MicroPlex Library Preparation Kit v3

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<li><strong>Reduce potential bias</strong> - few PCR amplification cycles needed</li>
<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
<li><strong>Great multiplexing flexibility</strong> with 24 dual indexes (8 nt)</li>
<li><strong>Validated with the IP-<a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit">Star<sup>&reg;</sup></a></strong><a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit"> Automated Platform</a></li>
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<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
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<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
</div>
</li>
</ul>
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<li><strong>1 tube</strong>, <strong>2 hours</strong>, <strong>3 steps</strong> protocol</li>
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<li><strong>Reduce potential bias</strong> - few PCR amplification cycles needed</li>
<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
<li><strong>Great multiplexing flexibility</strong> with 24 dual indexes (8 nt)</li>
<li><strong>Validated with the IP-<a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit">Star<sup>&reg;</sup></a></strong><a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit"> Automated Platform</a></li>
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<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
<div id="first" class="content">
<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
</div>
</li>
</ul>
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<p>Diagenode&rsquo;s <strong>MicroPlex Library Preparation Kits v3</strong> have been extensively validated for ChIP-seq samples and are optimized to generate DNA libraries with high molecular complexity from the lowest input amounts &ndash; down to 50 pg. The kit MicroPlex v3 includes all buffers and enzymes necessary for the library preparation. For flexibility of the choice different formats of compatible primer indexes are available separately:</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns">C05010003 - 24 Dual indexes for MicroPlex Kit v3 /48 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1">C05010004 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set I /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2">C05010005 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set II /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3">C05010006 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set III /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4">C05010007 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV /96 rxns</a></li>
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<p style="padding-left: 30px;">NEW! Unique dual indexes :</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1">C05010008 - 24 UDI for MicroPlex Kit v3 - Set I</a></li>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2">C05010009 - 24 UDI for MicroPlex Kit v3 - Set II</a></li>
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<p>Read more about <a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">library preparation for ChIP-seq</a></p>
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<li><strong>1 tube</strong>, <strong>2 hours</strong>, <strong>3 steps</strong> protocol</li>
<li><strong>Input</strong>: 50 pg &ndash; 50 ng</li>
<li><strong>Reduce potential bias</strong> - few PCR amplification cycles needed</li>
<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
<li><strong>Great multiplexing flexibility</strong> with 24 dual indexes (8 nt)</li>
<li><strong>Validated with the IP-<a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit">Star<sup>&reg;</sup></a></strong><a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit"> Automated Platform</a></li>
</ul>
<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
<div id="first" class="content">
<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
</div>
</li>
</ul>
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			'meta_description' => 'MicroPlex Library Preparation Kits v3 have been extensively validated for ChIP-seq samples and are optimized to generate DNA libraries with high molecular complexity from the lowest input amounts – down to 50 pg.',
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<div class="small-12 medium-12 large-12 columns">
<p><span style="font-weight: 400;">Most of the major next-generation sequencing platforms require ligation of specific adaptor oligos to </span><a href="../applications/dna-rna-shearing"><span style="font-weight: 400;">fragmented DNA or RNA</span></a><span style="font-weight: 400;"> prior to sequencing</span></p>
<p><span style="font-weight: 400;">After input DNA has been fragmented, it is end-repaired and blunt-ended</span><span style="font-weight: 400;">. The next step is a A-tailing in which dAMP is added to the 3&acute; end of the blunt phosphorylated DNA fragments to prevent concatemerization and to allow the ligation of adaptors with complementary dT overhangs. In addition, barcoded adapters can be incorporated to facilitate multiplexing prior to or during amplification.</span></p>
<center><img src="https://www.diagenode.com/img/categories/library-prep/flux.png" /></center>
<p><span style="font-weight: 400;">Diagenode offers a comprehensive product portfolio for library preparation:<br /></span></p>
<strong><a href="https://www.diagenode.com/en/categories/Library-preparation-for-RNA-seq">D-Plex&nbsp;RNA-seq Library Preparation Kits</a></strong><br />
<p><span style="font-weight: 400;">Diagenode&rsquo;s new RNA-sequencing solutions utilize the innovative c</span><span style="font-weight: 400;">apture and a</span><span style="font-weight: 400;">mplification by t</span><span style="font-weight: 400;">ailing and s</span><span style="font-weight: 400;">witching&rdquo;</span><span style="font-weight: 400;">, a ligation-free method to produce DNA libraries for next generation sequencing from low input amounts of RNA. </span><span style="font-weight: 400;"></span><a href="../categories/Library-preparation-for-RNA-seq">Learn more</a></p>
<strong><a href="../categories/library-preparation-for-ChIP-seq">ChIP-seq and DNA sequencing library preparation solutions</a></strong><br />
<p><span style="font-weight: 400;">Our kits have been optimized for DNA library preparation used for next generation sequencing for a wide range of inputs. Using a simple three-step protocols, our</span><a href="http://www.diagenode.com/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><span style="font-weight: 400;"> </span></a><span style="font-weight: 400;">kits are an optimal choice for library preparation from DNA inputs down to 50 pg.&nbsp;</span><a href="../categories/library-preparation-for-ChIP-seq">Learn more</a></p>
<a href="../p/bioruptor-pico-sonication-device"><span style="font-weight: 400;"></span><strong>Bioruptor Pico - short fragments</strong></a><a href="../categories/library-preparation-for-ChIP-seq-and-DNA-sequencing"><span style="font-weight: 400;"></span></a><br />
<p><span style="font-weight: 400;"></span><span style="font-weight: 400;">Our well-cited Bioruptor Pico is the shearing device of choice for chromatin and DNA fragmentation. Obtain uniform and tight fragment distributions &nbsp;between 150bp -2kb. </span><a href="../p/bioruptor-pico-sonication-device">Learn more</a></p>
<strong><a href="../p/megaruptor2-1-unit"><span href="../p/bioruptor-pico-sonication-device">Megaruptor</span>&reg; - long fragments</a></strong><a href="../p/bioruptor-pico-sonication-device"><span style="font-weight: 400;"></span></a><a href="../categories/library-preparation-for-ChIP-seq-and-DNA-sequencing"><span style="font-weight: 400;"></span></a><br />
<p><span style="font-weight: 400;"></span><span style="font-weight: 400;">The Megaruptor is designed to shear DNA from 3kb-75kb for long-read sequencing.&nbsp; <a href="../p/megaruptor2-1-unit">Learn more</a></span></p>
<span href="../p/bioruptor-pico-sonication-device"></span><span style="font-weight: 400;"></span></div>
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<div class="large-12 columns text-justify">
<p>Library preparation following ChIP can be challenging due to the limited amount of DNA recovered after ChIP. Diagenode has developed the optimal solutions for ChIP-seq using two different approaches: the ligation-based library preparation on purified DNA or the tagmentation-based ChIPmentation.</p>
</div>
</div>
<div class="row extra-spaced">
<div class="large-12 columns"><center><a href="https://www.diagenode.com/en/pages/form-microplex-promo" target="_blank"></a></center></div>
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<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div id="portal" class="main-portal">
<div class="portal-inner"><nav class="portal-nav">
<ul data-tab="" class="tips-menu">
<li><a href="#panel1" class="tips portal button">Ligation-based library prep</a></li>
<li><a href="#panel2" class="tips portal button">ChIPmentation</a></li>
<li><a href="#panel3" class="tips portal button">Kit choice guide</a></li>
<li><a href="#panel4" class="tips portal button">Resources</a></li>
