUE</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td class="text-center"> <div class="label alert" style="font-size: 17px;">FFPE SAMPLES</div> </td> <td class="text-center"></td> </tr> <tr style="background: #fff;"> <td colspan="6"></td> </tr> </tbody> </table> <div class="extra-spaced"> <h3>Guide for optimal chromatin preparation using Chromatin EasyShear Kits <i class="fa 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Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>®</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>®</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>®</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div> <div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 µl volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.1 ml Bioruptor® Microtubes (Cat. No. B01200041). <strong>Panel B, 100 µl volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using 0.65 ml Bioruptor® Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 µl volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor® Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016). Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37°C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 µl of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div> <div class="small-12 medium-12 large-12 columns"><br /><br /></div> <div class="small-12 medium-12 large-12 columns"> <p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p> </div> <div class="small-12 medium-12 large-12 columns"> <div class="page" title="Page 7"> <table> <tbody> <tr valign="middle"> <td></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td> <td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>SDS concentration</strong></p> </td> <td style="text-align: center;"> <p>< 0.1%</p> </td> <td style="text-align: center;"> <p>0.2%</p> </td> <td style="text-align: center;"> <p>1%</p> </td> <td style="text-align: center;"> <p>0.5%</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Nuclei isolation</strong></p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> <td style="text-align: center;"> <p>No</p> </td> <td style="text-align: center;"> <p>Yes</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Allows for shearing of... cells/tissue</strong></p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>100 million cells</p> </td> <td style="text-align: center;"> <p>up to 25 g of tissue</p> </td> </tr> <tr valign="middle" style="background-color: #fff;"> <td> <p><strong>Corresponding to shearing buffers from</strong></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p> <p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p> </td> <td style="text-align: center;"> <p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p> </td> </tr> </tbody> </table> <p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor® Pico</span></a></em></p> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'chromatin-shearing', 'meta_keywords' => 'Chromatin shearing,Chromatin Immunoprecipitation,Bioruptor,Sonication,Sonicator', 'meta_description' => 'Diagenode's Bioruptor® is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.', 'meta_title' => 'Chromatin shearing using Bioruptor® sonication device | Diagenode', 'modified' => '2017-11-15 10:14:02', 'created' => '2015-03-05 15:56:30', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3', 'position' => '10', 'parent_id' => null, 'name' => '次世代シーケンシング', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2 style="font-size: 22px;">DNA断片化、ライブラリー調製、自動化：NGSのワンストップショップ</h2> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-12 medium-12 large-12 columns"> <h4>1. 断片化装置を選択してください：150 bp〜75 kbの範囲でDNAを断片化します。</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-pico-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/bioruptor_pico.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/megaruptor2-1-unit"><img src="https://www.diagenode.com/img/product/shearing_technologies/B06010001_megaruptor2.jpg" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/bioruptor-one-sonication-device"><img src="https://www.diagenode.com/img/product/shearing_technologies/br-one-profil.png" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns">5μlまで断片化：150 bp〜2 kb<br />NGS DNAライブラリー調製およびFFPE核酸抽出に最適で、</td> <td class="small-4 medium-4 large-4 columns">2 kb〜75 kbの範囲をできます。<br />メイトペアライブラリー調製および長いフラグメントDNAシーケンシングに最適で、この軽量デスクトップデバイスで</td> <td class="small-4 medium-4 large-4 columns">20または50μlの断片化が可能です。</td> </tr> </tbody> </table> <table class="small-12 medium-12 large-12 columns"> <tbody> <tr> <th class="small-8 medium-8 large-8 columns"> <h4>2. 最適化されたライブラリー調整キットを選択してください。</h4> </th> <th class="small-4 medium-4 large-4 columns"> <h4>3. ライブラリー前処理自動化を選択して、比類のないデータ再現性を実感</h4> </th> </tr> <tr style="background-color: #ffffff;"> <td class="small-12 medium-12 large-12 columns"></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns"><a href="../p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><img src="https://www.diagenode.com/img/product/kits/microPlex_library_preparation.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns"><img src="https://www.diagenode.com/img/product/kits/box_kit.jpg" style="display: block; margin-left: auto; margin-right: auto;" height="173" width="250" /></a></td> <td class="small-4 medium-4 large-4 columns"><a href="../p/sx-8g-ip-star-compact-automated-system-1-unit"><img src="https://www.diagenode.com/img/product/automation/B03000002%20_ipstar_compact.png" style="display: block; margin-left: auto; margin-right: auto;" /></a></td> </tr> <tr> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">50pgの低入力：MicroPlex Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">5ng以上：iDeal Library Preparation Kit</td> <td class="small-4 medium-4 large-4 columns" style="text-align: center;">Achieve great NGS data easily</td> </tr> </tbody> </table> </div> </div> <blockquote> <div class="row"> <div class="small-12 medium-12 large-12 columns"><span class="label" style="margin-bottom: 16px; margin-left: -22px; font-size: 15px;">DiagenodeがNGS研究にぴったりなプロバイダーである理由</span> <p>Diagenodeは15年以上もエピジェネティクス研究に専念、専門としています。 ChIP研究クロマチン用のユニークな断片化システムの開発から始まり、 専門知識を活かし、5μlのせん断体積まで可能で、NGS DNAライブラリーの調製に最適な最先端DNA断片化装置の開発にたどり着きました。 我々は以来、ChIP-seq、Methyl-seq、NGSライブラリー調製用キットを研究開発し、業界をリードする免疫沈降研究と同様に、ライブラリー調製を自動化および完結させる独自の自動化システムを開発にも成功しました。</p> <ul> <li>信頼されるせん断装置</li> <li>様々なインプットからのライブラリ作成キット</li> <li>独自の自動化デバイス</li> </ul> </div> </div> </blockquote> <div class="row"> <div class="small-12 columns"> <ul class="accordion" data-accordion=""> <li class="accordion-navigation"><a href="#panel1a">次世代シーケンシングへの理解とその専門知識</a> <div id="panel1a" class="content"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p><strong>次世代シーケンシング (NGS)</strong> ）は、著しいスケールとハイスループットでシーケンシングを行い、1日に数十億もの塩基生成を可能にします。 NGSのハイスループットは迅速でありながら正確で、再現性のあるデータセットを実現し、さらにシーケンシング費用を削減します。 NGSは、ゲノムシーケンシング、ゲノム再シーケンシング、デノボシーケンシング、トランスクリプトームシーケンシング、その他にDNA-タンパク質相互作用の検出やエピゲノムなどを示します。 指数関数的に増加するシーケンシングデータの需要は、計算分析の障害や解釈、データストレージなどの課題を解決します。</p> <p>アプリケーションおよび出発物質に応じて、数百万から数十億の鋳型DNA分子を大規模に並行してシーケンシングすることが可能です。その為に、異なる化学物質を使用するいくつかの市販のNGSプラットフォームを利用することができます。 NGSプラットフォームの種類によっては、事前準備とライブラリー作成が必要です。</p> <p>NGSにとっても、特にデータ処理と分析に関した大きな課題はあります。第3世代技術はゲノミクス研究にさらに革命を起こすであろうと大きく期待されています。</p> </div> </div> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <p><strong>NGS アプリケーション</strong></p> <ul> <li>全ゲノム配列決定</li> <li>デノボシーケンシング</li> <li>標的配列</li> <li>Exomeシーケンシング</li> <li>トランスクリプトーム配列決定</li> <li>ゲノム配列決定</li> <li>ミトコンドリア配列決定</li> <li>DNA-タンパク質相互作用（ChIP-seq</li> <li>バリアント検出</li> <li>ゲノム仕上げ</li> </ul> </div> <div class="small-6 medium-6 large-6 columns"> <p><strong>研究分野におけるNGS:</strong></p> <ul> <li>腫瘍学</li> <li>リプロダクティブ・ヘルス</li> <li>法医学ゲノミクス</li> <li>アグリゲノミックス</li> <li>複雑な病気</li> <li>微生物ゲノミクス</li> <li>食品・環境ゲノミクス</li> <li>創薬ゲノミクス - パーソナライズド・メディカル</li> </ul> </div> <div class="small-12 medium-12 large-12 columns"> <p><strong>NGSの用語</strong></p> <dl> <dt>リード（読み取り）</dt> <dd>この装置から得られた連続した単一のストレッチ</dd> <dt>断片リード</dt> <dd>フラグメントライブラリからの読み込み。 シーケンシングプラットフォームに応じて、読み取りは通常約100〜300bp。</dd> <dt>断片ペアエンドリード</dt> <dd>断片ライブラリーからDNA断片の各末端2つの読み取り。</dd> <dt>メイトペアリード</dt> <dd>大きなDNA断片（通常は予め定義されたサイズ範囲）の各末端から2つの読み取り。</dd> <dt>カバレッジ（例）</dt> <dd>30×適用範囲とは、参照ゲノム中の各塩基対が平均30回の読み取りを示す。</dd> </dl> </div> </div> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h2>NGSプラットフォーム</h2> <h3><a href="http://www.illumina.com" target="_blank">イルミナ</a></h3> <p>イルミナは、クローン的に増幅された鋳型DNA（クラスター）上に位置する、蛍光標識された可逆的鎖ターミネーターヌクレオチドを用いた配列別合成技術を使用。 DNAクラスターは、ガラスフローセルの表面上に固定化され、 ワークフローは、4つのヌクレオチド（それぞれ異なる蛍光色素で標識された）の組み込み、4色イメージング、色素や末端基の切断、取り込み、イメージングなどを繰り返します。フローセルは大規模な並列配列決定を受ける。 この方法により、単一蛍光標識されたヌクレオチドの制御添加によるモノヌクレオチドのエラーを回避する可能性があります。 読み取りの長さは、通常約100〜150 bpです。</p> <h3><a href="http://www.lifetechnologies.com" target="_blank">イオン トレント</a></h3> <p>イオントレントは、半導体技術チップを用いて、合成中にヌクレオチドを取り込む際に放出されたプロトンを検出します。 これは、イオン球粒子と呼ばれるビーズの表面にエマルションPCR（emPCR）を使用し、リンクされた特定のアダプターを用いてDNA断片を増幅します。 各ビーズは1種類のDNA断片で覆われていて、異なるDNA断片を有するビーズは次いで、チップの陽子感知ウェル内に配置されます。 チップには一度に4つのヌクレオチドのうちの1つが浸水し、このプロセスは異なるヌクレオチドで15秒ごとに繰り返されます。 配列決定の間に4つの塩基の各々が1つずつ導入されます、組み込みの場合はプロトンが放出され、電圧信号が取り込みに比例して検出されます。.</p> <h3><a href="http://www.pacificbiosciences.com" target="_blank">パシフィック バイオサイエンス</a></h3> <p>パシフィックバイオサイエンスでは、20kbを超える塩基対の読み取りも、単一分子リアルタイム（SMRT）シーケンシングによる構造および細胞タイプの変化を観察することができます。 このプラットフォームでは、超長鎖二本鎖DNA（dsDNA）断片が、Megaruptor（登録商標）のようなDiagenode装置を用いたランダムシアリングまたは目的の標的領域の増幅によって生成されます。 SMRTbellライブラリーは、ユニバーサルヘアピンアダプターをDNA断片の各末端に連結することによって生成します。 サイズ選択条件による洗浄ステップの後、配列決定プライマーをSMRTbellテンプレートにアニーリングし、鋳型DNAに結合したDNAポリメラーゼを含む配列決定を、蛍光標識ヌクレオチドの存在下で開始。 各塩基が取り込まれると、異なる蛍光のパルスをリアルタイムで検出します。</p> <h3><a href="https://nanoporetech.com" target="_blank">オックスフォード ナノポア</a></h3> <p>Oxford Nanoporeは、単一のDNA分子配列決定に基づく技術を開発します。その技術により生物学的分子、すなわちDNAが一群の電気抵抗性高分子膜として位置するナノスケールの孔（ナノ細孔）またはその近くを通過し、イオン電流が変化します。 この変化に関する情報は、例えば4つのヌクレオチド（AまたはG r CまたはT）ならびに修飾されたヌクレオチドすべてを区別することによって分子情報に訳されます。 シーケンシングミニオンデバイスのフローセルは、数百個のナノポアチャネルのセンサアレイを含みます。 DNAサンプルは、Diagenode社のMegaruptor（登録商標）を用いてランダムシアリングによって生成され得る超長鎖DNAフラグメントが必要です。</p> <h3><a href="http://www.lifetechnologies.com/be/en/home/life-science/sequencing/next-generation-sequencing/solid-next-generation-sequencing.html" target="_blank">SOLiD</a></h3> <p>SOLiDは、ユニークな化学作用により、何千という個々のDNA分子の同時配列決定を可能にします。 それは、アダプター対ライブラリーのフラグメントが適切で、せん断されたゲノムDNAへのアダプターのライゲーションによるライブラリー作製から始まります。 次のステップでは、エマルジョンPCR（emPCR）を実施して、ビーズの表面上の個々の鋳型DNA分子をクローン的に増幅。 emPCRでは、個々の鋳型DNAをPCR試薬と混合し、水中油型エマルジョン内の疎水性シェルで囲まれた水性液滴内のプライマーコートビーズを、配列決定のためにロードするスライドガラスの表面にランダムに付着。 この技術は、シークエンシングプライマーへのライゲーションで競合する4つの蛍光標識されたジ塩基プローブのセットを使用します。</p> <h3><a href="http://454.com/products/technology.asp" target="_blank">454</a></h3> <p>454は、大規模並列パイロシーケンシングを利用しています。 始めに全ゲノムDNAまたは標的遺伝子断片の300〜800bp断片のライブラリー調製します。 次に、DNAフラグメントへのアダプターの付着および単一のDNA鎖の分離。 その後アダプターに連結されたDNAフラグメントをエマルジョンベースのクローン増幅（emPCR）で処理し、DNAライブラリーフラグメントをミクロンサイズのビーズ上に配置します。 各DNA結合ビーズを光ファイバーチップ上のウェルに入れ、器具に挿入します。 4つのDNAヌクレオチドは、配列決定操作中に固定された順序で連続して加えられ、並行して配列決定されます。</p> </div> </div> </div> </li> </ul> </div> </div>', 'in_footer' => true, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'next-generation-sequencing', 'meta_keywords' => 'Next-generation sequencing,NGS,Whole genome sequencing,NGS platforms,DNA/RNA shearing', 'meta_description' => 'Diagenode offers kits and DNA/RNA shearing technology prior to next-generation sequencing, many Next-generation sequencing platforms require preparation of the DNA.', 'meta_title' => 'Next-generation sequencing (NGS) Applications and Methods | Diagenode', 'modified' => '2018-07-26 05:24:29', 'created' => '2015-04-01 22:47:04', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '13', 'position' => '10', 'parent_id' => '3', 'name' => 'DNA/RNA shearing', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns">In recent years, advances in Next-Generation Sequencing (NGS) have revolutionized genomics and biology. This growth has fueled demands on upstream techniques for optimal sample preparation and genomic library construction. One of the most critical aspects of optimal library preparation is the quality of the DNA to be sequenced. The DNA must first be effectively and consistently sheared into the appropriate fragment size (depending on the sequencing platform) to enable sensitive and reliable NGS results. The <strong>Bioruptor</strong><sup>®</sup> <strong>Pico</strong> and the <strong>Megaruptor</strong><sup>®</sup> provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows. Follow our guidelines and find the good parameters for your expected DNA size: <a href="https://pybrevet.typeform.com/to/o8cQfM">DNA shearing with the Bioruptor<sup>®</sup></a>.</div> </div> <p></p> <div class="row"> <div class="small-7 medium-7 large-7 columns text-center"><img src="https://www.diagenode.com/img/applications/true-flexibility-with-br-ngs.jpg" /></div> <div class="small-5 medium-5 large-5 columns"><small><strong>Programmable DNA size distribution and high reproducibility with Bioruptor<sup>®</sup> Pico using 0.65 (panel A) or 0.1 ml (panel B) microtubes</strong>. <b>Panel A:</b> 200 bp after 13 cycles (13 sec ON/OFF) using 100 µl volume. Average size: 204; CV%:1.89%). <b>Panel B:</b> 200 bp after 20 cycles (30 sec ON/OFF) using 10 µl volume. (Average size: 215 bp; CV%: 6.6%). <b>Panel A & B:</b> peak electropherogram view. <b>Panel C & D:</b> virtual gel view.</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-10 medium-10 large-10 columns text-center end small-offset-1"><img src="https://www.diagenode.com/img/applications/megaruptor-short-frag.jpg" /></div> <div class="small-12 medium-12 large-12 columns"><small><strong> Reproducible and narrow DNA size distribution with Megaruptor® using short fragment size Hydropores Validation using two different DNA sources and two different methods of analysis. A:</strong> Shearing of lambda phage genomic DNA (20 ng/μl; 150 μl/sample) sheared at different speed settings and analyzed on 1% agarose gel. <strong>B:</strong> Bioanalyzer profiles of human genomic DNA (20 ng/μl; 150 μl/sample) sheared at different software settings of 2 and 5 kb. Three independent experiments were run for each setting. (Agilent DNA 12000 kit was used for separation and fragment sizing).</small></div> </div> <p><br /><br /></p> <div class="row"> <div class="small-4 medium-4 large-4 columns text-center"><img src="https://www.diagenode.com/img/applications/megaruptor-long-frag.jpg" /></div> <div class="small-8 medium-8 large-8 columns"><small><strong> Demonstrated shearing to fragment sizes between 15 kb and 75 kb with Megaruptor® using long fragment size Hydropores. </strong>Image shows DNA size distribution of human genomic DNA sheared with long fragment Hydropores. DNA was analyzed by pulsed field gel electrophoresis (PFGE) in 1% agarose gel and a mean size of smears was estimated using Image Lab 4.1 software.<br /> * indicates unsheared DNA </small></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'dna-rna-shearing', 'meta_keywords' => 'DNA/RNA shearing,Bioruptor® Pico,Megaruptor®,Next-Generation Sequencing ', 'meta_description' => 'Bioruptor® Pico and the Megaruptor® provide superior sample yields, fragment size, and consistency, which are essential for Next-Generation Sequencing workflows.', 'meta_title' => 'DNA shearing & RNA shearing for Next-Generation Sequencing (NGS) | Diagenode', 'modified' => '2017-12-08 14:44:11', 'created' => '2014-10-29 12:45:41', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '17', 'position' => '10', 'parent_id' => '4', 'name' => 'Protein extraction', 'description' => '<div class="row"> <div class="large-12 columns">Various biochemical and analytical techniques require the extraction of protein from tissues or mammalian, yeast and bacterial cells. Obtaining high quality and yields of proteins is important for further downstream protein characterization such as in PAGE, western blotting, mass spectrometry or protein purification. The efficient disruption and homogenization of tissues and cultured cells obtained in just one step using <strong>Diagenode's Bioruptor</strong><sup>®</sup> deliver high quality protein.</div> </div> <p></p> <div class="row"> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_standard_plus.png" /> <p><small>Western blot analysis of GAPDH and HSP90 proteins in tissues (various mouse tissues) and cultured cell extracts (HeLA).</small></p> </div> <div class="small-6 medium-6 large-6 columns text-center"><img src="https://www.diagenode.com/img/applications/protein_extraction_pico.png" /> <p><small>Western blot analysis of GAPDH and ß-tubulin proteins in tissues (mouse liver) and cultured cell extracts (HeLA).</small></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'protein-extraction', 'meta_keywords' => 'Protein extraction,Bioruptor,Sonication,Protein Analysis', 'meta_description' => 'Diagenode provides efficient disruption and homogenization of tissues and cultured cells obtained in just one step using Bioruptor® deliver high quality protein.', 'meta_title' => 'Protein extraction using Bioruptor® Sonication device | Diagenode', 'modified' => '2017-10-16 14:39:42', 'created' => '2014-07-02 04:41:03', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '6', 'position' => '10', 'parent_id' => '1', 'name' => 'メチル化DNA結合タンパク質', 'description' => '<div class="row"> <div class="large-12 columns">MBD方法は、メチル化DNAに対するH6-GST-MBD融合タンパク質の非常に高い親和性に基づいています。 このタンパク質は、N末端His6タグを含むグルタチオン-S-トランスフェラーゼ（GST）とのC末端融合物として、ヒトMeCP2のメチル結合ドメイン（MBD）を含有します。 このH6-GST-MBD融合タンパク質を用いて、メチル化CpGを含むDNAを特異的に単離する事が可能です。<br /><br />DiagenodeのMethylCap®キットは、二本鎖DNAの高濃縮と、メチル化CpG密度の関数における微分分画を可能にします。 分画はサンプルの複雑さを軽減し、次世代のシーケンシングを容易にします。 MethylCapアッセイに先立ち、DNAを最初に抽出し、Picoruptorソニケーターを用いて断片化します。<br /> <h3>概要</h3> <p class="text-center"><br /><img src="https://www.diagenode.com/img/applications/methyl_binding_domain_overview.jpg" /></p> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'methylbinding-domain-protein', 'meta_keywords' => 'Epigenetic,Methylbinding Domain Protein,MBD,DNA methylation,DNA replication,MethylCap,MethylCap assay,', 'meta_description' => 'Methylbinding Domain Protein(MBD) approach is based on the very high affinity of a H6-GST-MBD fusion protein for methylated DNA. This protein consists of the methyl binding domain (MBD) of human MeCP2, as a C-terminal fusion with Glutathione-S-transferase', 'meta_title' => 'Epigenetic Methylbinding Domain Protein(MBD) - DNA methylation | Diagenode', 'modified' => '2019-03-22 12:32:12', 'created' => '2015-06-02 17:05:42', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '9', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-seq', 'description' => '<div class="row"> <div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div> <div class="large-12 columns"></div> <h5 class="large-12 columns"><strong></strong></h5> <h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5> <div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div> <div class="large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by sonication to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with <strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: Reverse cross-links, elute, and purify </li> <li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify IP'd material</li> <li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chromatin-immunoprecipitation-sequencing', 'meta_keywords' => 'Chromatin Immunoprecipitation Sequencing,ChIP-Seq,ChIP-seq grade antibodies,DNA purification,qPCR,Shearing of chromatin', 'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing', 'meta_title' => 'Chromatin Immunoprecipitation - ChIP-seq Kits - Dna methylation | Diagenode', 'modified' => '2017-11-14 09:57:16', 'created' => '2015-04-12 18:08:46', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '11', 'position' => '10', 'parent_id' => '3', 'name' => 'FFPE DNA extraction', 'description' => '<div class="row"> <div class="large-12 columns">Diagenode's high yields FFPE DNA extraction using Bioruptor<sup><span>®</span></sup> is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no toxic reagents, digest tissues, and purify DNA with high yields and low sample degradation. The DNA can then be analyzed by traditional methods or can be sheared with the Bioruptor<sup>®</sup> Pico ultrasonicator for downstream NGS library prep using the MicroPlex Library Preparation Kit.