<li><a href="#panel5" class="tips portal button">FAQs</a></li>
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<div class="content active" id="panel1">
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<div class="small-12 medium-12 large-12 columns">
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v5" style="color: #13b29c;"><i class="fa fa-caret-right"></i> Standard input library prep</a>
<div id="v5" class="content">
<div class="small-12 medium-12 large-12 columns">
<p>The <strong>iDeal Library Preparation Kit</strong> reliably converts DNA into indexed libraries for next-generation sequencing, with input amounts down to <strong>5 ng</strong>. Our kit offers a simple and fast workflow, high yields, and ready-to-sequence DNA on the Illumina platform.</p>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> <strong>Sample</strong>: Fragmented dsDNA</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Input</strong>: 5 ng &ndash; 1 &micro;g</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Fast protocol</strong>: 3 hours</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Easy processing</strong>: 3 steps</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Indexing</strong>: single indexes for multiplexing up to 24 samples</li>
<li><i class="fa fa-arrow-circle-right"></i> Manual and automated protocols available</li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<ul class="square">
<li>MeDIP-seq library prep</li>
<li>Genomic DNA sequencing</li>
<li>High input ChIP-seq</li>
</ul>
</div>
<div class="extra-spaced">
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010020</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" style="color: #b21329;" target="_blank">iDeal Library Preparation Kit x24 (incl. Index Primer Set 1)</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010021</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" style="color: #b21329;" target="_blank">Index Primer Set 2 (iDeal Lib. Prep Kit x24)</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
</li>
</ul>
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v4" style="color: #13b29c;"><i class="fa fa-caret-right"></i> Low input library prep</a>
<div id="v4" class="content active"><center><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" target="_blank"><img src="https://www.diagenode.com/img/banners/banner-microplex-v3-580.jpg" class="extra-spaced" /></a></center>
<div align="center"><a href="https://www.diagenode.com/pages/form-microplex3" class="center alert radius button extra-spaced"><i class="fa fa-info"></i> Contact us</a></div>
<div class="extra-spaced">
<p>Diagenode&rsquo;s <strong>MicroPlex Library Preparation kits</strong> have been extensively validated for ChIP-seq samples. Generated libraries are compatible with single-end or paired-end sequencing. MicroPlex chemistry (using stem-loop adapters ) is specifically developed and optimized to generate DNA libraries with high molecular complexity from the lowest input amounts. Only <strong>50 pg to 50 ng</strong> of fragmented double-stranded DNA is required for library preparation. The entire <strong>three-step workflow</strong> takes place in a <strong>single tube</strong> or well in about <strong>2 hours</strong>. No intermediate purification steps and no sample transfers are necessary to prevent handling errors and loss of valuable samples.</p>
</div>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> <strong>Sample</strong>: Fragmented dsDNA</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Low input</strong>: 50 pg &ndash; 50 ng</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Fast protocol</strong>: 2 hours</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Easy processing</strong>: 3 steps in 1 tube</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>No intermediate purification</strong></li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
<li><i class="fa fa-arrow-circle-right"></i> Manual and automated protocols available</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<ul class="square">
<li>ChIP-seq library prep from ChIP-derived DNA</li>
<li>Low input DNA sequencing</li>
</ul>
</div>
<h2>Two versions are available:</h2>
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v2" style="color: #13b29c;"><i class="fa fa-caret-right"></i> MicroPlex Library Preparation Kit v2 with single indexes</a>
<div id="v2" class="content">
<p>The MicroPlex Library Preparation Kit v2 contains all necessary reagents including single indexes for multiplexing up to 48 samples using single barcoding.</p>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010012</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v2 (12 indexes)</a></td>
<td class="format">12 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</li>
<li class="accordion-navigation"><a href="#v3" style="color: #13b29c;"><i class="fa fa-caret-right"></i> MicroPlex Library Preparation Kit v3 with dual indexes &nbsp;&nbsp;<strong><span class="diacol">NEW!</span></strong></a>
<div id="v3" class="content active">
<p>In this version the library preparation reagents and the dual indexes are available separately allowing for the flexibility choosing the number of indexes. MicroPlex v3 has multiplexing capacities up to 384 samples.</p>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010001</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v3 /48 rxns</a></td>
<td class="format">48 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010002</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v3 /96 rxns</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
<h4>DUAL INDEXES</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010003</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" style="color: #b21329;" target="_blank">24 Dual indexes for MicroPlex Kit v3</a></td>
<td class="format">48 rxns</td>
<td><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010004</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set I</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010005</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set II</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010006</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set III</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010007</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</li>
</ul>
</div>
</li>
</ul>
</div>
</div>
</div>
<div class="content active" id="panel2">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<p>The TAG Kit for ChIPmentation offers an optimized ChIP-seq library preparation solution based on tagmentation. This kit includes reagents for tagmentation-based library preparation integrated in the IP and is compatible with any ChIP protocol based on magnetic beads. The primer indexes for multiplexing&nbsp;must be purchased separately and are available as a reference: <a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" target="_blank">24 SI for ChIPmentation</a>, Cat. No. C01011031. Alternatively, for histone marks, Diagenode proposes the complete solution (including all buffers for ChIP, tagmentation and multiplexing): <a href="https://www.diagenode.com/en/p/manual-chipmentation-kit-for-histones-24-rxns" target="_blank">ChIPmentation for Histones</a>.</p>
</div>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> Sample: chromatin-antibody-magnetic beads complexes</li>
<li><i class="fa fa-arrow-circle-right"></i> Input: chromatin from 5 K &ndash; 4 M cells</li>
<li><i class="fa fa-arrow-circle-right"></i> Easy and fast protocol</li>
<li><i class="fa fa-arrow-circle-right"></i> Compatible with any ChIP protocol based on magnetic beads</li>
<li><i class="fa fa-arrow-circle-right"></i> No adapter dimers</li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<p class="lead"><em><strong>TAG kit for ChIPmentation</strong></em></p>
<ul class="square">
<li>ChIPmentation library preparation</li>
</ul>
<p class="lead"><em><strong>24 SI for for ChIPmentation</strong></em></p>
<ul class="square">
<li>ChIPmentation library preparation</li>
<li>Tagmentation-based library preparation methods like ATAC-seq, CUT&amp;Tag</li>
</ul>
</div>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C01011030</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" style="color: #b21329;" target="_blank">TAG Kit for ChIPmentation</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C01011031</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" style="color: #b21329;" target="_blank">24 SI for ChIPmentation</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
<div class="content" id="panel3">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<h3 class="text-center diacol"><em>How to choose your library preparation kit?</em></h3>
</div>
<table class="noborder">
<tbody>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Sample</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Chromatin-antibody-beads complex</p>
</td>
<td colspan="2">
<p class="text-center" style="font-size: 15px;">Purified DNA</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Purified DNA</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td colspan="2"><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Application</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">ChIPmentation</p>
</td>
<td colspan="2">
<p class="text-center" style="font-size: 15px;">ChIP-seq library prep<br /> Low input DNA sequencing</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">MeDIP-seq library prep<br /> Genomic DNA sequencing<br /> High input ChIP-seq</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td colspan="2"><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Input</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Chromatin: 5 K to 4 M cells</p>
</td>
<td colspan="2&quot;">
<p class="text-center" style="font-size: 15px;">DNA: 50 pg &ndash; 50 ng</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">DNA: 5 ng &ndash; 1 &micro;g</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow-45-left.png" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow-45-right.png" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Multiplexing</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 24 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 384 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 48 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 24 samples</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Indexes</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Dual indexes (DI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Kit</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>TAG Kit for ChIPmentation</strong><br /> (indexes not included in the kit)</p>
<p class="text-center"><strong>Kit</strong><br /> <a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" target="_blank">C01011030 &ndash; 24 rxns</a></p>
<p class="text-center"><strong>Single indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" target="_blank">C01011031 &ndash; 24 SI/24 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>MicroPlex Library Preparation Kit v3</strong><br />(dual indexes not included in the kit)</p>
<p class="text-center"><strong>Kit</strong><br /> <a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" target="_blank">C05010001 - 48 rxns</a><br /> <a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" target="_blank">C05010002 - 96 rxns</a></p>
<br />
<p class="text-center"><strong>Unique dual indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1" target="_blank">C05010008 - Set I 24 UDI / 24 rxns</a><br /> <a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2" target="_blank">C05010009 - Set II 24 UDI/ 24 rxns</a></p>
<p class="text-center"><strong>Dual indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" target="_blank">C05010003 - 24 DI/ 48 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" target="_blank">C05010004 - Set I 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" target="_blank">C05010005 - Set II 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" target="_blank">C05010006 - Set III 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" target="_blank">C05010007 - Set IV 96 DI/ 96 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>MicroPlex Library Preparation Kit v2</strong><br />(single indexes included in the kit)</p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" target="_blank">C05010012 - 12 SI/ 12 rxns</a><br /> <a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x48-12-indices-48-rxns" target="_blank">C05010013 - 12 SI/ 48 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>iDeal Library Preparation Kit</strong><br />(Set 1 of indexes included in the kit)</p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" target="_blank">C05010020 - 12 SI/ 24 rxns</a></p>
<p class="text-center" style="font-size: 15px;"><strong>Index Primer Set 2</strong></p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" target="_blank">C05010021 - 12 SI/ 24 rxns</a></p>
</td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
<div class="content" id="panel4">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<p>Combined chromatin immunoprecipitation and next-generation sequencing (ChIP-seq) has become the gold standard to investigate genome-wide epigenetic profiles. However, ChIP from a limited amount of cells has been a challenge. Here we provide a complete and robust workflow solution for successful ChIP-seq from small numbers of cells using the True MicroChIP kit and MicroPlex Library Preparation kit.</p>
<blockquote><span class="label-green" style="margin-bottom: 16px; margin-left: -22px;">APPLICATION NOTE</span>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><center><img src="https://www.diagenode.com/img/categories/microplex/chip-efficiency-on-10000-cells.jpg" /></center>
<p><small><em>ChIP efficiency on 10,000 cells</em></small></p>
</div>
<div class="small-12 medium-6 large-6 columns">
<p><strong>From minuscule amounts to magnificent results:</strong><br /> reliable ChIP-seq data from 10,000 cells with the True MicroChIP&trade; and the MicroPlex Library Preparation&trade; kits.</p>
<a href="https://www.diagenode.com/files/application_notes/True_MicroChIP_and_MicroPlex_kits_Application_Note.pdf" class="details small button" target="_blank">DOWNLOAD</a></div>
</div>
</blockquote>
<blockquote><span class="label-green" style="margin-bottom: 16px; margin-left: -22px;">APPLICATION NOTE</span>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><center><img src="https://www.diagenode.com/img/categories/microplex/quality-control-check.jpg" /></center>
<p class="text-left"><small><em>Quality control check of a ChIP-seq library on the Fragment Analyzer. High Efficiency ChIP performed on 10,000 cells</em></small></p>
</div>
<div class="small-12 medium-6 large-6 columns">
<p class="text-left"><strong>Best Workflow Practices for ChIP-seq Analysis with Small Samples</strong></p>
<a href="https://www.diagenode.com/files/application_notes/Diagenode_AATI_Joint.pdf" class="details small button" target="_blank">DOWNLOAD</a></div>
</div>
</blockquote>
</div>
</div>
</div>
<div class="content" id="panel5">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<h2>TAG Kit for ChIPmentation</h2>
<ol>
<li><strong>What is the difference between tagmentation and ChIPmentation?</strong><br />Tagmentation is a reaction where an enzyme (a transposase) cleaves DNA and incorporates sequencing adaptors at the ends of the fragments in one step. In our ChIPmentation technology we combine chromatin immunoprecipitation and tagmentation in one streamlined workflow where the tagmentation step occurs directly on chromatin.<br /><br /></li>
<li><strong>What is the expected concentration of ChIPmentation libraries?</strong><br />The concentration of libraries that you need to reach will depend on the sensitivity of the machine and kits that you will use to perform the quality control and the sequencing of your libraries. Usually a concentration of 4-8 ng/&mu;l is enough for a quality control using the Qubit High Sensitivity assay (ThermoFischer Scientific) and the High Sensitivity chip for BioAnalyzer (Agilent) and for sequencing on Illumina HiSeq3000/4000.<br /><br /></li>
<li><strong>Does the ChIPmentation approach work on plants?</strong><br />Our ChIPmentation solution has been validated on human cells and we do not have any data on plants. It should be compatible. We would recommend using our Universal Plant ChIP Kit in combination with the TAG Kit for ChIPmentation and the 24 SI for ChIPmentation.<br /><br /></li>
<li><strong>What is the size of the fragments after the tagmentation?</strong><br />The size of the fragments at the end of the ChIPmentation protocol can vary depending on many parameters like the shearing efficiency, the antibody used or the tagmentation time. However, with our standard protocol we usually obtain a library peak which is around 200-300 bp (see example of results at the end of the manual). If many fragments larger than 500 bp are present , the best would be to contact your sequencing provider to ask what their requirements are, because it can vary depending on the sequencer. If you want to remove the large fragments you can use the size selection protocol described in the manual.<br /><br /></li>
<li><strong>What is the size of the adapters?</strong><br />The sum of the adapters is 128 bp.</li>
</ol>
</div>
<div class="extra-spaced">
<h2>MicroPlex Library Preparation Kit</h2>
<ol>
<li><strong>Can I use the available Illumina primers and validate them with the MicroPlex Kit v2?</strong><br /> Although the final flanking sequences of MicroPlex are the same as those used by Illumina, the PCR primers are not identical and part of them is supplied with the buffer. For this reason Illumina primers will not work as substitute.<br /><br /></li>
<li><strong>The BioAnalyzer profile of purified library shows the presence of low molecular weight peaks (primers/adaptors) in the samples. Should I re- purify the samples or they can be used directly to the sequencing? If the second purification is recommended, which ratio sample/AMPure beads should I use?</strong><br /> You can do a second round of purification using 1:1 ratio of AMPure beads to sample and this should get rid of the majority of the dimers.<br /><br /></li>