</div> <div class="small-12 medium-12 large-12 columns text-center"><img src="https://www.diagenode.com/img/applications/ffpe_workflow.png" /></div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => false, 'slug' => 'ffpe-dna-extraction', 'meta_keywords' => 'FFPE DNA extraction,Next-Gen Sequencing,Bioruptor® ultrasonicator', 'meta_description' => 'Diagenode's high yields FFPE DNA extraction using Bioruptor is a superior method for extracting DNA for Next-Gen Sequencing. Our FFPE DNA Extraction kit contains optimized reagents that are added directly to the FFPE samples to remove paraffin with no tox', 'meta_title' => 'FFPE DNA extraction using Bioruptor® ultrasonicator | Diagenode', 'modified' => '2017-10-16 14:34:57', 'created' => '2014-10-01 01:24:40', 'ProductsApplication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '10', 'position' => '10', 'parent_id' => '2', 'name' => 'ChIP-qPCR', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns text-justify"> <p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p> <p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p> </div> <div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div> <div class="small-12 medium-12 large-12 columns"><br /> <ol> <li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li> <li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li> <li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong> against the histone or transcription factor of interest</li> <li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li> <li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li> </ol> </div> </div> <div class="row" style="margin-top: 32px;"> <div class="small-12 medium-10 large-9 small-centered columns"> <div class="radius panel" style="background-color: #fff;"> <h3 class="text-center" style="color: #b21329;">Need guidance?</h3> <p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div> <div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div> </div> </div> </div> </div>', 'in_footer' => false, 'in_menu' => true, 'online' => true, 'tabular' => true, 'slug' => 'chip-qpcr', 'meta_keywords' => 'Chromatin immunoprecipitation,ChIP Quantitative PCR,polymerase chain reaction (PCR)', 'meta_description' => 'Diagenode's ChIP qPCR kits can be used to quantify enriched DNA after chromatin immunoprecipitation. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of', 'meta_title' => 'ChIP Quantitative PCR (ChIP-qPCR) | Diagenode', 'modified' => '2018-01-09 16:46:56', 'created' => '2014-12-11 00:22:08', 'ProductsApplication' => array( [maximum depth reached] ) ) ), 'Category' => array( (int) 0 => array( 'id' => '6', 'position' => '1', 'parent_id' => '1', 'name' => 'Bioruptor<sup>®</sup>', 'description' => '<div class="row"> <div class="small-12 medium-12 large-12 columns"><br /> <p><span>Diagenode focuses on state-of-the-art preparation of high quality biological and chemical samples by developing the industry’s most advanced water bath sonicators and hydrodynamic devices. Our instruments are ideal for a number of applications in various fields of studies including environmental research, toxicology, genomics and epigenomics, cancer research, stem cells and development, neuroscience, clinical applications, agriculture, and many more.</span></p> <p><a href="https://www.diagenode.com/files/products/shearing_technology/bioruptor/TAB-BR-comparaison.pdf" target="_blank"><img src="https://www.diagenode.com/img/bouton-comparaison.png" /></a></p> </div> <!-- <center> <div class="small-12 medium-4 large-4 columns"> <script>// <![CDATA[ var date = new Date(); var heure = date.getHours(); var jour = date.getDay(); var semaine = Math.floor(date.getDate() / 7) + 1; if (jour === 2 && ( (heure >= 9 && heure < 9.5) || (heure >= 18 && heure < 18.5) )) { document.write('<a href="https://us02web.zoom.us/j/85467619762"><img src="https://www.diagenode.com/img/epicafe-ON.gif"></a>'); } else { document.write('<a href="https://go.diagenode.com/l/928883/2023-04-26/3kq1v"><img 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crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script async="" src="https://edge.fullstory.com/s/fs.js" crossorigin="anonymous"></script> <script>// <![CDATA[ (function (d) { var js, id = "genially-embed-js", ref = d.getElementsByTagName("script")[0]; if (d.getElementById(id)) { return; } js = d.createElement("script"); js.id = id; js.async = true; js.src = "https://view.genial.ly/static/embed/embed.js"; ref.parentNode.insertBefore(js, ref); }(document)); // ]]></script> </div> </div>--> <p><span> <br /></span></p> <div class="spacer"></div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">Reproductibility is our priority</h2> </div> </div> <div><img src="https://www.diagenode.com/img/shearing/reproductibility.png" alt="reproductibility" /> <p class="bottom_note"></p> </div> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;">An affordable instrument for wide range of applications</h2> </div> </div> <p style="text-align: center;">Designed for any researchers, the Bioruptor gives the user the right level of flexibility.</p> <table style="width: 972px;"> <tbody> <tr style="height: 56px;"> <th style="width: 380px; height: 56px;"></th> <th class="text-center" style="width: 126px; height: 56px;">Bioruptor</th> <th class="text-center" style="width: 141px; height: 56px;">Cup Horn Sonicators</th> <th class="text-center" style="width: 156px; height: 56px;">Focused <br />ultra-sonicators</th> <th class="text-center" style="width: 155px; height: 56px;">Multi Sample Sonicator</th> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Instrument pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Consumables pricing</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-usd" aria-hidden="true"></i><i class="fa fa-usd" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Range of applications</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Scalable and sample volume flexibility</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> <tr style="height: 38px;"> <td style="width: 380px; height: 38px;">Throughput</td> <td style="width: 126px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 141px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 156px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> <td style="width: 155px; height: 38px;"><center><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i><i class="fa fa-flask" aria-hidden="true"></i></center></td> </tr> </tbody> </table> <div class="content_block"> <div class="centered row"> <h2 style="text-align: center;"></h2> <h2 style="text-align: center;">Bioruptor ultrasonication for best results in:</h2> <p><b><span>✓ Chromatin shearing</span><span> </span><span style="font-weight: 400;">- Industry leader in accurate and tight fragment ranges</span></b></p> <p><b><span>✓ DNA shearing</span><span> </span><span style="font-weight: 400;">- Excellent results for optimal fragment lengths in NGS library prep</span></b></p> <p><b><span>✓<span> </span></span>Protein aggregation studies </b><span style="font-weight: 400;">- Standardizing seeding with the robust Bioruptor.<br /></span><i><span style="font-weight: 400;">Read the app note by Dr. Kelvin Luk at the University of Pennsylvania </span></i><a href="https://www.diagenode.com/en/documents/standardizing-seeding-experiments-for-the-understanding-of-parkinson-disease" style="color: #13b29c;"><i><span style="font-weight: 400;">“Standardizing seeding experiments using the Bioruptor® for the understanding of the neuronal alpha-synuclein pathology”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>3D genome analysis with Hi-C</b><span style="font-weight: 400;"> - Preparing chromatin libraries with high-quality sonication.<br /></span><i><span style="font-weight: 400;">Read the app note, “</span></i><a href="https://www.diagenode.com/en/documents/applicationnote-arima-low-input" style="color: #13b29c;"><i><span style="font-weight: 400;">Unlock Low-Input 3D Genome Analysis with the Arima-HiC Kit”</span></i></a></p> <p><b><b><span>✓<span> </span></span></b>Mass spectrometry</b> <b>and increasing protein identification</b><span style="font-weight: 400;">- Sample preparation using Preomics iST and Bioruptor sonication.<br /></span><i><span style="font-weight: 400;">Read the app note “</span></i><a href="https://www.diagenode.com/en/documents/wp-ist-adaptators" style="color: #13b29c;"><i><span style="font-weight: 400;">Increase your iST ultrasonication throughput with the new Bioruptor® Pico cartridge holder”</span></i></a></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>Cell lysis, liposome prep, protein extraction, RNA extraction and more</b></span></p> <p><i><span style="font-weight: 400;"><b><span>✓ </span></b></span></i><span style="font-weight: 400;"><b>CUT&RUN –Sonication of input DNA (for enrichment comparison) for NGS</b></span></p> </div> </div> <p><a href="https://www.diagenode.com/en/categories/bioruptor-maintenance"><img src="https://www.diagenode.com/img/banners/maintenance-banner-br.png" /></a></p> <p><a href="https://go.diagenode.com/bioruptor-upgrade"><img src="https://www.diagenode.com/img/banners/banner-br-trade.png" 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When studying samples that are difficult to obtain or grow, low input solutions can help you understand genome structure across a new range of low input samples. In addition, the Diagenode Bioruptor Pico assures that chromatin is sheared to optimal fragment lengths.</span></p>', 'image_id' => '247', 'type' => 'Application Note', 'url' => 'files/application_notes/ApplicationNote-Arima-Low-Input.pdf', 'slug' => 'applicationnote-arima-low-input', 'meta_keywords' => 'application note arima low input', 'meta_description' => 'application note arima low input', 'modified' => '2021-02-09 09:55:59', 'created' => '2021-02-09 09:55:59', 'ProductsDocument' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1074', 'name' => 'Datasheet of Bioruptor tubes', 'description' => '<p>Datasheet of Diagenode tubes for Bioruptor Pico and Bioruptor Plus.</p>', 'image_id' => null, 'type' => 'Datasheet', 'url' => 'files/products/shearing_technology/bioruptor_accessories/TDS-BioruptorTubes.pdf', 'slug' => 'tds-bioruptor-tubes', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2022-02-23 12:21:44', 'created' => '2020-03-23 10:41:46', 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'modified' => '2020-01-10 10:53:08', 'created' => '2020-01-10 10:53:08', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '1805', 'name' => 'product/shearing_technologies/B01080000-3.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:46', 'created' => '2020-01-10 10:53:46', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '1806', 'name' => 'product/shearing_technologies/B01080000-4.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:53:56', 'created' => '2020-01-10 10:53:56', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '1807', 'name' => 'product/shearing_technologies/B01080000-5.jpg', 'alt' => 'Bioruptor Pico', 'modified' => '2020-01-10 10:54:06', 'created' => '2020-01-10 10:54:06', 'ProductsImage' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => '2018-02-14 15:41:46', 'ProductsImage' => array( [maximum depth reached] ) ) ), 'Promotion' => array(), 'Protocol' => array( (int) 0 => array( 'id' => '73', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:16:00', 'created' => '0000-00-00 00:00:00', 'ProductsProtocol' => array( [maximum depth reached] ) ) ), 'Publication' => array( (int) 0 => array( 'id' => '4881', 'name' => 'LEO1 Is Required for Efficient Entry into Quiescence, Control of H3K9 Methylation and Gene Expression in Human Fibroblasts', 'authors' => 'Laurent M. et al.', 'description' => '<p><span>(1) Background: The LEO1 (Left open reading frame 1) protein is a conserved subunit of the PAF1C complex (RNA polymerase II-associated factor 1 complex). PAF1C has well-established mechanistic functions in elongation of transcription and RNA processing. We previously showed, in fission yeast, that LEO1 controls histone H3K9 methylation levels by affecting the turnover of histone H3 in chromatin, and that it is essential for the proper regulation of gene expression during cellular quiescence. Human fibroblasts enter a reversible quiescence state upon serum deprivation in the growth media. Here we investigate the function of LEO1 in human fibroblasts. (2) Methods: We knocked out the </span><span class="html-italic">LEO1</span><span><span> </span>gene using CRISPR/Cas9 methodology in human fibroblasts and verified that the LEO1 protein was undetectable by Western blot. We characterized the phenotype of the<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout cells with FACS analysis and cell growth assays. We used RNA-sequencing using spike-in controls to measure gene expression and spike-in controlled ChIP-sequencing experiments to measure the histone modification H3K9me2 genome-wide. (3) Results: Gene expression levels are altered in quiescent cells, however factors controlling chromatin and gene expression changes in quiescent human cells are largely unknown. The<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>knockout fibroblasts are viable but have reduced metabolic activity compared to wild-type cells.<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells showed a slower entry into quiescence and a different morphology compared to wild-type cells. Gene expression was generally reduced in quiescent wild-type cells. The downregulated genes included genes involved in cell proliferation. A small number of genes were upregulated in quiescent wild-type cells including several genes involved in ERK1/ERK2 and Wnt signaling. In quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells, many genes were mis-regulated compared to wild-type cells. This included genes involved in Calcium ion transport and cell morphogenesis. Finally, spike-in controlled ChIP-sequencing experiments demonstrated that the histone modification H3K9me2 levels are globally increased in quiescent<span> </span></span><span class="html-italic">ΔLEO1</span><span><span> </span>cells. (4) Conclusions: Thus, LEO1 is important for proper entry into cellular quiescence, control of H3K9me2 levels, and gene expression in human fibroblasts.</span></p>', 'date' => '2023-11-17', 'pmid' => 'https://www.mdpi.com/2218-273X/13/11/1662', 'doi' => 'https://doi.org/10.3390/biom13111662', 'modified' => '2023-11-21 12:01:53', 'created' => '2023-11-21 12:01:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '4845', 'name' => 'DeSUMOylation of chromatin-bound proteins limits the rapidtranscriptional reprogramming induced by daunorubicin in acute myeloidleukemias.', 'authors' => 'Boulanger M. et al.', 'description' => '<p>Genotoxicants have been used for decades as front-line therapies against cancer on the basis of their DNA-damaging actions. However, some of their non-DNA-damaging effects are also instrumental for killing dividing cells. We report here that the anthracycline Daunorubicin (DNR), one of the main drugs used to treat Acute Myeloid Leukemia (AML), induces rapid (3 h) and broad transcriptional changes in AML cells. The regulated genes are particularly enriched in genes controlling cell proliferation and death, as well as inflammation and immunity. These transcriptional changes are preceded by DNR-dependent deSUMOylation of chromatin proteins, in particular at active promoters and enhancers. Surprisingly, inhibition of SUMOylation with ML-792 (SUMO E1 inhibitor), dampens DNR-induced transcriptional reprogramming. Quantitative proteomics shows that the proteins deSUMOylated in response to DNR are mostly transcription factors, transcriptional co-regulators and chromatin organizers. Among them, the CCCTC-binding factor CTCF is highly enriched at SUMO-binding sites found in cis-regulatory regions. This is notably the case at the promoter of the DNR-induced NFKB2 gene. DNR leads to a reconfiguration of chromatin loops engaging CTCF- and SUMO-bound NFKB2 promoter with a distal cis-regulatory region and inhibition of SUMOylation with ML-792 prevents these changes.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37462077', 'doi' => '10.1093/nar/gkad581', 'modified' => '2023-08-01 14:16:43', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '4846', 'name' => 'RNA polymerase II CTD is dispensable for transcription and requiredfor termination in human cells.', 'authors' => 'Yahia Y. et al.', 'description' => '<p>The largest subunit of RNA polymerase (Pol) II harbors an evolutionarily conserved C-terminal domain (CTD), composed of heptapeptide repeats, central to the transcriptional process. Here, we analyze the transcriptional phenotypes of a CTD-Δ5 mutant that carries a large CTD truncation in human cells. Our data show that this mutant can transcribe genes in living cells but displays a pervasive phenotype with impaired termination, similar to but more severe than previously characterized mutations of CTD tyrosine residues. The CTD-Δ5 mutant does not interact with the Mediator and Integrator complexes involved in the activation of transcription and processing of RNAs. Examination of long-distance interactions and CTCF-binding patterns in CTD-Δ5 mutant cells reveals no changes in TAD domains or borders. Our data demonstrate that the CTD is largely dispensable for the act of transcription in living cells. We propose a model in which CTD-depleted Pol II has a lower entry rate onto DNA but becomes pervasive once engaged in transcription, resulting in a defect in termination.