<li><strong>I am going to use the MicroPlex Library Preparation Kit v2 on ChIP samples . Our thermocycler has ramp rate 1.5&deg;/s max while the protocol recommends using a ramp rate 3 to 5&deg;/s. How would this affect the library prep?</strong><br /> We have not used a thermocycler with a ramp rate of 1.5 &deg;C, which seems faster than most of thermocyclers. Too fast of a ramp rate may affect the primer annealing and ligation steps.<br /><br /></li>
<li><strong>What is the function of the replication stop site in the adapter loops?</strong><br /> The replication stop site in the adaptor loops function to stop the polymerase from continuing to copy the rest of the stem loop.<br /><br /></li>
<li><strong>I want to do ChIP-seq. Which ChIP-seq kit can I use for sample preparation prior to Microplex Library Preparation Kit v2?</strong><br /> In our portfolio there are several ChIP-seq kits compatible with Microplex Library Preparation Kit v2. Depending on your sample type and target studied you can use the following kits: iDeal ChIP-seq Kit for Transcription Factors (Cat. No. C01010055), iDeal ChIP-seq Kit for Histones (Cat. No. C01010051), True MicroChIP kit (Cat. No. C01010130), Universal Plant ChIP-seq Kit (Cat. No. C01010152). All these kits exist in manual and automated versions.<br /><br /></li>
<li><strong>Is Microplex Library Preparation Kit v2 compatible with exome enrichment methods?</strong><br /> Microplex Library Preparation Kit v2 is compatible with major exome and target enrichment products, including Agilent SureSelect<sup>&reg;</sup>, Roche NimbleGen<sup>&reg;</sup> SeqCap<sup>&reg;</sup> EZ and custom panels.<br /><br /></li>
<li><strong>What is the nick that is mentioned in the kit method overview?</strong><br /> The nick is simply a gap between a stem adaptor and 3&rsquo; DNA end, as shown on the schema in the kit method overview.<br /><br /></li>
<li><strong>Are the indexes of the MicroPlex library preparation kit v2 located at i5 or i7?</strong><br /> The libraries generated with the MicroPlex kit v2 contain indices located at i7.<br /><br /></li>
<li><strong>Is there a need to use custom index read primers for the sequencing to read the 8nt iPCRtags?</strong><br /> There is no need for using custom Sequencing primer to sequence MicroPlex libraires. MicroPlex libraries can be sequenced using standard Illumina Sequencing kits and protocols.<br /><br /></li>
<li><strong>What is the advantage of using stem-loop adapter in the MicroPlex kit?</strong><br /> There are several advantages of using stem-loop adaptors. First of all, stem-loop adaptors prevent from self-ligation thus increases the ligation efficiency between the adapter and DNA fragment. Moreover, the background is reduced using ds adaptors with no single-stranded tails. Finally, adaptor-adaptor ligation is reduced using blocked 5&rsquo; ends.<br /><br /></li>
</ol>
</div>
<div class="extra-spaced">
<h2>IDeal Library Preparation Kit</h2>
<ol>
<li><strong>Are the index from the iDeal library Prep kit compatible with the MicroPlex library prep kit?</strong><br /> No, it is important to use only the indexes provided in the MicroPlex kit to ensure proper library preparation with this kit</li>
</ol>
</div>
</div>
</div>
</div>
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			'description' => '<p><span>Anti-PD-L1-based combination immunotherapy has become the first-line treatment for unresectable hepatocellular carcinoma (HCC). However, the objective response rate is lower than 40%, highlighting the need to identify mechanisms of tolerance to immune checkpoint inhibitors and accurate biomarkers of response. Here, we employed next-generation sequencing to analyze HCC samples from 10 patients receiving anti-PD-L1 therapy. Activation of the renin-angiotensin system was elevated in nonresponders compared with responders, and ACE2 expression was significantly downregulated in nonresponders. ACE2 deficiency promoted HCC development and anti-PD-L1 resistance, whereas ACE2 overexpression inhibited HCC progression in immune competent mice. Mass cytometry by time of flight (CyTOF) revealed that ACE2 deficient murine orthotopic tumor tissues featured elevated M2-like tumor-associated macrophages (TAMs), displayed a CCR5+PD-L1+ immunosuppressive phenotype, and exhibited high VEGF&alpha; expression. ACE2 downregulated tumor intrinsic CCL5 expression by suppressing NF-&kappa;B signaling through the ACE2/angiotensin-(1&ndash;7)/Mas receptor axis. The lower CCL5 levels led to reduced activation of the JAK-STAT3 pathway and suppressed PD-L1 and VEGF&alpha; expression in macrophages, blocking macrophage infiltration and M2-like polarization. Pharmacological targeting of CCR5 using maraviroc enhanced the tumor suppressive effect of anti-PD-L1 therapy. Together, these findings suggest that activation of the ACE2 axis overcomes the immunosuppressive microenvironment of HCC and may serve as an immunotherapeutic target and predictive biomarker of response to PD-L1 blockade.</span></p>',
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			'name' => 'Extracellular vesicle-mediated trafficking of molecular cues during human brain development',
			'authors' => 'Forero A. et al.',
			'description' => '<p><span>Cellular crosstalk is an essential process influenced by numerous factors, including secreted vesicles that transfer nucleic acids, lipids, and proteins between cells. Extracellular vesicles (EVs) have been the center of many studies focusing on neurodegenerative disorders, but whether EVs display cell-type-specific features for cellular crosstalk during neurodevelopment is unknown. Here, using human-induced pluripotent stem cell-derived cerebral organoids, neural progenitors, neurons, and astrocytes, we identify heterogeneity in EV protein content and dynamics in a cell-type-specific and time-dependent manner. Our results support the trafficking of key molecules via EVs in neurodevelopment, such as the transcription factor YAP1, and their localization to differing cell compartments depending on the EV recipient cell type. This study sheds new light on the biology of EVs during human brain development.</span></p>',
			'date' => '2024-10-22',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01106-9',
			'doi' => '10.1016/j.celrep.2024.114755',
			'modified' => '2024-09-23 10:19:53',
			'created' => '2024-09-23 10:19:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 2 => array(
			'id' => '4982',
			'name' => 'The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency',
			'authors' => 'Mathew Sheridan et al.',
			'description' => '<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Background</h3>
<p>The epigenetic factors KAT6A (MOZ/MYST3) and KMT2A (MLL/MLL1) interact in normal hematopoiesis to regulate progenitors&rsquo; self-renewal. Both proteins are recurrently translocated in AML, leading to impairment of critical differentiation pathways in these malignant cells. We evaluated the potential of different KAT6A therapeutic targeting strategies to alter the growth of KAT6A and KMT2A rearranged AMLs.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Methods</h3>
<p>We investigated the action and potential mechanisms of the first-in-class KAT6A inhibitor, WM-1119 in KAT6A and KMT2A rearranged&nbsp;(KAT6Ar and KMT2Ar) AML using cellular (flow cytometry, colony assays, cell growth) and molecular (shRNA knock-down, CRISPR knock-out, bulk and single-cell RNA-seq, ChIP-seq) assays. We also used two novel genetic murine KAT6A models combined with the most common KMT2Ar AML, KMT2A::MLLT3 AML. In these murine models, the catalytic activity of KAT6A, or the whole protein, can be conditionally abrogated or deleted. These models allowed us to compare the effects of specific KAT6A KAT activity inhibition with the complete deletion of the whole protein. Finally, we also tested these therapeutic approaches on human AML cell lines and primary patient AMLs.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Results</h3>
<p>We found that WM-1119 completely abrogated the proliferative and clonogenic potential of KAT6Ar cells<span>&nbsp;</span><i>in vitro.</i><span>&nbsp;</span>WM-1119 treatment was associated with a dramatic increase in myeloid differentiation program. The treatment also decreased stemness and leukemia pathways at the transcriptome level and led to loss of binding of the fusion protein at critical regulators of these pathways. In contrast, our pharmacologic and genetic results indicate that the catalytic activity of KAT6A plays a more limited role in KMT2Ar leukemogenicity, while targeting the whole KAT6A protein dramatically affects leukemic potential in murine KMT2A::MLLT3 AML.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Conclusion</h3>
<p>Our study indicates that inhibiting KAT6A KAT activity holds compelling promise for KAT6Ar AML patients. In contrast, targeted degradation of KAT6A, and not just its catalytic activity, may represent a more appropriate therapeutic approach for KMT2Ar AMLs.</p>',
			'date' => '2024-10-08',
			'pmid' => 'https://jhoonline.biomedcentral.com/articles/10.1186/s13045-024-01610-0',
			'doi' => 'https://doi.org/10.1186/s13045-024-01610-0',
			'modified' => '2024-10-11 10:00:42',
			'created' => '2024-10-11 10:00:42',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 3 => array(
			'id' => '4983',
			'name' => 'Integrated multi-omics analysis of PBX1 in mouse adult neural stem- and progenitor cells identifies a transcriptional module that functionally links PBX1 to TCF3/4',
			'authors' => 'Vera Laub et al.',
			'description' => '<p><span>Developmental transcription factors act in networks, but how these networks achieve cell- and tissue specificity is still poorly understood. Here, we explored pre-B cell leukemia homeobox 1 (PBX1) in adult neurogenesis combining genomic, transcriptomic, and proteomic approaches. ChIP-seq analysis uncovered PBX1 binding to numerous genomic sites. Integration of PBX1 ChIP-seq with ATAC-seq data predicted interaction partners, which were subsequently validated by mass spectrometry. Whole transcriptome spatial RNA analysis revealed shared expression dynamics of&nbsp;</span><em>Pbx1</em><span><span>&nbsp;</span>and interacting factors. Among these were class I bHLH proteins TCF3 and TCF4. RNA-seq following<span>&nbsp;</span></span><em>Pbx1</em><span>,<span>&nbsp;</span></span><em>Tcf3</em><span><span>&nbsp;</span>or<span>&nbsp;</span></span><em>Tcf4</em><span><span>&nbsp;</span>knockdown identified proliferation- and differentiation associated genes as shared targets, while sphere formation assays following knockdown argued for functional cooperativity of PBX1 and TCF3 in progenitor cell proliferation. Notably, while physiological PBX1-TCF interaction has not yet been described, chromosomal translocation resulting in genomic<span>&nbsp;</span></span><em>TCF3::PBX1</em><span><span>&nbsp;</span>fusion characterizes a subtype of acute lymphoblastic leukemia. Introducing<span>&nbsp;</span></span><em>Pbx1</em><span><span>&nbsp;</span>into Nalm6 cells, a pre-B cell line expressing<span>&nbsp;</span></span><em>TCF3</em><span><span>&nbsp;</span>but lacking<span>&nbsp;</span></span><em>PBX1</em><span>, upregulated the leukemogenic genes<span>&nbsp;</span></span><em>BLK</em><span><span>&nbsp;</span>and<span>&nbsp;</span></span><em>NOTCH3</em><span>, arguing that functional PBX1-TCF cooperativity likely extends to hematopoiesis. Our study hence uncovers a transcriptional module orchestrating the balance between progenitor cell proliferation and differentiation in adult neurogenesis with potential implications for leukemia etiology.</span></p>',
			'date' => '2024-10-08',
			'pmid' => 'https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkae864/7815639',
			'doi' => 'https://doi.org/10.1093/nar/gkae864',
			'modified' => '2024-10-11 10:02:42',
			'created' => '2024-10-11 10:02:42',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 4 => array(
			'id' => '4985',
			'name' => 'HNF1β bookmarking involves Topoisomerase 1 activation and DNA topology relaxation in mitotic chromatin',
			'authors' => 'Alessia Bagattin et al.',
			'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HNF1&beta; mitotic site binding is preserved with a specific methanol/formaldehyde ChIP</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">BTBD2, an HNF1&beta; partner, mediates mitosis-specific interaction with TOP1</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">HNF1&beta; recruits TOP1 and induces DNA relaxation around bookmarked HNF1&beta; sites</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">An HNF1&beta; mutation, found in MODY patients, disrupts the interaction with TOP1</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">HNF1&beta; (<i>HNF1B</i>) is a transcription factor frequently mutated in patients with developmental renal disease. It binds to mitotic chromatin and reactivates gene expression after mitosis, a phenomenon referred to as bookmarking. Using a crosslinking method that circumvents the artifacts of formaldehyde, we demonstrate that&nbsp;HNF1&beta; remains associated with chromatin in a sequence-specific way in both interphase and mitosis. We identify an HNF1&beta;-interacting protein, BTBD2, that enables the interaction and activation of Topoisomerase 1 (TOP1) exclusively during mitosis. Our study identifies a shared microhomology domain between HNF1&beta; and TOP1, where a mutation, found in &ldquo;maturity onset diabetes of the young&rdquo; patients, disrupts their interaction. Importantly, HNF1&beta; recruits TOP1 and induces DNA relaxation around HNF1&beta; mitotic chromatin sites, elucidating its crucial role in chromatin remodeling and gene reactivation after mitotic exit. These findings shed light on how HNF1&beta; reactivates target gene expression after mitosis, providing insights into its crucial role in maintenance of cellular identity.</div>
</section>',
			'date' => '2024-10-08',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01156-2',
			'doi' => '10.1016/j.celrep.2024.114805',
			'modified' => '2024-10-14 09:04:44',
			'created' => '2024-10-14 09:04:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 5 => array(
			'id' => '4978',
			'name' => 'RNA polymerase II transcription initiation in holo-TFIID-depleted mouse embryonic stem cells',
			'authors' => 'Hisler V. et al.',
			'description' => '<p><span>The recognition of core promoter sequences by TFIID is the first step in RNA polymerase II (Pol II) transcription initiation. Metazoan holo-TFIID is a trilobular complex, composed of the TATA binding protein (TBP) and 13 TBP-associated factors (TAFs). Why and how TAFs are necessary for the formation of TFIID domains and how they contribute to transcription initiation remain unclear. Inducible TAF7 or TAF10 depletion, followed by comprehensive analysis of TFIID subcomplex formation, chromatin binding, and nascent transcription in mouse embryonic stem cells, result in the formation of a TAF7-lacking TFIID or a minimal core-TFIID complex, respectively. These partial complexes support TBP recruitment at promoters and nascent Pol II transcription at most genes early after depletion, but importantly, TAF10 is necessary for efficient Pol II pausing. We show that partially assembled TFIID complexes can sustain Pol II transcription initiation but cannot replace holo-TFIID over several cell divisions and/or development.</span></p>',
			'date' => '2024-09-30',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01142-2',
			'doi' => 'https://doi.org/10.1016/j.celrep.2024.114791',
			'modified' => '2024-10-04 10:18:22',
			'created' => '2024-10-04 10:18:22',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '4963',
			'name' => 'An atlas of the human liver diurnal transcriptome and its perturbation by hepatitis C virus infection',
			'authors' => 'Mukherji A. et al.',
			'description' => '<p><span>Chronic liver disease and cancer are global health challenges. The role of the circadian clock as a regulator of liver physiology and disease is well established in rodents, however, the identity and epigenetic regulation of rhythmically expressed genes in human disease is less well studied. Here we unravel the rhythmic transcriptome and epigenome of human hepatocytes using male human liver chimeric mice. We identify a large number of rhythmically expressed protein coding genes in human hepatocytes of male chimeric mice, which includes key transcription factors, chromatin modifiers, and critical enzymes. We show that hepatitis C virus (HCV) infection, a major cause of liver disease and cancer, perturbs the transcriptome by altering the rhythmicity of the expression of more than 1000 genes, and affects the epigenome, leading to an activation of critical pathways mediating metabolic alterations, fibrosis, and cancer. HCV-perturbed rhythmic pathways remain dysregulated in patients with advanced liver disease. Collectively, these data support a role for virus-induced perturbation of the hepatic rhythmic transcriptome and pathways in cancer development and may provide opportunities for cancer prevention and biomarkers to predict HCC risk.</span></p>',
			'date' => '2024-08-29',
			'pmid' => 'https://www.nature.com/articles/s41467-024-51698-8',
			'doi' => 'https://doi.org/10.1038/s41467-024-51698-8',
			'modified' => '2024-09-02 10:17:48',
			'created' => '2024-09-02 10:17:48',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '4968',
			'name' => 'Innate immune training restores pro-reparative myeloid functions to promote remyelination in the aged central nervous system',
			'authors' => 'Tiwari V. et al.',
			'description' => '<p><span>The reduced ability of the central nervous system to regenerate with increasing age limits functional recovery following demyelinating injury. Previous work has shown that myelin debris can overwhelm the metabolic capacity of microglia, thereby impeding tissue regeneration in aging, but the underlying mechanisms are unknown. In a model of demyelination, we found that a substantial number of genes that were not effectively activated in aged myeloid cells displayed epigenetic modifications associated with restricted chromatin accessibility. Ablation of two class I histone deacetylases in microglia was sufficient to restore the capacity of aged mice to remyelinate lesioned tissue. We used Bacillus Calmette-Guerin (BCG), a live-attenuated vaccine, to train the innate immune system and detected epigenetic reprogramming of brain-resident myeloid cells and functional restoration of myelin debris clearance and lesion recovery. Our results provide insight into aging-associated decline in myeloid function and how this decay can be prevented by innate immune reprogramming.</span></p>',