</p>', 'date' => '2023-07-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37424514', 'doi' => '10.15252/embr.202256150', 'modified' => '2023-08-01 14:17:54', 'created' => '2023-08-01 15:59:38', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '4793', 'name' => 'Targeting lymphoid-derived IL-17 signaling to delay skin aging.', 'authors' => 'Paloma S. et al.', 'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, γδ T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-κB in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218', 'doi' => '10.1038/s43587-023-00431-z', 'modified' => '2023-06-14 15:56:56', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '4796', 'name' => 'Nicotinamide N-methyltransferase sustains a core epigenetic programthat promotes metastatic colonization in breast cancer.', 'authors' => 'Couto J.P. et al.', 'description' => '<p><span>Metastatic colonization of distant organs accounts for over 90% of deaths related to solid cancers, yet the molecular determinants of metastasis remain poorly understood. Here, we unveil a mechanism of colonization in the aggressive basal-like subtype of breast cancer that is driven by the NAD</span><sup>+</sup><span><span> </span>metabolic enzyme nicotinamide N-methyltransferase (NNMT). We demonstrate that NNMT imprints a basal genetic program into cancer cells, enhancing their plasticity. In line, NNMT expression is associated with poor clinical outcomes in patients with breast cancer. Accordingly, ablation of NNMT dramatically suppresses metastasis formation in pre-clinical mouse models. Mechanistically, NNMT depletion results in a methyl overflow that increases histone H3K9 trimethylation (H3K9me3) and DNA methylation at the promoters of PR/SET Domain-5 (PRDM5) and extracellular matrix-related genes. PRDM5 emerged in this study as a pro-metastatic gene acting via induction of cancer-cell intrinsic transcription of collagens. Depletion of PRDM5 in tumor cells decreases COL1A1 deposition and impairs metastatic colonization of the lungs. These findings reveal a critical activity of the NNMT-PRDM5-COL1A1 axis for cancer cell plasticity and metastasis in basal-like breast cancer.</span></p>', 'date' => '2023-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37259596', 'doi' => '10.15252/embj.2022112559', 'modified' => '2023-06-15 08:35:19', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 5 => array( 'id' => '4812', 'name' => 'SOX expression in prostate cancer drives resistance to nuclear hormonereceptor signaling inhibition through the WEE1/CDK1 signaling axis.', 'authors' => 'Williams A. et al.', 'description' => '<p><span>The development of androgen receptor signaling inhibitor (ARSI) drug resistance in prostate cancer (PC) remains therapeutically challenging. Our group has described the role of sex determining region Y-box 2 (SOX2) overexpression in ARSI-resistant PC. Continuing this work, we report that NR3C1, the gene encoding glucocorticoid receptor (GR), is a novel SOX2 target in PC, positively regulating its expression. Similar to ARSI treatment, SOX2-positive PC cells are insensitive to GR signaling inhibition using a GR modulating therapy. To understand SOX2-mediated nuclear hormone receptor signaling inhibitor (NHRSI) insensitivity, we performed RNA-seq in SOX2-positive and -negative PC cells following NHRSI treatment. RNA-seq prioritized differentially regulated genes mediating the cell cycle, including G2 checkpoint WEE1 Kinase (WEE1) and cyclin-dependent kinase 1 (CDK1). Additionally, WEE1 and CDK1 were differentially expressed in PC patient tumors dichotomized by high vs low SOX2 gene expression. Importantly, pharmacological targeting of WEE1 (WEE1i) in combination with an ARSI or GR modulator re-sensitizes SOX2-positive PC cells to nuclear hormone receptor signaling inhibition in vitro, and WEE1i combined with ARSI significantly slowed tumor growth in vivo. Collectively, our data suggest SOX2 predicts NHRSI resistance, and simultaneously indicates the addition of WEE1i to improve therapeutic efficacy of NHRSIs in SOX2-positive PC.</span></p>', 'date' => '2023-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37169162', 'doi' => '10.1016/j.canlet.2023.216209', 'modified' => '2023-06-15 08:58:59', 'created' => '2023-06-13 21:11:31', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 6 => array( 'id' => '4787', 'name' => 'The Effect of Metformin and Carbohydrate-Controlled Diet onDNA Methylation and Gene Expression in the Endometrium of Womenwith Polycystic Ovary Syndrome.', 'authors' => 'Garcia-Gomez E. et al.', 'description' => '<p>Polycystic ovary syndrome (PCOS) is an endocrine disease associated with infertility and metabolic disorders in reproductive-aged women. In this study, we evaluated the expression of eight genes related to endometrial function and their DNA methylation levels in the endometrium of PCOS patients and women without the disease (control group). In addition, eight of the PCOS patients underwent intervention with metformin (1500 mg/day) and a carbohydrate-controlled diet (type and quantity) for three months. Clinical and metabolic parameters were determined, and RT-qPCR and MeDIP-qPCR were used to evaluate gene expression and DNA methylation levels, respectively. Decreased expression levels of , , and genes and increased DNA methylation levels of the promoter were found in the endometrium of PCOS patients compared to controls. After metformin and nutritional intervention, some metabolic and clinical variables improved in PCOS patients. This intervention was associated with increased expression of , , and genes and reduced DNA methylation levels of the promoter in the endometrium of PCOS women. Our preliminary findings suggest that metformin and a carbohydrate-controlled diet improve endometrial function in PCOS patients, partly by modulating DNA methylation of the gene promoter and the expression of genes implicated in endometrial receptivity and insulin signaling.</p>', 'date' => '2023-04-01', 'pmid' => 'https://doi.org/10.3390%2Fijms24076857', 'doi' => '10.3390/ijms24076857', 'modified' => '2023-06-12 08:58:33', 'created' => '2023-05-05 12:34:24', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 7 => array( 'id' => '4763', 'name' => 'Chromatin profiling identifies transcriptional readthrough as a conservedmechanism for piRNA biogenesis in mosquitoes.', 'authors' => 'Qu J. et al.', 'description' => '<p>The piRNA pathway in mosquitoes differs substantially from other model organisms, with an expanded PIWI gene family and functions in antiviral defense. Here, we define core piRNA clusters as genomic loci that show ubiquitous piRNA expression in both somatic and germline tissues. These core piRNA clusters are enriched for non-retroviral endogenous viral elements (nrEVEs) in antisense orientation and depend on key biogenesis factors, Veneno, Tejas, Yb, and Shutdown. Combined transcriptome and chromatin state analyses identify transcriptional readthrough as a conserved mechanism for cluster-derived piRNA biogenesis in the vector mosquitoes Aedes aegypti, Aedes albopictus, Culex quinquefasciatus, and Anopheles gambiae. Comparative analyses between the two Aedes species suggest that piRNA clusters function as traps for nrEVEs, allowing adaptation to environmental challenges such as virus infection. Our systematic transcriptome and chromatin state analyses lay the foundation for studies of gene regulation, genome evolution, and piRNA function in these important vector species.</p>', 'date' => '2023-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36930642', 'doi' => '10.1016/j.celrep.2023.112257', 'modified' => '2023-04-17 09:12:37', 'created' => '2023-04-14 13:41:22', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 8 => array( 'id' => '4720', 'name' => 'Activation of AKT induces EZH2-mediated β-catenin trimethylation incolorectal cancer.', 'authors' => 'Ghobashi A. H. et al.', 'description' => '<p>Colorectal cancer (CRC) develops in part through the deregulation of different signaling pathways, including activation of the WNT/β-catenin and PI3K/AKT pathways. Enhancer of zeste homolog 2 (EZH2) is a lysine methyltransferase that is involved in regulating stem cell development and differentiation and is overexpressed in CRC. However, depending on the study EZH2 has been found to be both positively and negatively correlated with the survival of CRC patients suggesting that EZH2's role in CRC may be context specific. In this study, we explored how PI3K/AKT activation alters EZH2's role in CRC. We found that activation of AKT by PTEN knockdown or by hydrogen peroxide treatment induced EZH2 phosphorylation at serine 21. Phosphorylation of EZH2 resulted in EZH2-mediated methylation of β-catenin and an associated increased interaction between β-catenin, TCF1, and RNA polymerase II. AKT activation increased β-catenin's enrichment across the genome and EZH2 inhibition reduced this enrichment by reducing the methylation of β-catenin. Furthermore, PTEN knockdown increased the expression of epithelial-mesenchymal transition (EMT)-related genes, and somewhat unexpectedly EZH2 inhibition further increased the expression of these genes. Consistent with these findings, EZH2 inhibition enhanced the migratory phenotype of PTEN knockdown cells. Overall, we demonstrated that EZH2 modulates AKT-induced changes in gene expression through the AKT/EZH2/ β-catenin axis in CRC with active PI3K/AKT signaling. Therefore, it is important to consider the use of EZH2 inhibitors in CRC with caution as these inhibitors will inhibit EZH2-mediated methylation of histone and non-histone targets such as β-catenin, which can have tumor-promoting effects.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1101%2F2023.01.31.526429', 'doi' => '10.1101/2023.01.31.526429', 'modified' => '2023-03-28 09:13:16', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 9 => array( 'id' => '4667', 'name' => 'Detailed molecular and epigenetic characterization of the Pig IPECJ2and Chicken SL-29 cell lines', 'authors' => 'de Vos J. et al.', 'description' => '<p>The pig IPECJ2 and chicken SL-29 cell lines are of interest because of their untransformed nature and wide use in functional studies. Molecular characterization of these cell lines is important to gain insight into possible molecular aberrations. The aims of this paper are providing a molecular and epigenetic characterization of the IPEC-J2 and SL-29 cell lines and providing a cell-line reference for the FAANG community, and future biomedical research. Whole genome sequencing , gene expression, DNA methylation , chromatin accessibility and ChIP-seq of four histone marks (H3K4me1, H3K4me3, H3K27ac, H3K27me3) and an insulator (CTCF) are used to achieve these aims. Heteroploidy (aneuploidy) of various chromosomes was observed from whole genome sequencing analysis in both cell lines. Furthermore, higher gene expression for genes located on chromosomes with aneuploidy in comparison to diploid chromosomes was observed. Regulatory complexity of gene expression, DNA methylation and chromatin accessibility was investigated through an integrative approach.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.isci.2023.106252', 'doi' => '10.1016/j.isci.2023.106252', 'modified' => '2023-04-07 16:52:26', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 10 => array( 'id' => '4673', 'name' => 'Signal-induced enhancer activation requires Ku70 to readtopoisomerase1-DNA covalent complexes.', 'authors' => 'Tan Y. et al.', 'description' => '<p>Enhancer activation serves as the main mechanism regulating signal-dependent transcriptional programs, ensuring cellular plasticity, yet central questions persist regarding their mechanism of activation. Here, by successfully mapping topoisomerase I-DNA covalent complexes genome-wide, we find that most, if not all, acutely activated enhancers, including those induced by 17β-estradiol, dihydrotestosterone, tumor necrosis factor alpha and neuronal depolarization, are hotspots for topoisomerase I-DNA covalent complexes, functioning as epigenomic signatures read by the classic DNA damage sensor protein, Ku70. Ku70 in turn nucleates a heterochromatin protein 1 gamma (HP1γ)-mediator subunit Med26 complex to facilitate acute, but not chronic, transcriptional activation programs. Together, our data uncover a broad, unappreciated transcriptional code, required for most, if not all, acute signal-dependent enhancer activation events in both mitotic and postmitotic cells.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36747093', 'doi' => '10.1038/s41594-022-00883-8', 'modified' => '2023-04-14 09:24:10', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 11 => array( 'id' => '4668', 'name' => 'Cotranscriptional demethylation induces global loss of H3K4me2 fromactive genes in Arabidopsis', 'authors' => 'Mori S. et al.', 'description' => '<p>Based on studies of animals and yeasts, methylation of histone H3 lysine 4 (H3K4me1/2/3, for mono-, di-, and tri-methylation, respectively) is regarded as the key epigenetic modification of transcriptionally active genes. In plants, however, H3K4me2 correlates negatively with transcription, and the regulatory mechanisms of this counterintuitive H3K4me2 distribution in plants remain largely unexplored. A previous genetic screen for factors regulating plant regeneration identified Arabidopsis LYSINE-SPECIFIC DEMETHYLASE 1-LIKE 3 (LDL3), which is a major H3K4me2 demethylase. Here, we show that LDL3-mediated H3K4me2 demethylation depends on the transcription elongation factor Paf1C and phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII). In addition, LDL3 binds to phosphorylated RNAPII. These results suggest that LDL3 is recruited to transcribed genes by binding to elongating RNAPII and demethylates H3K4me2 cotranscriptionally. Importantly, the negative correlation between H3K4me2 and transcription is disrupted in the ldl3 mutant, demonstrating the genome-wide impacts of the transcription-driven LDL3 pathway to control H3K4me2 in plants. Our findings implicate H3K4me2 in plants as chromatin memory for transcriptionally repressive states, which ensures robust gene control.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.02.17.528985v1', 'doi' => '10.1101/2023.02.17.528985', 'modified' => '2023-04-14 09:31:55', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 12 => array( 'id' => '4670', 'name' => 'Epigenetic regulation of plastin 3 expression by the macrosatelliteDXZ4 and the transcriptional regulator CHD4.', 'authors' => 'Strathmann E. A. et al.', 'description' => '<p>Dysregulated Plastin 3 (PLS3) levels associate with a wide range of skeletal and neuromuscular disorders and the most common types of solid and hematopoietic cancer. Most importantly, PLS3 overexpression protects against spinal muscular atrophy. Despite its crucial role in F-actin dynamics in healthy cells and its involvement in many diseases, the mechanisms that regulate PLS3 expression are unknown. Interestingly, PLS3 is an X-linked gene and all asymptomatic SMN1-deleted individuals in SMA-discordant families who exhibit PLS3 upregulation are female, suggesting that PLS3 may escape X chromosome inactivation. To elucidate mechanisms contributing to PLS3 regulation, we performed a multi-omics analysis in two SMA-discordant families using lymphoblastoid cell lines and iPSC-derived spinal motor neurons originated from fibroblasts. We show that PLS3 tissue-specifically escapes X-inactivation. PLS3 is located ∼500 kb proximal to the DXZ4 macrosatellite, which is essential for X chromosome inactivation. By applying molecular combing in a total of 25 lymphoblastoid cell lines (asymptomatic individuals, individuals with SMA, control subjects) with variable PLS3 expression, we found a significant correlation between the copy number of DXZ4 monomers and PLS3 levels. Additionally, we identified chromodomain helicase DNA binding protein 4 (CHD4) as an epigenetic transcriptional regulator of PLS3 and validated co-regulation of the two genes by siRNA-mediated knock-down and overexpression of CHD4. We show that CHD4 binds the PLS3 promoter by performing chromatin immunoprecipitation and that CHD4/NuRD activates the transcription of PLS3 by dual-luciferase promoter assays. Thus, we provide evidence for a multilevel epigenetic regulation of PLS3 that may help to understand the protective or disease-associated PLS3 dysregulation.</p>', 'date' => '2023-02-01', 'pmid' => 'https://doi.org/10.1016%2Fj.ajhg.2023.02.004', 'doi' => '10.1016/j.ajhg.2023.02.004', 'modified' => '2023-04-14 09:36:04', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 13 => array( 'id' => '4672', 'name' => 'A dataset of definitive endoderm and hepatocyte differentiations fromhuman induced pluripotent stem cells.', 'authors' => 'Tanaka Y. et al.', 'description' => '<p>Hepatocytes are a major parenchymal cell type in the liver and play an essential role in liver function. Hepatocyte-like cells can be differentiated in vitro from induced pluripotent stem cells (iPSCs) via definitive endoderm (DE)-like cells and hepatoblast-like cells. Here, we explored the in vitro differentiation time-course of hepatocyte-like cells. We performed methylome and transcriptome analyses for hepatocyte-like cell differentiation. We also analyzed DE-like cell differentiation by methylome, transcriptome, chromatin accessibility, and GATA6 binding profiles, using finer time-course samples. In this manuscript, we provide a detailed description of the dataset and the technical validations. Our data may be valuable for the analysis of the molecular mechanisms underlying hepatocyte and DE differentiations.