			'date' => '2024-07-24',
			'pmid' => 'https://www.cell.com/immunity/fulltext/S1074-7613(24)00348-0',
			'doi' => '',
			'modified' => '2024-09-02 17:05:54',
			'created' => '2024-09-02 17:05:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '4954',
			'name' => 'A multiomic atlas of the aging hippocampus reveals molecular changes in response to environmental enrichment',
			'authors' => 'Perez R. F. at al. ',
			'description' => '<p><span>Aging involves the deterioration of organismal function, leading to the emergence of multiple pathologies. Environmental stimuli, including lifestyle, can influence the trajectory of this process and may be used as tools in the pursuit of healthy aging. To evaluate the role of epigenetic mechanisms in this context, we have generated bulk tissue and single cell multi-omic maps of the male mouse dorsal hippocampus in young and old animals exposed to environmental stimulation in the form of enriched environments. We present a molecular atlas of the aging process, highlighting two distinct axes, related to inflammation and to the dysregulation of mRNA metabolism, at the functional RNA and protein level. Additionally, we report the alteration of heterochromatin domains, including the loss of bivalent chromatin and the uncovering of a heterochromatin-switch phenomenon whereby constitutive heterochromatin loss is partially mitigated through gains in facultative heterochromatin. Notably, we observed the multi-omic reversal of a great number of aging-associated alterations in the context of environmental enrichment, which was particularly linked to glial and oligodendrocyte pathways. In conclusion, our work describes the epigenomic landscape of environmental stimulation in the context of aging and reveals how lifestyle intervention can lead to the multi-layered reversal of aging-associated decline.</span></p>',
			'date' => '2024-07-16',
			'pmid' => 'https://www.nature.com/articles/s41467-024-49608-z',
			'doi' => 'https://doi.org/10.1038/s41467-024-49608-z',
			'modified' => '2024-07-29 11:33:49',
			'created' => '2024-07-29 11:33:49',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '4952',
			'name' => 'Epigenetic alterations affecting hematopoietic regulatory networks as drivers of mixed myeloid/lymphoid leukemia',
			'authors' => 'Roger Mulet-Lazaro et al.',
			'description' => '<p><span>Leukemias with ambiguous lineage comprise several loosely defined entities, often without a clear mechanistic basis. Here, we extensively profile the epigenome and transcriptome of a subgroup of such leukemias with CpG Island Methylator Phenotype. These leukemias exhibit comparable hybrid myeloid/lymphoid epigenetic landscapes, yet heterogeneous genetic alterations, suggesting they are defined by their shared epigenetic profile rather than common genetic lesions. Gene expression enrichment reveals similarity with early T-cell precursor acute lymphoblastic leukemia and a lymphoid progenitor cell of origin. In line with this, integration of differential DNA methylation and gene expression shows widespread silencing of myeloid transcription factors. Moreover, binding sites for hematopoietic transcription factors, including CEBPA, SPI1 and LEF1, are uniquely inaccessible in these leukemias. Hypermethylation also results in loss of CTCF binding, accompanied by changes in chromatin interactions involving key transcription factors. In conclusion, epigenetic dysregulation, and not genetic lesions, explains the mixed phenotype of this group of leukemias with ambiguous lineage. The data collected here constitute a useful and comprehensive epigenomic reference for subsequent studies of acute myeloid leukemias, T-cell acute lymphoblastic leukemias and mixed-phenotype leukemias.</span></p>',
			'date' => '2024-07-07',
			'pmid' => 'https://www.nature.com/articles/s41467-024-49811-y',
			'doi' => 'https://doi.org/10.1038/s41467-024-49811-y',
			'modified' => '2024-07-10 12:21:42',
			'created' => '2024-07-10 12:21:42',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '4911',
			'name' => 'Multiomics uncovers the epigenomic and transcriptomic response to viral and bacterial stimulation in turbot',
			'authors' => 'Aramburu O. et al.',
			'description' => '<p><span>Uncovering the epigenomic regulation of immune responses is essential for a comprehensive understanding of host defence mechanisms but remains poorly described in farmed fish. Here, we report the first annotation of the innate immune regulatory response in the genome of turbot (</span><em>Scophthalmus maximus</em><span>), a farmed flatfish. We integrated RNA-Seq with ATAC-Seq and ChIP-Seq (histone marks H3K4me3, H3K27ac and H3K27me3) using samples from head kidney. Sampling was performed 24 hours post-stimulation with viral (poly I:C) and bacterial (inactivate<span>&nbsp;</span></span><em>Vibrio anguillarum</em><span>) mimics<span>&nbsp;</span></span><em>in vivo</em><span><span>&nbsp;</span>and<span>&nbsp;</span></span><em>in vitro</em><span><span>&nbsp;</span>(primary leukocyte cultures). Among the 8,797 differentially expressed genes (DEGs), we observed enrichment of transcriptional activation pathways in response to<span>&nbsp;</span></span><em>Vibrio</em><span><span>&nbsp;</span>and immune response pathways - including interferon stimulated genes - for poly I:C. Meanwhile, metabolic and cell cycle were downregulated by both mimics. We identified notable differences in chromatin accessibility (20,617<span>&nbsp;</span></span><em>in vitro</em><span>, 59,892<span>&nbsp;</span></span><em>in vivo</em><span>) and H3K4me3 bound regions (11,454<span>&nbsp;</span></span><em>in vitro</em><span>, 10,275<span>&nbsp;</span></span><em>in viv</em><span>o) - i.e. marking active promoters - between stimulations and controls. Overlaps of DEGs with promoters showing differential accessibility or histone mark binding revealed a significant coupling of the transcriptome and chromatin state. DEGs with activation marks in their promoters were enriched for similar functions to the global DEG set, but not in all cases, suggesting key regulatory genes were in poised or bivalent states. Active promoters and putative enhancers were differentially enriched in transcription factor binding motifs, many of them common to viral and bacterial responses. Finally, an in-depth analysis of immune response changes in chromatin state surrounding key DEGs encoding transcription factors was performed. This comprehensive multi-omics investigation provides an improved understanding of the epigenomic basis for the turbot immune responses and provides novel functional genomic information that can be leveraged in selective breeding towards enhanced disease resistance.</span></p>',
			'date' => '2024-02-15',
			'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.02.15.580452v1',
			'doi' => 'https://doi.org/10.1101/2024.02.15.580452',
			'modified' => '2024-02-22 11:41:27',
			'created' => '2024-02-22 11:41:27',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '4884',
			'name' => 'SMARCB1 loss activates patient-specific distal oncogenic enhancers in malignant rhabdoid tumors',
			'authors' => 'Liu, N.Q. et al.',
			'description' => '<p><span>Malignant rhabdoid tumor (MRT) is a highly malignant and often lethal childhood cancer. MRTs are genetically defined by bi-allelic inactivating mutations in&nbsp;</span><i>SMARCB1</i><span>, a member of the BRG1/BRM-associated factors (BAF) chromatin remodeling complex. Mutations in BAF complex members are common in human cancer, yet their contribution to tumorigenesis remains in many cases poorly understood. Here, we study derailed regulatory landscapes as a consequence of<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>loss in the context of MRT. Our multi-omics approach on patient-derived MRT organoids reveals a dramatic reshaping of the regulatory landscape upon<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>reconstitution. Chromosome conformation capture experiments subsequently reveal patient-specific looping of distal enhancer regions with the promoter of the<span>&nbsp;</span></span><i>MYC</i><span><span>&nbsp;</span>oncogene. This intertumoral heterogeneity in<span>&nbsp;</span></span><i>MYC</i><span><span>&nbsp;</span>enhancer utilization is also present in patient MRT tissues as shown by combined single-cell RNA-seq and ATAC-seq. We show that loss of<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>activates patient-specific epigenetic reprogramming underlying MRT tumorigenesis.</span></p>',
			'date' => '2023-12-01',
			'pmid' => 'https://www.nature.com/articles/s41467-023-43498-3#Abs1',
			'doi' => '10.1038/s41467-023-43498-3',
			'modified' => '2023-12-05 08:45:53',
			'created' => '2023-12-05 08:45:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '4885',
			'name' => 'The genetic landscape of origins of replication in P. falciparum',
			'authors' => 'Casilda Muñoz Castellano et al.',
			'description' => '<p><span>Various origin mapping approaches have enabled genome-wide identification of origins of replication (ORI) in model organisms, but only a few studies have focused on divergent organisms. By employing three complementary approaches we provide a high-resolution map of ORIs in&nbsp;</span><em>Plasmodium falciparum</em><span>, the deadliest human malaria parasite. We profiled the distribution of origin of recognition complex (ORC) binding sites by ChIP-seq of two<span>&nbsp;</span></span><em>Pf</em><span>ORC subunits and mapped active ORIs using NFS and SNS-seq. We show that ORIs lack sequence specificity but are not randomly distributed, and group in clusters. Licensing is biased towards regions of higher GC content and associated with G-quadruplex forming sequences (G4FS). While strong transcription likely enhances firing, active origins are depleted from transcription start sites. Instead, most accumulate in transcriptionally active gene bodies. Single molecule analysis of nanopore reads containing multiple initiation events, which could have only come from individual nuclei, showed a relationship between the replication fork pace and the distance to the nearest origin. While some similarities were drawn with the canonic eukaryote model, the distribution of ORIs in<span>&nbsp;</span></span><em>P. falciparum</em><span><span>&nbsp;</span>is likely shaped by unique genomic features such as extreme AT-richness&mdash;a product of evolutionary pressure imposed by the parasitic lifestyle.</span></p>',
			'date' => '2023-12-01',
			'pmid' => 'https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkad1103/7457016#428428709',
			'doi' => 'doi.org/10.1093/nar/gkad1103',
			'modified' => '2023-12-05 08:47:24',
			'created' => '2023-12-05 08:47:24',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '4843',
			'name' => 'Differentiation block in acute myeloid leukemia regulated by intronicsequences of FTO',
			'authors' => 'Camera  F. et al.',
			'description' => '<p>Iroquois transcription factor gene IRX3 is highly expressed in 20&acirc;&euro;&ldquo;30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences &acirc;&circ;&frac14;220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with the IRX3 promoter, which correlate with IRX3 expression. Deletion of these intronic elements confirms a role in positively regulating IRX3. RNAseq revealed long non-coding (lnc) transcripts arising from this locus. FTO-lncAML knockdown (KD) induced differentiation of AML cells, loss of clonogenic activity, and reduced FTO intron 8:IRX3 promoter contacts. While both FTO-lncAML KD and IRX3 KD induced differentiation, FTO-lncAML but not IRX3 KD led to HOXA downregulation suggesting transcript activity in trans. FTO-lncAMLhigh AML samples expressed higher levels of HOXA and lower levels of differentiation genes. Thus, a regulatory module in FTO intron 8 consisting of clustered enhancer elements and a long non-coding RNA is active in human AML, impeding myeloid differentiation.</p>',
			'date' => '2023-08-01',
			'pmid' => 'https://www.sciencedirect.com/science/article/pii/S2589004223013962',
			'doi' => '10.1016/j.isci.2023.107319',
			'modified' => '2023-08-01 14:14:01',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '4851',
			'name' => 'Supraphysiological Androgens Promote the Tumor Suppressive Activity of the Androgen Receptor Through cMYC Repression and Recruitment of the DREAM Complex',
			'authors' => 'Nyquist  M. et al.',
			'description' => '<p>The androgen receptor (AR) pathway regulates key cell survival programs in prostate epithelium. The AR represents a near-universal driver and therapeutic vulnerability in metastatic prostate cancer, and targeting AR has a remarkable therapeutic index. Though most approaches directed toward AR focus on inhibiting AR signaling, laboratory and now clinical data have shown that high dose, supraphysiological androgen treatment (SPA) results in growth repression and improved outcomes in subsets of prostate cancer patients. A better understanding of the mechanisms contributing to SPA response and resistance could help guide patient selection and combination therapies to improve efficacy. To characterize SPA signaling, we integrated metrics of gene expression changes induced by SPA together with cistrome data and protein-interactomes. These analyses indicated that the Dimerization partner, RB-like, E2F and Multi-vulval class B (DREAM) complex mediates growth repression and downregulation of E2F targets in response to SPA. Notably, prostate cancers with complete genomic loss of RB1 responded to SPA treatment whereas loss of DREAM complex components such as RBL1/2 promoted resistance. Overexpression of MYC resulted in complete resistance to SPA and attenuated the SPA/AR-mediated repression of E2F target genes. These findings support a model of SPA-mediated growth repression that relies on the negative regulation of MYC by AR leading to repression of E2F1 signaling via the DREAM complex. The integrity of MYC signaling and DREAM complex assembly may consequently serve as determinants of SPA responses and as pathways mediating SPA resistance.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/37352376/',
			'doi' => '10.1158/0008-5472.CAN-22-2613',
			'modified' => '2023-08-01 18:09:31',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '4852',
			'name' => 'In skeletal muscle and neural crest cells, SMCHD1 regulates biologicalpathways relevant for Bosma syndrome and facioscapulohumeral dystrophyphenotype.',
			'authors' => 'Laberthonnière  C. et al.',
			'description' => '<p>Many genetic syndromes are linked to mutations in genes encoding factors that guide chromatin organization. Among them, several distinct rare genetic diseases are linked to mutations in SMCHD1 that encodes the structural maintenance of chromosomes flexible hinge domain containing 1 chromatin-associated factor. In humans, its function as well as the impact of its mutations remains poorly defined. To fill this gap, we determined the episignature associated with heterozygous SMCHD1 variants in primary cells and cell lineages derived from induced pluripotent stem cells for Bosma arhinia and microphthalmia syndrome (BAMS) and type 2 facioscapulohumeral dystrophy (FSHD2). In human tissues, SMCHD1 regulates the distribution of methylated CpGs, H3K27 trimethylation and CTCF at repressed chromatin but also at euchromatin. Based on the exploration of tissues affected either in FSHD or in BAMS, i.e. skeletal muscle fibers and neural crest stem cells, respectively, our results emphasize multiple functions for SMCHD1, in chromatin compaction, chromatin insulation and gene regulation with variable targets or phenotypical outcomes. We concluded that in rare genetic diseases, SMCHD1 variants impact gene expression in two ways: (i) by changing the chromatin context at a number of euchromatin loci or (ii) by directly regulating some loci encoding master transcription factors required for cell fate determination and tissue differentiation.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37334829',
			'doi' => '10.1093/nar/gkad523',
			'modified' => '2023-08-01 14:35:38',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '4861',
			'name' => 'Hypomethylation and overexpression of Th17-associated genes is ahallmark of intestinal CD4+ lymphocytes in Crohn's disease.',
			'authors' => 'Sun  Z. et al.',
			'description' => '<p>BACKGROUND: The development of Crohn's disease (CD) involves immune cell signaling pathways regulated by epigenetic modifications. Aberrant DNA methylation has been identified in peripheral blood and bulk intestinal tissue from CD patients. However, the DNA methylome of disease-associated intestinal CD4 + lymphocytes has not been evaluated. MATERIALS AND METHODS: Genome-wide DNA methylation sequencing was performed from terminal ileum CD4 + cells from 21 CD patients and 12 age and sex matched controls. Data was analyzed for differentially methylated CpGs (DMCs) and methylated regions (DMRs). Integration was performed with RNA-sequencing data to evaluate the functional impact of DNA methylation changes on gene expression. DMRs were overlapped with regions of differentially open chromatin (by ATAC-seq) and CCCTC-binding factor (CTCF) binding sites (by ChIP-seq) between peripherally-derived Th17 and Treg cells. RESULTS: CD4+ cells in CD patients had significantly increased DNA methylation compared to those from the controls. A total of 119,051 DMCs and 8,113 DMRs were detected. While hyper-methylated genes were mostly related to cell metabolism and homeostasis, hypomethylated genes were significantly enriched within the Th17 signaling pathway. The differentially enriched ATAC regions in Th17 cells (compared to Tregs) were hypomethylated in CD patients, suggesting heightened Th17 activity. There was significant overlap between hypomethylated DNA regions and CTCF-associated binding sites. CONCLUSIONS: The methylome of CD patients demonstrate an overall dominant hypermethylation yet hypomethylation is more concentrated in proinflammatory pathways, including Th17 differentiation. Hypomethylation of Th17-related genes associated with areas of open chromatin and CTCF binding sites constitutes a hallmark of CD-associated intestinal CD4 + cells.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37280154',
			'doi' => '10.1093/ecco-jcc/jjad093',