</p>', 'date' => '2023-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36788249', 'doi' => '10.1038/s41597-023-02001-9', 'modified' => '2023-04-14 09:41:29', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 14 => array( 'id' => '4643', 'name' => 'The mineralocorticoid receptor modulates timing and location of genomicbinding by glucocorticoid receptor in response to synthetic glucocorticoidsin keratinocytes.', 'authors' => 'Carceller-Zazo E. et al.', 'description' => '<p>Glucocorticoids (GCs) exert potent antiproliferative and anti-inflammatory properties, explaining their therapeutic efficacy for skin diseases. GCs act by binding to the GC receptor (GR) and the mineralocorticoid receptor (MR), co-expressed in classical and non-classical targets including keratinocytes. Using knockout mice, we previously demonstrated that GR and MR exert essential nonoverlapping functions in skin homeostasis. These closely related receptors may homo- or heterodimerize to regulate transcription, and theoretically bind identical GC-response elements (GRE). We assessed the contribution of MR to GR genomic binding and the transcriptional response to the synthetic GC dexamethasone (Dex) using control (CO) and MR knockout (MR ) keratinocytes. GR chromatin immunoprecipitation (ChIP)-seq identified peaks common and unique to both genotypes upon Dex treatment (1 h). GREs, AP-1, TEAD, and p53 motifs were enriched in CO and MR peaks. However, GR genomic binding was 35\% reduced in MR , with significantly decreased GRE enrichment, and reduced nuclear GR. Surface plasmon resonance determined steady state affinity constants, suggesting preferred dimer formation as MR-MR > GR-MR ~ GR-GR; however, kinetic studies demonstrated that GR-containing dimers had the longest lifetimes. Despite GR-binding differences, RNA-seq identified largely similar subsets of differentially expressed genes in both genotypes upon Dex treatment (3 h). However, time-course experiments showed gene-dependent differences in the magnitude of expression, which correlated with earlier and more pronounced GR binding to GRE sites unique to CO including near Nr3c1. Our data show that endogenous MR has an impact on the kinetics and differential genomic binding of GR, affecting the time-course, specificity, and magnitude of GC transcriptional responses in keratinocytes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36527388', 'doi' => '10.1096/fj.202201199RR', 'modified' => '2023-03-28 08:55:08', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 15 => array( 'id' => '4605', 'name' => 'Gene Regulatory Interactions at Lamina-Associated Domains', 'authors' => 'Madsen-Østerbye J. et al.', 'description' => '<p>The nuclear lamina provides a repressive chromatin environment at the nuclear periphery. However, whereas most genes in lamina-associated domains (LADs) are inactive, over ten percent reside in local euchromatic contexts and are expressed. How these genes are regulated and whether they are able to interact with regulatory elements remain unclear. Here, we integrate publicly available enhancer-capture Hi-C data with our own chromatin state and transcriptomic datasets to show that inferred enhancers of active genes in LADs are able to form connections with other enhancers within LADs and outside LADs. Fluorescence in situ hybridization analyses show proximity changes between differentially expressed genes in LADs and distant enhancers upon the induction of adipogenic differentiation. We also provide evidence of involvement of lamin A/C, but not lamin B1, in repressing genes at the border of an in-LAD active region within a topological domain. Our data favor a model where the spatial topology of chromatin at the nuclear lamina is compatible with gene expression in this dynamic nuclear compartment.</p>', 'date' => '2023-01-01', 'pmid' => 'https://doi.org/10.3390%2Fgenes14020334', 'doi' => '10.3390/genes14020334', 'modified' => '2023-04-04 08:57:32', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 16 => array( 'id' => '4578', 'name' => 'The aryl hydrocarbon receptor cell intrinsically promotes resident memoryCD8 T cell differentiation and function.', 'authors' => 'Dean J. W. et al.', 'description' => '<p>The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4 T cells; however, its cell-intrinsic role in CD8 T cells remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8 T cell (T) differentiation and function. Genetic ablation of Ahr in mouse CD8 T cells leads to increased CD127KLRG1 short-lived effector cells and CD44CD62L T central memory cells but reduced granzyme-B-producing CD69CD103 T cells. Genome-wide analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8 T cell population, revealed by single-cell RNA-seq, is diminished upon Ahr deletion, compromising anti-tumor immunity. Human intestinal intraepithelial CD8 T cells also highly express AHR that regulates in vitro T differentiation and granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8 T cell immunity.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36640340', 'doi' => '10.1016/j.celrep.2022.111963', 'modified' => '2023-04-11 10:14:26', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 17 => array( 'id' => '4577', 'name' => 'Impact of Fetal Exposure to Endocrine Disrupting ChemicalMixtures on FOXA3 Gene and Protein Expression in Adult RatTestes.', 'authors' => 'Walker C. et al.', 'description' => '<p>Perinatal exposure to endocrine disrupting chemicals (EDCs) has been shown to affect male reproductive functions. However, the effects on male reproduction of exposure to EDC mixtures at doses relevant to humans have not been fully characterized. In previous studies, we found that in utero exposure to mixtures of the plasticizer di(2-ethylhexyl) phthalate (DEHP) and the soy-based phytoestrogen genistein (Gen) induced abnormal testis development in rats. In the present study, we investigated the molecular basis of these effects in adult testes from the offspring of pregnant SD rats gavaged with corn oil or Gen + DEHP mixtures at 0.1 or 10 mg/kg/day. Testicular transcriptomes were determined by microarray and RNA-seq analyses. A protein analysis was performed on paraffin and frozen testis sections, mainly by immunofluorescence. The transcription factor forkhead box protein 3 (FOXA3), a key regulator of Leydig cell function, was identified as the most significantly downregulated gene in testes from rats exposed in utero to Gen + DEHP mixtures. FOXA3 protein levels were decreased in testicular interstitium at a dose previously found to reduce testosterone levels, suggesting a primary effect of fetal exposure to Gen + DEHP on adult Leydig cells, rather than on spermatids and Sertoli cells, also expressing FOXA3. Thus, FOXA3 downregulation in adult testes following fetal exposure to Gen + DEHP may contribute to adverse male reproductive outcomes.</p>', 'date' => '2023-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36674726', 'doi' => '10.3390/ijms24021211', 'modified' => '2023-04-11 10:18:58', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 18 => array( 'id' => '4721', 'name' => 'Transfer of blocker-based qPCR reactions for DNA methylation analysisinto a microfluidic LoC system using thermal modeling.', 'authors' => 'Kärcher J.et al.', 'description' => '<p>Changes in the DNA methylation landscape are associated with many diseases like cancer. Therefore, DNA methylation analysis is of great interest for molecular diagnostics and can be applied, e.g., for minimally invasive diagnostics in liquid biopsy samples like blood plasma. Sensitive detection of local methylation, which occurs in various cancer types, can be achieved with quantitative HeavyMethyl-PCR using oligonucleotides that block the amplification of unmethylated DNA. A transfer of these quantitative PCRs (qPCRs) into point-of-care (PoC) devices like microfluidic Lab-on-Chip (LoC) cartridges can be challenging as LoC systems show significantly different thermal properties than qPCR cyclers. We demonstrate how an adequate thermal model of the specific LoC system can help us to identify a suitable thermal profile, even for complex HeavyMethyl qPCRs, with reduced experimental effort. Using a simulation-based approach, we demonstrate a proof-of-principle for the successful LoC transfer of colorectal /-qPCR from Epi Procolon® colorectal carcinoma test, by avoidance of oligonucleotide interactions.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36506005', 'doi' => '10.1063/5.0108374', 'modified' => '2023-03-28 09:15:30', 'created' => '2023-02-28 12:19:11', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 19 => array( 'id' => '4575', 'name' => 'Intranasal administration of Acinetobacter lwoffii in a murine model ofasthma induces IL-6-mediated protection associated with cecal microbiotachanges.', 'authors' => 'Alashkar A. B. et al.', 'description' => '<p>BACKGROUND: Early-life exposure to certain environmental bacteria including Acinetobacter lwoffii (AL) has been implicated in protection from chronic inflammatory diseases including asthma later in life. However, the underlying mechanisms at the immune-microbe interface remain largely unknown. METHODS: The effects of repeated intranasal AL exposure on local and systemic innate immune responses were investigated in wild-type and Il6 , Il10 , and Il17 mice exposed to ovalbumin-induced allergic airway inflammation. Those investigations were expanded by microbiome analyses. To assess for AL-associated changes in gene expression, the picture arising from animal data was supplemented by in vitro experiments of macrophage and T-cell responses, yielding expression and epigenetic data. RESULTS: The asthma preventive effect of AL was confirmed in the lung. Repeated intranasal AL administration triggered a proinflammatory immune response particularly characterized by elevated levels of IL-6, and consequently, IL-6 induced IL-10 production in CD4 T-cells. Both IL-6 and IL-10, but not IL-17, were required for asthma protection. AL had a profound impact on the gene regulatory landscape of CD4 T-cells which could be largely recapitulated by recombinant IL-6. AL administration also induced marked changes in the gastrointestinal microbiome but not in the lung microbiome. By comparing the effects on the microbiota according to mouse genotype and AL-treatment status, we have identified microbial taxa that were associated with either disease protection or activity. CONCLUSION: These experiments provide a novel mechanism of Acinetobacter lwoffii-induced asthma protection operating through IL-6-mediated epigenetic activation of IL-10 production and with associated effects on the intestinal microbiome.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36458896', 'doi' => '10.1111/all.15606', 'modified' => '2023-04-11 10:23:07', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 20 => array( 'id' => '4574', 'name' => 'Trichoderma root colonization triggers epigenetic changes in jasmonic andsalicylic acid pathway-related genes.', 'authors' => 'Agostini R. B. et al.', 'description' => '<p>Beneficial interactions between plant-roots and Trichoderma spp. lead to a local and systemic enhancement of the plant immune system through a mechanism known as priming of defenses. In recent reports, we outlined a repertoire of genes and proteins differentially regulated in distant tissues of maize plants previously inoculated with Trichoderma atroviride. To further investigate the mechanisms involved in the systemic activation of plant responses, we continued evaluating the regulatory aspects of a selected group of genes when priming is triggered in maize plants. We conducted a time-course expression experiment from the beginning of the interaction between T. atroviride and maize roots, along plant vegetative growth and during Colletotrichum graminicola leaf infection. In addition to gene expression studies, the levels of jasmonic and salicylic acid were determined in the same samples for a comprehensive understanding of the gene expression results. Lastly, chromatin structure and modification assays were designed to evaluate the role of epigenetic marks during the long-lasting activation of the primed state of maize plants. The overall analysis of the results allowed us to shed some light on the interplay between the phytohormones and epigenetic regulatory events in the systemic and long-lasting regulation of maize plant defenses after Trichoderma inoculation.</p>', 'date' => '2022-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36575905', 'doi' => '10.1093/jxb/erac518', 'modified' => '2023-04-14 09:08:14', 'created' => '2023-02-21 09:59:46', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 21 => array( 'id' => '4474', 'name' => 'DNA sequence and chromatin modifiers cooperate to confer epigeneticbistability at imprinting control regions.', 'authors' => 'Butz S. et al.', 'description' => '<p>Genomic imprinting is regulated by parental-specific DNA methylation of imprinting control regions (ICRs). Despite an identical DNA sequence, ICRs can exist in two distinct epigenetic states that are memorized throughout unlimited cell divisions and reset during germline formation. Here, we systematically study the genetic and epigenetic determinants of this epigenetic bistability. By iterative integration of ICRs and related DNA sequences to an ectopic location in the mouse genome, we first identify the DNA sequence features required for maintenance of epigenetic states in embryonic stem cells. The autonomous regulatory properties of ICRs further enabled us to create DNA-methylation-sensitive reporters and to screen for key components involved in regulating their epigenetic memory. Besides DNMT1, UHRF1 and ZFP57, we identify factors that prevent switching from methylated to unmethylated states and show that two of these candidates, ATF7IP and ZMYM2, are important for the stability of DNA and H3K9 methylation at ICRs in embryonic stem cells.</p>', 'date' => '2022-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36333500', 'doi' => '10.1038/s41588-022-01210-z', 'modified' => '2022-11-18 12:20:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 22 => array( 'id' => '4493', 'name' => 'Smc5/6 silences episomal transcription by a three-step function.', 'authors' => 'Abdul F. et al.', 'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36097294', 'doi' => '10.1038/s41594-022-00829-0', 'modified' => '2022-11-18 12:41:42', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 23 => array( 'id' => '4495', 'name' => 'Exploration of nuclear body-enhanced sumoylation reveals that PMLrepresses 2-cell features of embryonic stem cells.', 'authors' => 'Tessier S. et al.', 'description' => '<p>Membrane-less organelles are condensates formed by phase separation whose functions often remain enigmatic. Upon oxidative stress, PML scaffolds Nuclear Bodies (NBs) to regulate senescence or metabolic adaptation. PML NBs recruit many partner proteins, but the actual biochemical mechanism underlying their pleiotropic functions remains elusive. Similarly, PML role in embryonic stem cell (ESC) and retro-element biology is unsettled. Here we demonstrate that PML is essential for oxidative stress-driven partner SUMO2/3 conjugation in mouse ESCs (mESCs) or leukemia, a process often followed by their poly-ubiquitination and degradation. Functionally, PML is required for stress responses in mESCs. Differential proteomics unravel the KAP1 complex as a PML NB-dependent SUMO2-target in arsenic-treated APL mice or mESCs. PML-driven KAP1 sumoylation enables activation of this key epigenetic repressor implicated in retro-element silencing. Accordingly, Pml mESCs re-express transposable elements and display 2-Cell-Like features, the latter enforced by PML-controlled SUMO2-conjugation of DPPA2. Thus, PML orchestrates mESC state by coordinating SUMO2-conjugation of different transcriptional regulators, raising new hypotheses about PML roles in cancer.</p>', 'date' => '2022-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36175410', 'doi' => '10.1038/s41467-022-33147-6', 'modified' => '2022-11-21 10:21:48', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 24 => array( 'id' => '4502', 'name' => 'Loss of epigenetic regulation disrupts lineage integrity, inducesaberrant alveogenesis and promotes breast cancer.', 'authors' => 'Langille E. et al.', 'description' => '<p>Systematically investigating the scores of genes mutated in cancer and discerning disease drivers from inconsequential bystanders is a prerequisite for Precision Medicine but remains challenging. Here, we developed a somatic CRISPR/Cas9 mutagenesis screen to study 215 recurrent 'long-tail' breast cancer genes, which revealed epigenetic regulation as a major tumor suppressive mechanism. We report that components of the BAP1 and the COMPASS-like complexes, including KMT2C/D, KDM6A, BAP1 and ASXL1/2 ("EpiDrivers"), cooperate with PIK3CAH1047R to transform mouse and human breast epithelial cells. Mechanistically, we find that activation of PIK3CAH1047R and concomitant EpiDriver loss triggered an alveolar-like lineage conversion of basal mammary epithelial cells and accelerated formation of luminal-like tumors, suggesting a basal origin for luminal tumors. EpiDrivers mutations are found in ~39\% of human breast cancers and ~50\% of ductal-carcinoma-in-situ express casein suggesting that lineage infidelity and alveogenic mimicry may significantly contribute to early steps of breast cancer etiology.</p>', 'date' => '2022-09-01', 'pmid' => 'https://aacrjournals.org/cancerdiscovery/article-abstract/doi/10.1158/2159-8290.CD-21-0865/709222/Loss-of-epigenetic-regulation-disrupts-lineage?redirectedFrom=fulltext', 'doi' => '10.1158/2159-8290.CD-21-0865', 'modified' => '2022-11-21 10:34:24', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 25 => array( 'id' => '4449', 'name' => 'RAD51 protects human cells from transcription-replication conflicts.', 'authors' => 'Bhowmick R. et al.', 'description' => '<p>Oncogene activation during tumorigenesis promotes DNA replication stress (RS), which subsequently drives the formation of cancer-associated chromosomal rearrangements. Many episodes of physiological RS likely arise due to conflicts between the DNA replication and transcription machineries operating simultaneously at the same loci. One role of the RAD51 recombinase in human cells is to protect replication forks undergoing RS. Here, we have identified a key role for RAD51 in preventing transcription-replication conflicts (TRCs) from triggering replication fork breakage. The genomic regions most affected by RAD51 deficiency are characterized by being replicated and transcribed in early S-phase and show significant overlap with loci prone to cancer-associated amplification. Consistent with a role for RAD51 in protecting against transcription-replication conflicts, many of the adverse effects of RAD51 depletion are ameliorated by inhibiting early S-phase transcription. We propose a model whereby RAD51 suppresses fork breakage and subsequent inadvertent amplification of genomic loci prone to experiencing TRCs.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36002000', 'doi' => '10.1016/j.molcel.2022.07.010', 'modified' => '2022-10-14 16:44:54', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 26 => array( 'id' => '4511', 'name' => 'The Arabidopsis APOLO and human UPAT sequence-unrelated longnoncoding RNAs can modulate DNA and histone methylation machineries inplants.', 'authors' => 'Fonouni-Farde C. et al.', 'description' => '<p>BACKGROUND: RNA-DNA hybrid (R-loop)-associated long noncoding RNAs (lncRNAs), including the Arabidopsis lncRNA AUXIN-REGULATED PROMOTER LOOP (APOLO), are emerging as important regulators of three-dimensional chromatin conformation and gene transcriptional activity. RESULTS: Here, we show that in addition to the PRC1-component LIKE HETEROCHROMATIN PROTEIN 1 (LHP1), APOLO interacts with the methylcytosine-binding protein VARIANT IN METHYLATION 1 (VIM1), a conserved homolog of the mammalian DNA methylation regulator UBIQUITIN-LIKE CONTAINING PHD AND RING FINGER DOMAINS 1 (UHRF1). The APOLO-VIM1-LHP1 complex directly regulates the transcription of the auxin biosynthesis gene YUCCA2 by dynamically determining DNA methylation and H3K27me3 deposition over its promoter during the plant thermomorphogenic response. Strikingly, we demonstrate that the lncRNA UHRF1 Protein Associated Transcript (UPAT), a direct interactor of UHRF1 in humans, can be recognized by VIM1 and LHP1 in plant cells, despite the lack of sequence homology between UPAT and APOLO. In addition, we show that increased levels of APOLO or UPAT hamper VIM1 and LHP1 binding to YUCCA2 promoter and globally alter the Arabidopsis transcriptome in a similar manner. CONCLUSIONS: Collectively, our results uncover a new mechanism in which a plant lncRNA coordinates Polycomb action and DNA methylation through the interaction with VIM1, and indicates that evolutionary unrelated lncRNAs with potentially conserved structures may exert similar functions by interacting with homolog partners.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36038910', 'doi' => '10.1186/s13059-022-02750-7', 'modified' => '2022-11-21 10:43:16', 'created' => '2022-11-15 09:26:20', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 27 => array( 'id' => '4552', 'name' => 'Prolonged FOS activity disrupts a global myogenic transcriptionalprogram by altering 3D chromatin architecture in primary muscleprogenitor cells.', 'authors' => 'Barutcu A Rasim et al.', 'description' => '<p>BACKGROUND: The AP-1 transcription factor, FBJ osteosarcoma oncogene (FOS), is induced in adult muscle satellite cells (SCs) within hours following muscle damage and is required for effective stem cell activation and muscle repair. However, why FOS is rapidly downregulated before SCs enter cell cycle as progenitor cells (i.e., transiently expressed) remains unclear. Further, whether boosting FOS levels in the proliferating progeny of SCs can enhance their myogenic properties needs further evaluation. METHODS: We established an inducible, FOS expression system to evaluate the impact of persistent FOS activity in muscle progenitor cells ex vivo. We performed various assays to measure cellular proliferation and differentiation, as well as uncover changes in RNA levels and three-dimensional (3D) chromatin interactions. RESULTS: Persistent FOS activity in primary muscle progenitor cells severely antagonizes their ability to differentiate and form myotubes within the first 2 weeks in culture. RNA-seq analysis revealed that ectopic FOS activity in muscle progenitor cells suppressed a global pro-myogenic transcriptional program, while activating a stress-induced, mitogen-activated protein kinase (MAPK) transcriptional signature. Additionally, we observed various FOS-dependent, chromosomal re-organization events in A/B compartments, topologically associated domains (TADs), and genomic loops near FOS-regulated genes. CONCLUSIONS: Our results suggest that elevated FOS activity in recently activated muscle progenitor cells perturbs cellular differentiation by altering the 3D chromosome organization near critical pro-myogenic genes. This work highlights the crucial importance of tightly controlling FOS expression in the muscle lineage and suggests that in states of chronic stress or disease, persistent FOS activity in muscle precursor cells may disrupt the muscle-forming process.</p>', 'date' => '2022-08-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35971133', 'doi' => '10.1186/s13395-022-00303-x', 'modified' => '2022-11-24 10:11:55', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 28 => array( 'id' => '4452', 'name' => 'Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.', 'authors' => 'Schomann T. et al.', 'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>', 'date' => '2022-07-01', 'pmid' => 'https://doi.org/10.3390%2Fbiom12081048', 'doi' => '10.3390/biom12081048', 'modified' => '2022-10-21 09:33:25', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 29 => array( 'id' => '4446', 'name' => 'Variation in PU.1 binding and chromatin looping at neutrophil enhancersinfluences autoimmune disease susceptibility', 'authors' => 'Watt S. et al. ', 'description' => '<p>Neutrophils play fundamental roles in innate inflammatory response, shape adaptive immunity1, and have been identified as a potentially causal cell type underpinning genetic associations with immune system traits and diseases2,3 The majority of these variants are non-coding and the underlying mechanisms are not fully understood. Here, we profiled the binding of one of the principal myeloid transcriptional regulators, PU.1, in primary neutrophils across nearly a hundred volunteers, and elucidate the coordinated genetic effects of PU.1 binding variation, local chromatin state, promoter-enhancer interactions and gene expression. We show that PU.1 binding and the associated chain of molecular changes underlie genetically-driven differences in cell count and autoimmune disease susceptibility. Our results advance interpretation for genetic loci associated with neutrophil biology and immune disease.</p>', 'date' => '2022-05-01', 'pmid' => 'https://www.biorxiv.org/content/10.1101/620260v1.abstract', 'doi' => '10.1101/620260', 'modified' => '2022-10-14 16:39:03', 'created' => '2022-09-28 09:53:13', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 30 => array( 'id' => '4217', 'name' => 'CREBBP/EP300 acetyltransferase inhibition disrupts FOXA1-bound enhancers to inhibit the proliferation of ER+ breast cancer cells.', 'authors' => 'Bommi-Reddy A. et al.', 'description' => '<p><span>Therapeutic targeting of the estrogen receptor (ER) is a clinically validated approach for estrogen receptor positive breast cancer (ER+ BC), but sustained response is limited by acquired resistance. Targeting the transcriptional coactivators required for estrogen receptor activity represents an alternative approach that is not subject to the same limitations as targeting estrogen receptor itself. In this report we demonstrate that the acetyltransferase activity of coactivator paralogs CREBBP/EP300 represents a promising therapeutic target in ER+ BC. Using the potent and selective inhibitor CPI-1612, we show that CREBBP/EP300 acetyltransferase inhibition potently suppresses in vitro and in vivo growth of breast cancer cell line models and acts in a manner orthogonal to directly targeting ER. CREBBP/EP300 acetyltransferase inhibition suppresses ER-dependent transcription by targeting lineage-specific enhancers defined by the pioneer transcription factor FOXA1. These results validate CREBBP/EP300 acetyltransferase activity as a viable target for clinical development in ER+ breast cancer.</span></p>', 'date' => '2022-03-30', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/35353838/', 'doi' => '10.1371/journal.pone.0262378', 'modified' => '2022-04-12 10:56:54', 'created' => '2022-04-12 10:56:54', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 31 => array( 'id' => '4407', 'name' => 'Transient regulation of focal adhesion via Tensin3 is required fornascent oligodendrocyte differentiation', 'authors' => 'Merour E. et al.', 'description' => '<p>The differentiation of oligodendroglia from oligodendrocyte precursor cells (OPCs) to complex and extensive myelinating oligodendrocytes (OLs) is a multistep process that involves largescale morphological changes with significant strain on the cytoskeleton. While key chromatin and transcriptional regulators of differentiation have been identified, their target genes responsible for the morphological changes occurring during OL myelination are still largely unknown. Here, we show that the regulator of focal adhesion, Tensin3 (Tns3), is a direct target gene of Olig2, Chd7, and Chd8, transcriptional regulators of OL differentiation. Tns3 is transiently upregulated and localized to cell processes of immature OLs, together with integrin-β1, a key mediator of survival at this transient stage. Constitutive Tns3 loss-of-function leads to reduced viability in mouse and humans, with surviving knockout mice still expressing Tns3 in oligodendroglia. Acute deletion of Tns3 in vivo, either in postnatal neural stem cells (NSCs) or in OPCs, leads to a two-fold reduction in OL numbers. We find that the transient upregulation of Tns3 is required to protect differentiating OPCs and immature OLs from cell death by preventing the upregulation of p53, a key regulator of apoptosis. Altogether, our findings reveal a specific time window during which transcriptional upregulation of Tns3 in immature OLs is required for OL differentiation likely by mediating integrin-β1 survival signaling to the actin cytoskeleton as OL undergo the large morphological changes required for their terminal differentiation.</p>', 'date' => '2022-02-01', 'pmid' => 'https://doi.org/10.1101%2F2022.02.25.481980', 'doi' => '10.1101/2022.02.25.481980', 'modified' => '2022-08-11 15:05:41', 'created' => '2022-08-11 12:14:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 32 => array( 'id' => '4238', 'name' => 'The long noncoding RNA H19 regulates tumor plasticity inneuroendocrine prostate cancer', 'authors' => 'Singh N. et al.', 'description' => '<p>Neuroendocrine (NE) prostate cancer (NEPC) is a lethal subtype of castration-resistant prostate cancer (PCa) arising either de novo or from transdifferentiated prostate adenocarcinoma following androgen deprivation therapy (ADT). Extensive computational analysis has identified a high degree of association between the long noncoding RNA (lncRNA) H19 and NEPC, with the longest isoform highly expressed in NEPC. H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown). It contributes to treatment resistance, with the knockdown of H19 re-sensitizing PCa to ADT. It is also essential for the proliferation and invasion of NEPC. H19 levels are negatively regulated by androgen signaling via androgen receptor (AR). When androgen is absent SOX2 levels increase, driving H19 transcription and facilitating transdifferentiation. H19 facilitates the PRC2 complex in regulating methylation changes at H3K27me3/H3K4me3 histone sites of AR-driven and NEPC-related genes. Additionally, this lncRNA induces alterations in genome-wide DNA methylation on CpG sites, further regulating genes associated with the NEPC phenotype. Our clinical data identify H19 as a candidate diagnostic marker and predictive marker of NEPC with elevated H19 levels associated with an increased probability of biochemical recurrence and metastatic disease in patients receiving ADT. Here we report H19 as an early upstream regulator of cell fate, plasticity, and treatment resistance in NEPC that can reverse/transform cells to a treatable form of PCa once therapeutically deactivated.</p>', 'date' => '2021-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34934057', 'doi' => '10.1038/s41467-021-26901-9', 'modified' => '2022-05-19 17:06:50', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 33 => array( 'id' => '4239', 'name' => 'Epromoters function as a hub to recruit key transcription factorsrequired for the inflammatory response', 'authors' => 'Santiago-Algarra D. et al. ', 'description' => '<p>Gene expression is controlled by the involvement of gene-proximal (promoters) and distal (enhancers) regulatory elements. Our previous results demonstrated that a subset of gene promoters, termed Epromoters, work as bona fide enhancers and regulate distal gene expression. Here, we hypothesized that Epromoters play a key role in the coordination of rapid gene induction during the inflammatory response. Using a high-throughput reporter assay we explored the function of Epromoters in response to type I interferon. We find that clusters of IFNa-induced genes are frequently associated with Epromoters and that these regulatory elements preferentially recruit the STAT1/2 and IRF transcription factors and distally regulate the activation of interferon-response genes. Consistently, we identified and validated the involvement of Epromoter-containing clusters in the regulation of LPS-stimulated macrophages. Our findings suggest that Epromoters function as a local hub recruiting the key TFs required for coordinated regulation of gene clusters during the inflammatory response.</p>', 'date' => '2021-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34795220', 'doi' => '10.1038/s41467-021-26861-0', 'modified' => '2022-05-19 17:10:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 34 => array( 'id' => '4231', 'name' => 'Differential contribution to gene expression prediction of histonemodifications at enhancers or promoters.', 'authors' => 'González-Ramírez M. et al.', 'description' => '<p>The ChIP-seq signal of histone modifications at promoters is a good predictor of gene expression in different cellular contexts, but whether this is also true at enhancers is not clear. To address this issue, we develop quantitative models to characterize the relationship of gene expression with histone modifications at enhancers or promoters. We use embryonic stem cells (ESCs), which contain a full spectrum of active and repressed (poised) enhancers, to train predictive models. As many poised enhancers in ESCs switch towards an active state during differentiation, predictive models can also be trained on poised enhancers throughout differentiation and in development. Remarkably, we determine that histone modifications at enhancers, as well as promoters, are predictive of gene expression in ESCs and throughout differentiation and development. Importantly, we demonstrate that their contribution to the predictive models varies depending on their location in enhancers or promoters. Moreover, we use a local regression (LOESS) to normalize sequencing data from different sources, which allows us to apply predictive models trained in a specific cellular context to a different one. We conclude that the relationship between gene expression and histone modifications at enhancers is universal and different from promoters. Our study provides new insight into how histone modifications relate to gene expression based on their location in enhancers or promoters.</p>', 'date' => '2021-09-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473698/', 'doi' => '10.1371/journal.pcbi.1009368', 'modified' => '2022-05-19 16:50:59', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 35 => array( 'id' => '4315', 'name' => 'Atg7 deficiency in microglia drives an altered transcriptomic profileassociated with an impaired neuroinflammatory response', 'authors' => 'Friess L. et al.', 'description' => '<p>Microglia, resident immunocompetent cells of the central nervous system, can display a range of reaction states and thereby exhibit distinct biological functions across development, adulthood and under disease conditions. Distinct gene expression profiles are reported to define each of these microglial reaction states. Hence, the identification of modulators of selective microglial transcriptomic signature, which have the potential to regulate unique microglial function has gained interest. Here, we report the identification of ATG7 (Autophagy-related 7) as a selective modulator of an NF-κB-dependent transcriptional program controlling the pro-inflammatory response of microglia. We also uncover that microglial Atg7-deficiency was associated with reduced microglia-mediated neurotoxicity, and thus a loss of biological function associated with the pro-inflammatory microglial reactive state. Further, we show that Atg7-deficiency in microglia did not impact on their ability to respond to alternative stimulus, such as one driving them towards an anti-inflammatory/tumor supportive phenotype. The identification of distinct regulators, such as Atg7, controlling specific microglial transcriptional programs could lead to developing novel therapeutic strategies aiming to manipulate selected microglial phenotypes, instead of the whole microglial population with is associated with several pitfalls. Supplementary Information The online version contains supplementary material available at 10.1186/s13041-021-00794-7.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34082793', 'doi' => '10.1186/s13041-021-00794-7', 'modified' => '2022-08-02 16:47:13', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 36 => array( 'id' => '4349', 'name' => 'Lasp1 regulates adherens junction dynamics and fibroblast transformationin destructive arthritis', 'authors' => 'Beckmann D. et al.', 'description' => '<p>The LIM and SH3 domain protein 1 (Lasp1) was originally cloned from metastatic breast cancer and characterised as an adaptor molecule associated with tumourigenesis and cancer cell invasion. However, the regulation of Lasp1 and its function in the aggressive transformation of cells is unclear. Here we use integrative epigenomic profiling of invasive fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA) and from mouse models of the disease, to identify Lasp1 as an epigenomically co-modified region in chronic inflammatory arthritis and a functionally important binding partner of the Cadherin-11/β-Catenin complex in zipper-like cell-to-cell contacts. In vitro, loss or blocking of Lasp1 alters pathological tissue formation, migratory behaviour and platelet-derived growth factor response of arthritic FLS. In arthritic human TNF transgenic mice, deletion of Lasp1 reduces arthritic joint destruction. Therefore, we show a function of Lasp1 in cellular junction formation and inflammatory tissue remodelling and identify Lasp1 as a potential target for treating inflammatory joint disorders associated with aggressive cellular transformation.</p>', 'date' => '2021-06-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34131132', 'doi' => '10.1038/s41467-021-23706-8', 'modified' => '2022-08-03 17:02:30', 'created' => '2022-05-19 10:41:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 37 => array( 'id' => '4136', 'name' => 'The lncRNA and the transcription factor WRKY42 target common cell wallEXTENSIN encoding genes to trigger root hair cell elongation.', 'authors' => 'Pacheco, J. M. et al.', 'description' => '<p>Plant long noncoding RNAs (lncRNAs) are key chromatin dynamics regulators, directing the transcriptional programs driving a wide variety of developmental outputs. Recently, we uncovered how the lncRNA () directly recognizes the locus encoding the root hair (RH) master regulator () modulating its transcriptional activation and leading to low temperature-induced RH elongation. We further demonstrated that interacts with the transcription factor WRKY42 in a novel ribonucleoprotein complex shaping epigenetic environment and integrating signals governing RH growth and development. In this work, we expand this model showing that is able to bind and positively control the expression of several cell wall EXTENSIN (EXT) encoding genes, including , a key regulator for RH growth. Interestingly, emerged as a novel common target of and WRKY42. Furthermore, we showed that the ROS homeostasis-related gene is deregulated upon overexpression, likely through the RHD6-RSL4 pathway, and that is required for low temperature-dependent enhancement of RH growth. Collectively, our results uncover an intricate regulatory network involving the /WRKY42 hub in the control of master and effector genes during RH development.</p>', 'date' => '2021-05-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33944666', 'doi' => '10.1080/15592324.2021.1920191', 'modified' => '2021-12-13 09:06:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 38 => array( 'id' => '4143', 'name' => 'Placental uptake and metabolism of 25(OH)Vitamin D determines itsactivity within the fetoplacental unit', 'authors' => 'Ashley, B. et al.', 'description' => '<p>Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes, but the underlying mechanisms have not been elucidated. Using physiological human placental perfusion approaches and intact villous explants we demonstrate a role for the placenta in regulating the relationships between maternal 25(OH)D concentrations and fetal physiology. Here, we demonstrate active placental uptake of 25(OH)D3 by endocytosis and placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the fetal and maternal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than solely the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer, including transcriptional activation and inflammatory responses. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta; with widespread effects on the placenta itself. These data show complex and synergistic interplay between vitamin D and the placenta, and inform possible interventions to optimise placental function to better support fetal growth and the maternal adaptations to pregnancy.</p>', 'date' => '2021-05-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.01.431439', 'doi' => '10.1101/2021.03.01.431439', 'modified' => '2021-12-13 09:29:25', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 39 => array( 'id' => '4147', 'name' => 'Waves of sumoylation support transcription dynamics during adipocytedifferentiation', 'authors' => 'Zhao, X. et al.', 'description' => '<p>Tight control of gene expression networks required for adipose tissue formation and plasticity is essential for adaptation to energy needs and environmental cues. However, little is known about the mechanisms that orchestrate the dramatic transcriptional changes leading to adipocyte differentiation. We investigated the regulation of nascent transcription by the sumoylation pathway during adipocyte differentiation using SLAMseq and ChIPseq. We discovered that the sumoylation pathway has a dual function in differentiation; it supports the initial downregulation of pre-adipocyte-specific genes, while it promotes the establishment of the mature adipocyte transcriptional program. By characterizing sumoylome dynamics in differentiating adipocytes by mass spectrometry, we found that sumoylation of specific transcription factors like Pparγ/RXR and their co-factors is associated with the transcription of adipogenic genes. Our data demonstrate that the sumoylation pathway coordinates the rewiring of transcriptional networks required for formation of functional adipocytes. This study also provides an in-depth resource of gene transcription dynamics, SUMO-regulated genes and sumoylation sites during adipogenesis.</p>', 'date' => '2021-04-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.20.432084', 'doi' => '10.1101/2021.02.20.432084', 'modified' => '2021-12-14 09:23:28', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 40 => array( 'id' => '4171', 'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.', 'authors' => 'Ryan, Genevieve E. et al.', 'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse LβT2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733', 'doi' => '10.1016/j.mce.2021.111286', 'modified' => '2021-12-21 15:57:35', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 41 => array( 'id' => '4181', 'name' => 'Genetic perturbation of PU.1 binding and chromatin looping at neutrophilenhancers associates with autoimmune disease.', 'authors' => 'Watt, Stephen et al.', 'description' => '<p>Neutrophils play fundamental roles in innate immune response, shape adaptive immunity, and are a potentially causal cell type underpinning genetic associations with immune system traits and diseases. Here, we profile the binding of myeloid master regulator PU.1 in primary neutrophils across nearly a hundred volunteers. We show that variants associated with differential PU.1 binding underlie genetically-driven differences in cell count and susceptibility to autoimmune and inflammatory diseases. We integrate these results with other multi-individual genomic readouts, revealing coordinated effects of PU.1 binding variants on the local chromatin state, enhancer-promoter contacts and downstream gene expression, and providing a functional interpretation for 27 genes underlying immune traits. Collectively, these results demonstrate the functional role of PU.1 and its target enhancers in neutrophil transcriptional control and immune disease susceptibility.</p>', 'date' => '2021-04-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863903', 'doi' => '10.1038/s41467-021-22548-8', 'modified' => '2021-12-21 16:50:30', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 42 => array( 'id' => '4126', 'name' => 'Fra-1 regulates its target genes via binding to remote enhancers withoutexerting major control on chromatin architecture in triple negative breastcancers.', 'authors' => 'Bejjani, Fabienne and Tolza, Claire and Boulanger, Mathias and Downes,Damien and Romero, Raphaël and Maqbool, Muhammad Ahmad and Zine ElAabidine, Amal and Andrau, Jean-Christophe and Lebre, Sophie and Brehelin,Laurent and Parrinello, Hughes and Rohmer,', 'description' => '<p>The ubiquitous family of dimeric transcription factors AP-1 is made up of Fos and Jun family proteins. It has long been thought to operate principally at gene promoters and how it controls transcription is still ill-understood. The Fos family protein Fra-1 is overexpressed in triple negative breast cancers (TNBCs) where it contributes to tumor aggressiveness. To address its transcriptional actions in TNBCs, we combined transcriptomics, ChIP-seqs, machine learning and NG Capture-C. Additionally, we studied its Fos family kin Fra-2 also expressed in TNBCs, albeit much less. Consistently with their pleiotropic effects, Fra-1 and Fra-2 up- and downregulate individually, together or redundantly many genes associated with a wide range of biological processes. Target gene regulation is principally due to binding of Fra-1 and Fra-2 at regulatory elements located distantly from cognate promoters where Fra-1 modulates the recruitment of the transcriptional co-regulator p300/CBP and where differences in AP-1 variant motif recognition can underlie preferential Fra-1- or Fra-2 bindings. Our work also shows no major role for Fra-1 in chromatin architecture control at target gene loci, but suggests collaboration between Fra-1-bound and -unbound enhancers within chromatin hubs sometimes including promoters for other Fra-1-regulated genes. Our work impacts our view of AP-1.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33533919', 'doi' => '10.1093/nar/gkab053', 'modified' => '2021-12-07 10:09:23', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 43 => array( 'id' => '4139', 'name' => 'Cell-specific alterations inPitx1regulatory landscape activation caused bythe loss of a single enhancer', 'authors' => 'Rouco, R. et al.', 'description' => '<p>Most developmental genes rely on multiple transcriptional enhancers for their accurate expression during embryogenesis. Because enhancers may have partially redundant activities, the loss of one of them often leads to a partial loss of gene expression and concurrent moderate phenotypic outcome, if any. While such a phenomenon has been observed in many instances, the nature of the underlying mechanisms remains elusive. We used the Pitx1 testbed locus to characterize in detail the regulatory and cellular identity alterations following the deletion in vivo of one of its enhancers (Pen), which normally accounts for 30 percent of Pitx1 expression in hindlimb buds. By combining single cell transcriptomics and a novel in embryo cell tracing approach, we observed that this global decrease in Pitx1 expression results from both an increase in the number of non- or low-expressing cells, and a decrease in the number of high-expressing cells. We found that the over-representation of Pitx1 non/low-expressing cells originates from a failure of the Pitx1 locus to coordinate enhancer activities and 3D chromatin changes. The resulting increase in Pitx1 non/low-expressing cells eventually affects the proximal limb more severely than the distal limb, leading to a clubfoot phenotype likely produced through a localized heterochrony and concurrent loss of irregular connective tissue. This data suggests that, in some cases, redundant enhancers may be used to locally enforce a robust activation of their host regulatory landscapes.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.10.434611', 'doi' => '10.1101/2021.03.10.434611', 'modified' => '2021-12-13 09:18:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 44 => array( 'id' => '4141', 'name' => 'Transgenic mice for in vivo epigenome editing with CRISPR-based systems', 'authors' => 'Gemberling, M. et al.', 'description' => '<p>The discovery, characterization, and adaptation of the RNA-guided clustered regularly interspersed short palindromic repeat (CRISPR)-Cas9 system has greatly increased the ease with which genome and epigenome editing can be performed. Fusion of chromatin-modifying domains to the nuclease-deactivated form of Cas9 (dCas9) has enabled targeted gene activation or repression in both cultured cells and in vivo in animal models. However, delivery of the large dCas9 fusion proteins to target cell types and tissues is an obstacle to widespread adoption of these tools for in vivo studies. Here we describe the generation and validation of two conditional transgenic mouse lines for targeted gene regulation, Rosa26:LSL-dCas9-p300 for gene activation and Rosa26:LSL-dCas9-KRAB for gene repression. Using the dCas9p300 and dCas9KRAB transgenic mice we demonstrate activation or repression of genes in both the brain and liver in vivo, and T cells and fibroblasts ex vivo. We show gene regulation and targeted epigenetic modification with gRNAs targeting either transcriptional start sites (TSS) or distal enhancer elements, as well as corresponding changes to downstream phenotypes. These mouse lines are convenient and valuable tools for facile, temporally controlled, and tissue-restricted epigenome editing and manipulation of gene expression in vivo.</p>', 'date' => '2021-03-01', 'pmid' => 'https://doi.org/10.1101%2F2021.03.08.434430', 'doi' => '10.1101/2021.03.08.434430', 'modified' => '2021-12-13 09:23:10', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 45 => array( 'id' => '4163', 'name' => 'Transcriptional programming drives Ibrutinib-resistance evolution in mantlecell lymphoma.', 'authors' => 'Zhao, Xiaohong et al.', 'description' => '<p>Ibrutinib, a bruton's tyrosine kinase (BTK) inhibitor, provokes robust clinical responses in aggressive mantle cell lymphoma (MCL), yet many patients relapse with lethal Ibrutinib-resistant (IR) disease. Here, using genomic, chemical proteomic, and drug screen profiling, we report that enhancer remodeling-mediated transcriptional activation and adaptive signaling changes drive the aggressive phenotypes of IR. Accordingly, IR MCL cells are vulnerable to inhibitors of the transcriptional machinery and especially so to inhibitors of cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the positive transcription elongation factor b (P-TEFb) of RNA polymerase II (RNAPII). Further, CDK9 inhibition disables reprogrammed signaling circuits and prevents the emergence of IR in MCL. Finally, and importantly, we find that a robust and facile ex vivo image-based functional drug screening platform can predict clinical therapeutic responses of IR MCL and identify vulnerabilities that can be targeted to disable the evolution of IR.</p>', 'date' => '2021-03-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33730585', 'doi' => '10.1016/j.celrep.2021.108870', 'modified' => '2021-12-21 15:28:26', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 46 => array( 'id' => '4119', 'name' => 'Coordinated changes in gene expression, H1 variant distribution and genome3D conformation in response to H1 depletion', 'authors' => 'Serna-Pujol, Nuria and Salinas-Pena, Monica and Mugianesi, Francesca and LeDily, François and Marti-Renom, Marc A. and Jordan, Albert', 'description' => '<p>Up to seven members of the histone H1 family may contribute to chromatin compaction and its regulation in human somatic cells. In breast cancer cells, knock-down of multiple H1 variants deregulates many genes, promotes the appearance of genome-wide accessibility sites and triggers an interferon response via activation of heterochromatic repeats. However, how these changes in the expression profile relate to the re-distribution of H1 variants as well as to genome conformational changes have not been yet studied. Here, we combined ChIP-seq of five endogenous H1 variants with Chromosome Conformation Capture analysis in wild-type and H1 knock-down T47D cells. The results indicate that H1 variants coexist in the genome in two large groups depending on the local DNA GC content and that their distribution is robust with respect to multiple H1 depletion. Despite the small changes in H1 variants distribution, knock-down of H1 translated into more isolated but de-compacted chromatin structures at the scale of Topologically Associating Domains or TADs. Such changes in TAD structure correlated with a coordinated gene expression response of their resident genes. This is the first report describing simultaneous profiling of five endogenous H1 variants within a cell line and giving functional evidence of genome topology alterations upon H1 depletion in human cancer cells.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.12.429879', 'doi' => '10.1101/2021.02.12.429879', 'modified' => '2021-12-07 09:43:11', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 47 => array( 'id' => '4144', 'name' => 'REPROGRAMMING CBX8-PRC1 FUNCTION WITH A POSITIVE ALLOSTERICMODULATOR', 'authors' => 'Suh, J. L. et al.', 'description' => '<p>Canonical targeting of Polycomb Repressive Complex 1 (PRC1) to repress developmental genes is mediated by cell type-specific, paralogous chromobox (CBX) proteins (CBX2, 4, 6, 7 and 8). Based on their central role in silencing and their misregulation associated with human disease including cancer, CBX proteins are attractive targets for small molecule chemical probe development. Here, we have used a quantitative and target-specific cellular assay to discover a potent positive allosteric modulator (PAM) of CBX8. The PAM activity of UNC7040 antagonizes H3K27me3 binding by CBX8 while increasing interactions with nucleic acids and participation in variant PRC1. We show that treatment with UNC7040 leads to efficient PRC1 chromatin eviction, loss of silencing and reduced proliferation across different cancer cell lines. Our discovery and characterization of UNC7040 not only revealed the most cellularly potent CBX8-specific chemical probe to date, but also corroborates a mechanism of polycomb regulation by non-histone lysine methylated interaction partners.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.23.432388', 'doi' => '10.1101/2021.02.23.432388', 'modified' => '2021-12-13 09:35:04', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 48 => array( 'id' => '4145', 'name' => 'Germline activity of the heat shock factor HSF-1 programs theinsulin-receptor daf-2 in C. elegans', 'authors' => 'Das, S. et al.', 'description' => '<p>The mechanisms by which maternal stress alters offspring phenotypes remain poorly understood. Here we report that the heat shock transcription factor HSF-1, activated in the C. elegans maternal germline upon stress, epigenetically programs the insulin-like receptor daf-2 by increasing repressive H3K9me2 levels throughout the daf-2 gene. This increase occurs by the recruitment of the C. elegans SETDB1 homolog MET-2 by HSF-1. Increased H3K9me2 levels at daf-2 persist in offspring to downregulate daf-2, activate the C. elegans FOXO ortholog DAF-16 and enhance offspring stress resilience. Thus, HSF-1 activity in the mother promotes the early life programming of the insulin/IGF-1 signaling (IIS) pathway and determines the strategy of stress resilience in progeny.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.22.432344', 'doi' => '10.1101/2021.02.22.432344', 'modified' => '2021-12-14 09:13:54', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 49 => array( 'id' => '4151', 'name' => 'The epigenetic landscape in purified myonuclei from fast and slow muscles', 'authors' => 'Bengtsen, M. et al.', 'description' => '<p>Muscle cells have different phenotypes adapted to different usage and can be grossly divided into fast/glycolytic and slow/oxidative types. While most muscles contain a mixture of such fiber types, we aimed at providing a genome-wide analysis of chromatin environment by ChIP-Seq in two muscle extremes, the almost completely fast/glycolytic extensor digitorum longus (EDL) and slow/oxidative soleus muscles. Muscle is a heterogeneous tissue where less than 60\% of the nuclei are inside muscle fibers. Since cellular homogeneity is critical in epigenome-wide association studies we devised a new method for purifying skeletal muscle nuclei from whole tissue based on the nuclear envelope protein Pericentriolar material 1 (PCM1) being a specific marker for myonuclei. Using antibody labeling and a magnetic-assisted sorting approach we were able to sort out myonuclei with 95\% purity. The sorting eliminated influence from other cell types in the tissue and improved the myo-specific signal. A genome-wide comparison of the epigenetic landscape in EDL and soleus reflected the functional properties of the two muscles each with a distinct regulatory program involving distal enhancers, including a glycolytic super-enhancer in the EDL. The two muscles are also regulated by different sets of transcription factors; e.g. in soleus binding sites for MEF2C, NFATC2 and PPARA were enriched, while in EDL MYOD1 and SOX1 binding sites were found to be overrepresented. In addition, novel factors for muscle regulation such as MAF, ZFX and ZBTB14 were identified.</p>', 'date' => '2021-02-01', 'pmid' => 'https://doi.org/10.1101%2F2021.02.04.429545', 'doi' => '10.1101/2021.02.04.429545', 'modified' => '2021-12-14 09:40:02', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 50 => array( 'id' => '4166', 'name' => 'The glucocorticoid receptor recruits the COMPASS complex to regulateinflammatory transcription at macrophage enhancers.', 'authors' => 'Greulich, Franziska et al.', 'description' => '<p>Glucocorticoids (GCs) are effective anti-inflammatory drugs; yet, their mechanisms of action are poorly understood. GCs bind to the glucocorticoid receptor (GR), a ligand-gated transcription factor controlling gene expression in numerous cell types. Here, we characterize GR's protein interactome and find the SETD1A (SET domain containing 1A)/COMPASS (complex of proteins associated with Set1) histone H3 lysine 4 (H3K4) methyltransferase complex highly enriched in activated mouse macrophages. We show that SETD1A/COMPASS is recruited by GR to specific cis-regulatory elements, coinciding with H3K4 methylation dynamics at subsets of sites, upon treatment with lipopolysaccharide (LPS) and GCs. By chromatin immunoprecipitation sequencing (ChIP-seq) and RNA-seq, we identify subsets of GR target loci that display SETD1A occupancy, H3K4 mono-, di-, or tri-methylation patterns, and transcriptional changes. However, our data on methylation status and COMPASS recruitment suggest that SETD1A has additional transcriptional functions. Setd1a loss-of-function studies reveal that SETD1A/COMPASS is required for GR-controlled transcription of subsets of macrophage target genes. We demonstrate that the SETD1A/COMPASS complex cooperates with GR to mediate anti-inflammatory effects.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33567280', 'doi' => '10.1016/j.celrep.2021.108742', 'modified' => '2021-12-21 15:42:49', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 51 => array( 'id' => '4185', 'name' => 'A distinct metabolic response characterizes sensitivity to EZH2inhibition in multiple myeloma.', 'authors' => 'Nylund P. et al.', 'description' => '<p>Multiple myeloma (MM) is a heterogeneous haematological disease that remains clinically challenging. Increased activity of the epigenetic silencer EZH2 is a common feature in patients with poor prognosis. Previous findings have demonstrated that metabolic profiles can be sensitive markers for response to treatment in cancer. While EZH2 inhibition (EZH2i) has proven efficient in inducing cell death in a number of human MM cell lines, we hereby identified a subset of cell lines that despite a global loss of H3K27me3, remains viable after EZH2i. By coupling liquid chromatography-mass spectrometry with gene and miRNA expression profiling, we found that sensitivity to EZH2i correlated with distinct metabolic signatures resulting from a dysregulation of genes involved in methionine cycling. Specifically, EZH2i resulted in a miRNA-mediated downregulation of methionine cycling-associated genes in responsive cells. This induced metabolite accumulation and DNA damage, leading to G2 arrest and apoptosis. Altogether, we unveiled that sensitivity to EZH2i in human MM cell lines is associated with a specific metabolic and gene expression profile post-treatment.</p>', 'date' => '2021-02-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33579905', 'doi' => '10.1038/s41419-021-03447-8', 'modified' => '2022-01-05 14:59:39', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 52 => array( 'id' => '4108', 'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma', 'authors' => 'Laubscher et. al.', 'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that </span><em>SMARCA4</em><span><span> </span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span> </span></span><em>de novo</em><span><span> </span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>', 'date' => '2021-01-07', 'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1', 'doi' => ' 10.21203/rs.3.rs-131009/v1', 'modified' => '2021-07-07 11:52:23', 'created' => '2021-07-07 06:38:34', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 53 => array( 'id' => '4098', 'name' => 'A Tumor Suppressor Enhancer of PTEN in T-cell development and leukemia', 'authors' => 'L. Tottone at al.', 'description' => '<p>Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss of expression of PTEN is associated with the pathogenesis of various cancers, including T-cell leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts with the <em>PTEN</em> promoter in multiple hematopoietic populations, including T-cells, and acts as a hub of relevant transcription factors in T-ALL. Consistently, loss of PE leads to reduced <em>PTEN</em> levels in T-ALL cells. Moreover, PE-null mice show reduced <em>Pten</em> levels in thymocytes and accelerated development of NOTCH1-induced T-ALL. Furthermore, secondary loss of PE in established leukemias leads to accelerated progression and a gene expression signature driven by <em>Pten</em> loss. Finally, we uncovered recurrent deletions encompassing PE in T-ALL, which are associated with decreased <em>PTEN</em> levels. Altogether, our results identify PE as the first long-range tumor suppressor enhancer directly implicated in cancer.</p>', 'date' => '2021-01-01', 'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33458694/', 'doi' => '10.1158/2643-3230.BCD-20-0201 ', 'modified' => '2021-05-04 09:51:10', 'created' => '2021-05-04 09:51:10', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 54 => array( 'id' => '4157', 'name' => 'Stronger induction of trained immunity by mucosal BCG or MTBVAC vaccination compared to standard intradermal vaccination.', 'authors' => 'Vierboom, M.P.M. et al. ', 'description' => '<p>BCG vaccination can strengthen protection against pathogens through the induction of epigenetic and metabolic reprogramming of innate immune cells, a process called trained immunity. We and others recently demonstrated that mucosal or intravenous BCG better protects rhesus macaques from infection and TB disease than standard intradermal vaccination, correlating with local adaptive immune signatures. In line with prior mouse data, here, we show in rhesus macaques that intravenous BCG enhances innate cytokine production associated with changes in H3K27 acetylation typical of trained immunity. Alternative delivery of BCG does not alter the cytokine production of unfractionated bronchial lavage cells. However, mucosal but not intradermal vaccination, either with BCG or the -derived candidate MTBVAC, enhances innate cytokine production by blood- and bone marrow-derived monocytes associated with metabolic rewiring, typical of trained immunity. These results provide support to strategies for improving TB vaccination and, more broadly, modulating innate immunity via mucosal surfaces.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33521699', 'doi' => '10.1016/j.xcrm.2020.100185', 'modified' => '2021-12-16 10:50:01', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 55 => array( 'id' => '4193', 'name' => 'Postoperative abdominal sepsis induces selective and persistent changes inCTCF binding within the MHC-II region of human monocytes.', 'authors' => 'Siegler B. et al.', 'description' => '<p>BACKGROUND: Postoperative abdominal infections belong to the most common triggers of sepsis and septic shock in intensive care units worldwide. While monocytes play a central role in mediating the initial host response to infections, sepsis-induced immune dysregulation is characterized by a defective antigen presentation to T-cells via loss of Major Histocompatibility Complex Class II DR (HLA-DR) surface expression. Here, we hypothesized a sepsis-induced differential occupancy of the CCCTC-Binding Factor (CTCF), an architectural protein and superordinate regulator of transcription, inside the Major Histocompatibility Complex Class II (MHC-II) region in patients with postoperative sepsis, contributing to an altered monocytic transcriptional response during critical illness. RESULTS: Compared to a matched surgical control cohort, postoperative sepsis was associated with selective and enduring increase in CTCF binding within the MHC-II. In detail, increased CTCF binding was detected at four sites adjacent to classical HLA class II genes coding for proteins expressed on monocyte surface. Gene expression analysis revealed a sepsis-associated decreased transcription of (i) the classical HLA genes HLA-DRA, HLA-DRB1, HLA-DPA1 and HLA-DPB1 and (ii) the gene of the MHC-II master regulator, CIITA (Class II Major Histocompatibility Complex Transactivator). Increased CTCF binding persisted in all sepsis patients, while transcriptional recovery CIITA was exclusively found in long-term survivors. CONCLUSION: Our experiments demonstrate differential and persisting alterations of CTCF occupancy within the MHC-II, accompanied by selective changes in the expression of spatially related HLA class II genes, indicating an important role of CTCF in modulating the transcriptional response of immunocompromised human monocytes during critical illness.</p>', 'date' => '2021-01-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33939725', 'doi' => '10.1371/journal.pone.0250818', 'modified' => '2022-01-06 14:22:15', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 56 => array( 'id' => '4204', 'name' => 'S-adenosyl-l-homocysteine hydrolase links methionine metabolism to thecircadian clock and chromatin remodeling.', 'authors' => 'Greco C. M. et al. ', 'description' => '<p>Circadian gene expression driven by transcription activators CLOCK and BMAL1 is intimately associated with dynamic chromatin remodeling. However, how cellular metabolism directs circadian chromatin remodeling is virtually unexplored. We report that the S-adenosylhomocysteine (SAH) hydrolyzing enzyme adenosylhomocysteinase (AHCY) cyclically associates to CLOCK-BMAL1 at chromatin sites and promotes circadian transcriptional activity. SAH is a potent feedback inhibitor of S-adenosylmethionine (SAM)-dependent methyltransferases, and timely hydrolysis of SAH by AHCY is critical to sustain methylation reactions. We show that AHCY is essential for cyclic H3K4 trimethylation, genome-wide recruitment of BMAL1 to chromatin, and subsequent circadian transcription. Depletion or targeted pharmacological inhibition of AHCY in mammalian cells markedly decreases the amplitude of circadian gene expression. In mice, pharmacological inhibition of AHCY in the hypothalamus alters circadian locomotor activity and rhythmic transcription within the suprachiasmatic nucleus. These results reveal a previously unappreciated connection between cellular metabolism, chromatin dynamics, and circadian regulation.</p>', 'date' => '2020-12-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33328229', 'doi' => '10.1126/sciadv.abc5629', 'modified' => '2022-01-06 14:59:48', 'created' => '2021-12-06 15:53:19', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 57 => array( 'id' => '4040', 'name' => 'Genomic profiling of T-cell activation suggests increased sensitivity ofmemory T cells to CD28 costimulation.', 'authors' => 'Glinos, Dafni A and Soskic, Blagoje and Williams, Cayman and Kennedy, Alanand Jostins, Luke and Sansom, David M and Trynka, Gosia', 'description' => '<p>T-cell activation is a critical driver of immune responses. The CD28 costimulation is an essential regulator of CD4 T-cell responses, however, its relative importance in naive and memory T cells is not fully understood. Using different model systems, we observe that human memory T cells are more sensitive to CD28 costimulation than naive T cells. To deconvolute how the T-cell receptor (TCR) and CD28 orchestrate activation of human T cells, we stimulate cells using varying intensities of TCR and CD28 and profiled gene expression. We show that genes involved in cell cycle progression and division are CD28-driven in memory cells, but under TCR control in naive cells. We further demonstrate that T-helper differentiation and cytokine expression are controlled by CD28. Using chromatin accessibility profiling, we observe that AP1 transcriptional regulation is enriched when both TCR and CD28 are engaged, whereas open chromatin near CD28-sensitive genes is enriched for NF-kB motifs. Lastly, we show that CD28-sensitive genes are enriched in GWAS regions associated with immune diseases, implicating a role for CD28 in disease development. Our study provides important insights into the differential role of costimulation in naive and memory T-cell responses and disease susceptibility.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33223527', 'doi' => '10.1038/s41435-020-00118-0', 'modified' => '2021-02-19 12:08:04', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 58 => array( 'id' => '4060', 'name' => 'A genetic variant controls interferon-β gene expression in human myeloidcells by preventing C/EBP-β binding on a conserved enhancer.', 'authors' => 'Assouvie, Anaïs and Rotival, Maxime and Hamroune, Juliette and Busso,Didier and Romeo, Paul-Henri and Quintana-Murci, Lluis and Rousselet,Germain', 'description' => '<p>Interferon β (IFN-β) is a cytokine that induces a global antiviral proteome, and regulates the adaptive immune response to infections and tumors. Its effects strongly depend on its level and timing of expression. Therefore, the transcription of its coding gene IFNB1 is strictly controlled. We have previously shown that in mice, the TRIM33 protein restrains Ifnb1 transcription in activated myeloid cells through an upstream inhibitory sequence called ICE. Here, we show that the deregulation of Ifnb1 expression observed in murine Trim33-/- macrophages correlates with abnormal looping of both ICE and the Ifnb1 gene to a 100 kb downstream region overlapping the Ptplad2/Hacd4 gene. This region is a predicted myeloid super-enhancer in which we could characterize 3 myeloid-specific active enhancers, one of which (E5) increases the response of the Ifnb1 promoter to activation. In humans, the orthologous region contains several single nucleotide polymorphisms (SNPs) known to be associated with decreased expression of IFNB1 in activated monocytes, and loops to the IFNB1 gene. The strongest association is found for the rs12553564 SNP, located in the E5 orthologous region. The minor allele of rs12553564 disrupts a conserved C/EBP-β binding motif, prevents binding of C/EBP-β, and abolishes the activation-induced enhancer activity of E5. Altogether, these results establish a link between a genetic variant preventing binding of a transcription factor and a higher order phenotype, and suggest that the frequent minor allele (around 30\% worldwide) might be associated with phenotypes regulated by IFN-β expression in myeloid cells.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147208', 'doi' => '10.1371/journal.pgen.1009090', 'modified' => '2021-02-19 17:29:34', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 59 => array( 'id' => '4084', 'name' => 'BCG Vaccination Induces Long-Term Functional Reprogramming of HumanNeutrophils.', 'authors' => 'Moorlag, Simone J C F M and Rodriguez-Rosales, Yessica Alina and Gillard,Joshua and Fanucchi, Stephanie and Theunissen, Kate and Novakovic, Borisand de Bont, Cynthia M and Negishi, Yutaka and Fok, Ezio T and Kalafati,Lydia and Verginis, Panayotis and M', 'description' => '<p>The tuberculosis vaccine bacillus Calmette-Guérin (BCG) protects against some heterologous infections, probably via induction of non-specific innate immune memory in monocytes and natural killer (NK) cells, a process known as trained immunity. Recent studies have revealed that the induction of trained immunity is associated with a bias toward granulopoiesis in bone marrow hematopoietic progenitor cells, but it is unknown whether BCG vaccination also leads to functional reprogramming of mature neutrophils. Here, we show that BCG vaccination of healthy humans induces long-lasting changes in neutrophil phenotype, characterized by increased expression of activation markers and antimicrobial function. The enhanced function of human neutrophils persists for at least 3 months after vaccination and is associated with genome-wide epigenetic modifications in trimethylation at histone 3 lysine 4. Functional reprogramming of neutrophils by the induction of trained immunity might offer novel therapeutic strategies in clinical conditions that could benefit from modulation of neutrophil effector function.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33207187', 'doi' => '10.1016/j.celrep.2020.108387', 'modified' => '2021-03-15 17:07:29', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 60 => array( 'id' => '4086', 'name' => 'Macrophage Immune Memory Controls Endometriosis in Mice and Humans.', 'authors' => 'Jeljeli, Mohamed and Riccio, Luiza G C and Chouzenoux, Sandrine and Moresi,Fabiana and Toullec, Laurie and Doridot, Ludivine and Nicco, Carole andBourdon, Mathilde and Marcellin, Louis and Santulli, Pietro and Abrão,Mauricio S and Chapron, Charles and ', 'description' => '<p>Endometriosis is a frequent, chronic, inflammatory gynecological disease characterized by the presence of ectopic endometrial tissue causing pain and infertility. Macrophages have a central role in lesion establishment and maintenance by driving chronic inflammation and tissue remodeling. Macrophages can be reprogrammed to acquire memory-like characteristics after antigenic challenge to reinforce or inhibit a subsequent immune response, a phenomenon termed "trained immunity." Here, whereas bacille Calmette-Guérin (BCG) training enhances the lesion growth in a mice model of endometriosis, tolerization with repeated low doses of lipopolysaccharide (LPS) or adoptive transfer of LPS-tolerized macrophages elicits a suppressor effect. LPS-tolerized human macrophages mitigate the fibro-inflammatory phenotype of endometriotic cells in an interleukin-10 (IL-10)-dependent manner. A history of severe Gram-negative infection is associated with reduced infertility duration and alleviated symptoms, in contrast to patients with Gram-positive infection history. Thus, the manipulation of innate immune memory may be effective in dampening hyper-inflammatory conditions, opening the way to promising therapeutic approaches.</p>', 'date' => '2020-11-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33147452', 'doi' => '10.1016/j.celrep.2020.108325', 'modified' => '2021-03-15 17:14:08', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 61 => array( 'id' => '4050', 'name' => 'UTX/KDM6A suppresses AP-1 and a gliogenesis program during neuraldifferentiation of human pluripotent stem cells.', 'authors' => 'Xu, Beisi and Mulvey, Brett and Salie, Muneeb and Yang, Xiaoyang andMatsui, Yurika and Nityanandam, Anjana and Fan, Yiping and Peng, Jamy C', 'description' => '<p>BACKGROUND: UTX/KDM6A is known to interact and influence multiple different chromatin modifiers to promote an open chromatin environment to facilitate gene activation, but its molecular activities in developmental gene regulation remain unclear. RESULTS: We report that in human neural stem cells, UTX binding correlates with both promotion and suppression of gene expression. These activities enable UTX to modulate neural stem cell self-renewal, promote neurogenesis, and suppress gliogenesis. In neural stem cells, UTX has a less influence over histone H3 lysine 27 and lysine 4 methylation but more predominantly affects histone H3 lysine 27 acetylation and chromatin accessibility. Furthermore, UTX suppresses components of AP-1 and, in turn, a gliogenesis program. CONCLUSIONS: Our findings revealed that UTX coordinates dualistic gene regulation to govern neural stem cell properties and neurogenesis-gliogenesis switch.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32977832', 'doi' => '10.1186/s13072-020-00359-3', 'modified' => '2021-02-19 14:46:42', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 62 => array( 'id' => '4091', 'name' => 'Epigenetic regulation of the lineage specificity of primary human dermallymphatic and blood vascular endothelial cells.', 'authors' => 'Tacconi, Carlotta and He, Yuliang and Ducoli, Luca and Detmar, Michael', 'description' => '<p>Lymphatic and blood vascular endothelial cells (ECs) share several molecular and developmental features. However, these two cell types possess distinct phenotypic signatures, reflecting their different biological functions. Despite significant advances in elucidating how the specification of lymphatic and blood vascular ECs is regulated at the transcriptional level during development, the key molecular mechanisms governing their lineage identity under physiological or pathological conditions remain poorly understood. To explore the epigenomic signatures in the maintenance of EC lineage specificity, we compared the transcriptomic landscapes, histone composition (H3K4me3 and H3K27me3) and DNA methylomes of cultured matched human primary dermal lymphatic and blood vascular ECs. Our findings reveal that blood vascular lineage genes manifest a more 'repressed' histone composition in lymphatic ECs, whereas DNA methylation at promoters is less linked to the differential transcriptomes of lymphatic versus blood vascular ECs. Meta-analyses identified two transcriptional regulators, BCL6 and MEF2C, which potentially govern endothelial lineage specificity. Notably, the blood vascular endothelial lineage markers CD34, ESAM and FLT1 and the lymphatic endothelial lineage markers PROX1, PDPN and FLT4 exhibited highly differential epigenetic profiles and responded in distinct manners to epigenetic drug treatments. The perturbation of histone and DNA methylation selectively promoted the expression of blood vascular endothelial markers in lymphatic endothelial cells, but not vice versa. Overall, our study reveals that the fine regulation of lymphatic and blood vascular endothelial transcriptomes is maintained via several epigenetic mechanisms, which are crucial to the maintenance of endothelial cell identity.</p>', 'date' => '2020-09-01', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32918672', 'doi' => '10.1007/s10456-020-09743-9', 'modified' => '2021-03-17 17:09:36', 'created' => '2021-02-18 10:21:53', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 63 => array( 'id' => '4010', 'name' => 'Combined treatment with CBP and BET inhibitors reverses inadvertentactivation of detrimental super enhancer programs in DIPG cells.', 'authors' => 'Wiese, M and Hamdan, FH and Kubiak, K and Diederichs, C and Gielen, GHand Nussbaumer, G and Carcaboso, AM and Hulleman, E and Johnsen, SA andKramm, CM', 'description' => '<p>Diffuse intrinsic pontine gliomas (DIPG) are the most aggressive brain tumors in children with 5-year survival rates of only 2%. About 85% of all DIPG are characterized by a lysine-to-methionine substitution in histone 3, which leads to global H3K27 hypomethylation accompanied by H3K27 hyperacetylation. Hyperacetylation in DIPG favors the action of the Bromodomain and Extra-Terminal (BET) protein BRD4, and leads to the reprogramming of the enhancer landscape contributing to the activation of DIPG super enhancer-driven oncogenes. The activity of the acetyltransferase CREB-binding protein (CBP) is enhanced by BRD4 and associated with acetylation of nucleosomes at super enhancers (SE). In addition, CBP contributes to transcriptional activation through its function as a scaffold and protein bridge. Monotherapy with either a CBP (ICG-001) or BET inhibitor (JQ1) led to the reduction of tumor-related characteristics. Interestingly, combined treatment induced strong cytotoxic effects in H3.3K27M-mutated DIPG cell lines. RNA sequencing and chromatin immunoprecipitation revealed that these effects were caused by the inactivation of DIPG SE-controlled tumor-related genes. However, single treatment with ICG-001 or JQ1, respectively, led to activation of a subgroup of detrimental super enhancers. Combinatorial treatment reversed the inadvertent activation of these super enhancers and rescued the effect of ICG-001 and JQ1 single treatment on enhancer-driven oncogenes in H3K27M-mutated DIPG, but not in H3 wild-type pedHGG cells. In conclusion, combinatorial treatment with CBP and BET inhibitors is highly efficient in H3K27M-mutant DIPG due to reversal of inadvertent activation of detrimental SE programs in comparison with monotherapy.</p>', 'date' => '2020-08-21', 'pmid' => 'http://www.pubmed.gov/32826850', 'doi' => '10.1038/s41419-020-02800-7', 'modified' => '2020-12-18 13:25:09', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 64 => array( 'id' => '4028', 'name' => 'Methylation in pericytes after acute injury promotes chronic kidneydisease.', 'authors' => 'Chou, YH and Pan, SY and Shao, YH and Shih, HM and Wei, SY andLai, CF and Chiang, WC and Schrimpf, C and Yang, KC and Lai, LC andChen, YM and Chu, TS and Lin, SL', 'description' => '<p>The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury-induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-β1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD.</p>', 'date' => '2020-08-04', 'pmid' => 'http://www.pubmed.gov/32749240', 'doi' => '10.1172/JCI135773.', 'modified' => '2020-12-18 13:25:55', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 65 => array( 'id' => '4011', 'name' => 'Exploring the virulence gene interactome with CRISPR/dCas9 in the humanmalaria parasite.', 'authors' => 'Bryant, JM and Baumgarten, S and Dingli, F and Loew, D and Sinha, A andClaës, A and Preiser, PR and Dedon, PC and Scherf, A', 'description' => '<p>Mutually exclusive expression of the var multigene family is key to immune evasion and pathogenesis in Plasmodium falciparum, but few factors have been shown to play a direct role. We adapted a CRISPR-based proteomics approach to identify novel factors associated with var genes in their natural chromatin context. Catalytically inactive Cas9 ("dCas9") was targeted to var gene regulatory elements, immunoprecipitated, and analyzed with mass spectrometry. Known and novel factors were enriched including structural proteins, DNA helicases, and chromatin remodelers. Functional characterization of PfISWI, an evolutionarily divergent putative chromatin remodeler enriched at the var gene promoter, revealed a role in transcriptional activation. Proteomics of PfISWI identified several proteins enriched at the var gene promoter such as acetyl-CoA synthetase, a putative MORC protein, and an ApiAP2 transcription factor. These findings validate the CRISPR/dCas9 proteomics method and define a new var gene-associated chromatin complex. This study establishes a tool for targeted chromatin purification of unaltered genomic loci and identifies novel chromatin-associated factors potentially involved in transcriptional control and/or chromatin organization of virulence genes in the human malaria parasite.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32816370', 'doi' => 'https://dx.doi.org/10.15252%2Fmsb.20209569', 'modified' => '2020-12-18 13:26:33', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 66 => array( 'id' => '4019', 'name' => 'Targeted bisulfite sequencing for biomarker discovery.', 'authors' => 'Morselli, M and Farrell, C and Rubbi, L and Fehling, HL and Henkhaus, Rand Pellegrini, M', 'description' => '<p>Cytosine methylation is one of the best studied epigenetic modifications. In mammals, DNA methylation patterns vary among cells and is mainly found in the CpG context. DNA methylation is involved in important processes during development and differentiation and its dysregulation can lead to or is associated with diseases, such as cancer, loss-of-imprinting syndromes and neurological disorders. It has been also shown that DNA methylation at the cellular, tissue and organism level varies with age. To overcome the costs of Whole-Genome Bisulfite Sequencing, the gold standard method to detect 5-methylcytosines at a single base resolution, DNA methylation arrays have been developed and extensively used. This method allows one to assess the status of a fraction of the CpG sites present in the genome of an organism. In order to combine the relatively low cost of Methylation Arrays and digital signals of bisulfite sequencing, we developed a Targeted Bisulfite Sequencing method that can be applied to biomarker discovery for virtually any phenotype. Here we describe a comprehensive step-by-step protocol to build a DNA methylation-based epigenetic clock.</p>', 'date' => '2020-08-02', 'pmid' => 'http://www.pubmed.gov/32755621', 'doi' => '10.1016/j.ymeth.2020.07.006', 'modified' => '2020-12-18 13:27:14', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 67 => array( 'id' => '4031', 'name' => 'Battle of the sex chromosomes: competition between X- and Y-chromosomeencoded proteins for partner interaction and chromatin occupancy drivesmulti-copy gene expression and evolution in muroid rodents.', 'authors' => 'Moretti, C and Blanco, M and Ialy-Radio, C and Serrentino, ME and Gobé,C and Friedman, R and Battail, C and Leduc, M and Ward, MA and Vaiman, Dand Tores, F and Cocquet, J', 'description' => '<p>Transmission distorters (TDs) are genetic elements that favor their own transmission to the detriments of others. Slx/Slxl1 (Sycp3-like-X-linked and Slx-like1) and Sly (Sycp3-like-Y-linked) are TDs which have been co-amplified on the X and Y chromosomes of Mus species. They are involved in an intragenomic conflict in which each favors its own transmission, resulting in sex ratio distortion of the progeny when Slx/Slxl1 vs. Sly copy number is unbalanced. They are specifically expressed in male postmeiotic gametes (spermatids) and have opposite effects on gene expression: Sly knockdown leads to the upregulation of hundreds of spermatid-expressed genes, while Slx/Slxl1-deficiency downregulates them. When both Slx/Slxl1 and Sly are knocked-down, sex ratio distortion and gene deregulation are corrected. Slx/Slxl1 and Sly are, therefore, in competition but the molecular mechanism remains unknown. By comparing their chromatin binding profiles and protein partners, we show that SLX/SLXL1 and SLY proteins compete for interaction with H3K4me3-reader SSTY1 (Spermiogenesis-specific-transcript-on-the-Y1) at the promoter of thousands of genes to drive their expression, and that the opposite effect they have on gene expression is mediated by different abilities to recruit SMRT/N-Cor transcriptional complex. Their target genes are predominantly spermatid-specific multicopy genes encoded by the sex chromosomes and the autosomal Speer/Takusan. Many of them have co-amplified with Slx/Slxl1/Sly but also Ssty during muroid rodent evolution. Overall, we identify Ssty as a key element of the X vs. Y intragenomic conflict, which may have influenced gene content and hybrid sterility beyond Mus lineage since Ssty amplification on the Y pre-dated that of Slx/Slxl1/Sly.</p>', 'date' => '2020-07-13', 'pmid' => 'http://www.pubmed.gov/32658962', 'doi' => '10.1093/molbev/msaa175/5870835', 'modified' => '2020-12-18 13:27:51', 'created' => '2020-10-12 14:54:59', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 68 => array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( [maximum depth reached] ) ) ), 'Testimonial' => array(), 'Area' => array() ) $country = 'US' $countries_allowed = array( (int) 0 => 'CA', (int) 1 => 'US', (int) 2 => 'IE', (int) 3 => 'GB', (int) 4 => 'DK', (int) 5 => 'NO', (int) 6 => 'SE', (int) 7 => 'FI', (int) 8 => 'NL', (int) 9 => 'BE', (int) 10 => 'LU', (int) 11 => 'FR', (int) 12 => 'DE', (int) 13 => 'CH', (int) 14 => 'AT', (int) 15 => 'ES', (int) 16 => 'IT', (int) 17 => 'PT' ) $outsource = false $other_formats = array() $edit = '' $testimonials = '' $featured_testimonials = '' $related_products = '<li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/1-5-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201140</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: ADD TO CART MODAL --><div id="cartModal-3047" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <form action="/en/carts/add/3047" id="CartAdd/3047Form" method="post" accept-charset="utf-8"><div style="display:none;"><input type="hidden" name="_method" value="POST"/></div><input type="hidden" name="data[Cart][product_id]" value="3047" id="CartProductId"/> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <p>Add <input name="data[Cart][quantity]" placeholder="1" value="1" min="1" style="width:60px;display:inline" type="number" id="CartQuantity" required="required"/> <strong> Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico</strong> to my shopping cart.</p> <div class="row"> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="checkout" id="checkout" value="checkout" type="submit">Checkout</button> </div> <div class="small-6 medium-6 large-6 columns"> <button class="alert small button expand" onclick="$(this).addToCart('Tube holder for 1.5 ml tubes - Bioruptor<sup>®</sup> Pico', 'B01201140', '1850', $('#CartQuantity').val());" name="keepshop" id="keepshop" type="submit">Keep shopping</button> </div> </div> </div> </div> </form><a class="close-reveal-modal" aria-label="Close">×</a></div><!-- END: ADD TO CART MODAL --><a href="#" id="1-5-ml-tube-holder-dock-for-bioruptor-pico" data-reveal-id="cartModal-3047" class="" style="color:#B21329"><i class="fa fa-cart-plus"></i></a> </div> </div> <div class="small-12 columns" > <h6 style="height:60px">Tube holder for 1.5 ml tubes - Bioruptor® Pico</h6> </div> </div> </li> <li> <div class="row"> <div class="small-12 columns"> <a href="/en/p/0-65-ml-tube-holder-dock-for-bioruptor-pico"><img src="/img/product/shearing_technologies/tube-holder-pico-2.jpg" alt="Bioruptor Pico Tube Holder" class="th"/></a> </div> <div class="small-12 columns"> <div class="small-6 columns" style="padding-left:0px;padding-right:0px;margin-top:-6px;margin-left:-1px"> <span class="success label" style="">B01201143</span> </div> <div class="small-6 columns text-right" style="padding-left:0px;padding-right:0px;margin-top:-6px"> <!--a href="#" style="color:#B21329"><i class="fa fa-info-circle"></i></a--> <!-- BEGIN: QUOTE MODAL --><div id="quoteModal-3048" class="reveal-modal small" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog"> <div class="row"> <div class="small-12 medium-12 large-12 columns"> <h3>Get a quote</h3><p class="lead">You are about to request a quote for <strong>Tube holder for 0.65 ml tubes - Bioruptor<sup>®</sup> Pico</strong>. 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=> '1 pack', 'catalog_number' => 'B01200016', 'old_catalog_number' => 'O-ring-15', 'sf_code' => 'B01200016-', 'type' => 'ACC', 'search_order' => '01-Accessory', 'price_EUR' => '300', 'price_USD' => '350', 'price_GBP' => '250', 'price_JPY' => '46995', 'price_CNY' => '', 'price_AUD' => '875', 'country' => 'ALL', 'except_countries' => 'None', 'quote' => false, 'in_stock' => false, 'featured' => false, 'no_promo' => false, 'online' => true, 'master' => true, 'last_datasheet_update' => '0000-00-00', 'slug' => '15-ml-sonication-accessories-for-bioruptor-standard-plus-pico-1-pack', 'meta_title' => '15 ml sonication accessories for Bioruptor® Standard & Plus & Pico', 'meta_keywords' => '', 'meta_description' => '15 ml sonication accessories for Bioruptor® Standard & Plus & Pico', 'modified' => '2022-01-25 04:00:28', 'created' => '2015-06-29 14:08:20', 'ProductsRelated' => array( 'id' => '4591', 'product_id' => '3046', 'related_id' => '1796' ), 'Image' => array( (int) 0 => array( 'id' => '116', 'name' => 'product/shearing_technologies/B01200016_tube_holder.jpg', 'alt' => 'some alt', 'modified' => '2015-06-10 17:28:55', 'created' => '2015-06-10 17:28:55', 'ProductsImage' => array( [maximum depth reached] ) ) ) ) $list = '<div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-1.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-2.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-3.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-4.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B01080000-5.jpg" /></div><div><img src="https://www.diagenode.com/img/product/shearing_technologies/B010600010.jpg" /></div>' $img = array( 'id' => '1772', 'name' => 'product/shearing_technologies/B010600010.jpg', 'alt' => 'B010600010', 'modified' => '2018-02-14 15:41:46', 'created' => '2018-02-14 15:41:46', 'ProductsImage' => array( 'id' => '1093', 'product_id' => '3046', 'image_id' => '1772' ) ) $rrbs_service = array( (int) 0 => (int) 1894, (int) 1 => (int) 1895 ) $chipseq_service = array( (int) 0 => (int) 2683, (int) 1 => (int) 1835, (int) 2 => (int) 1836, (int) 3 => (int) 2684, (int) 4 => (int) 1838, (int) 5 => (int) 1839, (int) 6 => (int) 1856 ) $labelize = object(Closure) { } $old_catalog_number = '' $label = '<img src="/img/banners/banner-customizer-back.png" alt=""/>' $protocol = array( 'id' => '73', 'name' => 'DNA shearing guide', 'description' => '<p>DNA shearing for Next-Generation Sequencing with the Bioruptor Pico</p>', 'image_id' => null, 'type' => 'Protocol', 'url' => 'files/protocols/protocol-dna-shearing-bioruptor-pico.pdf', 'slug' => 'protocol-dna-shearing-bioruptor-pico', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2020-08-11 10:16:00', 'created' => '0000-00-00 00:00:00', 'ProductsProtocol' => array( 'id' => '241', 'product_id' => '3046', 'protocol_id' => '73' ) ) $document = array( 'id' => '1170', 'name' => 'Critical steps for Bioruptor® maintenance and efficient shearing', 'description' => '', 'image_id' => null, 'type' => 'Document', 'url' => 'files/products/shearing_technology/critical-steps-bioruptor-web.pdf', 'slug' => 'critical-steps-bioruptor-maintenance', 'meta_keywords' => '', 'meta_description' => '', 'modified' => '2023-08-31 14:27:41', 'created' => '2023-08-31 14:27:41', 'ProductsDocument' => array( 'id' => '3264', 'product_id' => '3046', 'document_id' => '1170' ) ) $publication = array( 'id' => '4549', 'name' => 'BET protein inhibition sensitizes glioblastoma cells to temozolomidetreatment by attenuating MGMT expression', 'authors' => 'Tancredi A. et al.', 'description' => '<p>Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of g-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylGuanin-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50\% of patients whose glioblastoma exert an unmethylated MGMT promoter.</p>', 'date' => '0000-00-00', 'pmid' => 'https://www.researchsquare.com/article/rs-1832996/v1', 'doi' => '10.21203/rs.3.rs-1832996/v1', 'modified' => '2022-11-24 10:06:26', 'created' => '2022-11-24 08:49:52', 'ProductsPublication' => array( 'id' => '6424', 'product_id' => '3046', 'publication_id' => '4549' ) ) $externalLink = ' <a href="https://www.researchsquare.com/article/rs-1832996/v1" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755 View::_evaluate() - CORE/Cake/View/View.php, line 971 View::_render() - CORE/Cake/View/View.php, line 933 View::render() - CORE/Cake/View/View.php, line 473 Controller::render() - CORE/Cake/Controller/Controller.php, line 963 Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 200 Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167 [main] - APP/webroot/index.php, line 118
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