			'modified' => '2023-08-01 14:52:39',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 17 => array(
			'id' => '4862',
			'name' => 'Mutant FUS induces chromatin reorganization in the hippocampus andalters memory processes.',
			'authors' => 'Tzeplaeff  L. et al.',
			'description' => '<p>Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalization to hippocampal function and memory formation are still not characterized. Herein, we show that in these mice, the hippocampus paradoxically displays nuclear FUS accumulation. Multi-omic analyses showed that FUS binds to a set of genes characterized by the presence of an ETS/ELK-binding motifs, and involved in RNA metabolism, transcription, ribosome/mitochondria and chromatin organization. Importantly, hippocampal nuclei showed a decompaction of the neuronal chromatin at highly expressed genes and an inappropriate transcriptomic response was observed after spatial training of Fus mice. Furthermore, these mice lacked precision in a hippocampal-dependent spatial memory task and displayed decreased dendritic spine density. These studies shows that mutated FUS affects epigenetic regulation of the chromatin landscape in hippocampal neurons, which could participate in FTD/ALS pathogenic events. These data call for further investigation in the neurological phenotype of FUS-related diseases and open therapeutic strategies towards epigenetic drugs.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37327984',
			'doi' => '10.1016/j.pneurobio.2023.102483',
			'modified' => '2023-08-01 14:55:49',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 18 => array(
			'id' => '4782',
			'name' => 'Transient suppression of SUMOylation in embryonic stem cells generatesembryo-like structures.',
			'authors' => 'Cossec  J-C. et al.',
			'description' => '<p>Recent advances in synthetic embryology have opened new avenues for understanding the complex events controlling mammalian peri-implantation development. Here, we show that mouse embryonic stem cells (ESCs) solely exposed to chemical inhibition of SUMOylation generate embryo-like structures comprising anterior neural and trunk-associated regions. HypoSUMOylation-instructed ESCs give rise to spheroids that self-organize into gastrulating structures containing cell types spatially and functionally related to embryonic and extraembryonic compartments. Alternatively, spheroids cultured in a droplet microfluidic device form elongated structures that undergo axial organization reminiscent of natural embryo morphogenesis. Single-cell transcriptomics reveals various cellular lineages, including properly positioned anterior neuronal cell types and paraxial mesoderm segmented into somite-like structures. Transient SUMOylation suppression gradually increases DNA methylation genome wide and repressive mark deposition at Nanog. Interestingly, cell-to-cell variations in SUMOylation levels occur during early embryogenesis. Our approach provides a proof of principle for potentially powerful strategies to explore early embryogenesis by targeting chromatin roadblocks of cell fate change.</p>',
			'date' => '2023-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37061916',
			'doi' => '10.1016/j.celrep.2023.112380',
			'modified' => '2023-06-13 09:20:06',
			'created' => '2023-05-05 12:34:24',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 19 => array(
			'id' => '4693',
			'name' => 'ZEB1 controls a lineage-specific transcriptional program essential formelanoma cell state transitions',
			'authors' => 'Tang  Y. et al.',
			'description' => '<p>Cell plasticity sustains intra-tumor heterogeneity and treatment resistance in melanoma. Deciphering the transcriptional mechanisms governing reversible phenotypic transitions between proliferative/differentiated and invasive/stem-like states is required in order to design novel therapeutic strategies. EMT-inducing transcription factors, extensively known for their role in metastasis in carcinoma, display cell-type specific functions in melanoma, with a decreased ZEB2/ZEB1 expression ratio fostering adaptive resistance to targeted therapies. While ZEB1 direct target genes have been well characterized in carcinoma models, they remain unknown in melanoma. Here, we performed a genome-wide characterization of ZEB1 transcriptional targets, by combining ChIP-sequencing and RNA-sequencing, upon phenotype switching in melanoma models. We identified and validated ZEB1 binding peaks in the promoter of key lineage-specific genes related to melanoma cell identity. Comparative analyses with breast carcinoma cells demonstrated melanoma-specific ZEB1 binding, further supporting lineage specificity. Gain- or loss-of-function of ZEB1, combined with functional analyses, further demonstrated that ZEB1 negatively regulates proliferative/melanocytic programs and positively regulates both invasive and stem-like programs. We then developed single-cell spatial multiplexed analyses to characterize melanoma cell states with respect to ZEB1/ZEB2 expression in human melanoma samples. We characterized the intra-tumoral heterogeneity of ZEB1 and ZEB2 and further validated ZEB1 increased expression in invasive cells, but also in stem-like cells, highlighting its relevance in vivo in both populations. Overall, our results define ZEB1 as a major transcriptional regulator of cell states transitions and provide a better understanding of lineage-specific transcriptional programs sustaining intra-tumor heterogeneity in melanoma.</p>',
			'date' => '2023-02-01',
			'pmid' => 'https://doi.org/10.1101%2F2023.02.10.526467',
			'doi' => '10.1101/2023.02.10.526467',
			'modified' => '2023-04-14 09:11:23',
			'created' => '2023-02-28 12:19:11',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 20 => 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) 21 => array(
			'id' => '4651',
			'name' => 'TCDD induces multigenerational alterations in the expression ofmicroRNA in the thymus through epigenetic modifications',
			'authors' => 'Singh  Narendra P et al.',
			'description' => '<p>2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a potent AhR ligand, is an environmental contaminant that is known for mediating toxicity across generations. However, whether TCDD can induce multigenerational changes in the expression of miRNAs (miRs) has not been previously studied. In the current study, we investigated the effect of administration of TCDD in pregnant mice (F0) on gestational day 14, on the expression of miRs in the thymus of F0 and subsequent generations (F1 and F2). Of the 3200 miRs screened, 160 miRs were dysregulated similarly in F0, F1, and F2 generations while 46 miRs were differentially altered in F0-F2 generations. Pathway analysis revealed that the changes in miR signature profile mediated by TCDD affected the genes that regulate cell signaling, apoptosis, thymic atrophy, cancer, immunosuppression, and other physiological pathways. A significant number of miRs that showed altered expression exhibited dioxin response elements (DRE) on their promoters. Focusing on one such miR, namely miR-203 that expressed DREs and was induced across F0-F2 by TCDD, promoter analysis showed that one of the DREs expressed by miR-203 was functional to TCDD-mediated upregulation. Also, the histone methylation status of H3K4me3 in the miR-203 promoter was significantly increased near the transcriptional start site (TSS) in TCDD-treated thymocytes across F0-F2 generations. Genome-wide ChIP-seq study suggested that TCDD may cause alterations in histone methylation in certain genes across the three generations. Together, the current study demonstrates that gestational exposure to TCDD can alter the expression of miRs in F0 through direct activation of DREs as well as across F0, F1, and F2 generations through epigenetic pathways.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://academic.oup.com/pnasnexus/advance-article/doi/10.1093/pnasnexus/pgac290/6886578',
			'doi' => 'https://doi.org/10.1093/pnasnexus/pgac290',
			'modified' => '2023-03-13 10:55:36',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 22 => array(
			'id' => '4632',
			'name' => 'The histone acetyltransferase KAT6A is recruited to unmethylatedCpG islands via a DNA binding winged helix domain.',
			'authors' => 'Weber  L.M. et al.',
			'description' => '<p>The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrate that a winged helix (WH) domain at the very N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A with unmethylated CpG islands (CGIs) genome-wide. Mutation of the essential amino acids for DNA binding completely abrogates the enrichment of KAT6A at CGIs. In contrast, deletion of a second WH domain or the histone tail binding PHD fingers only subtly influences the binding of KAT6A to CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36537216',
			'doi' => '10.1093/nar/gkac1188',
			'modified' => '2023-03-28 09:01:38',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 23 => array(
			'id' => '4629',
			'name' => 'Polyglutamine-expanded ATXN7 alters a specific epigenetic signatureunderlying photoreceptor identity gene expression in SCA7 mouseretinopathy.',
			'authors' => 'Niewiadomska-Cimicka  A.et al.',
			'description' => '<p>BACKGROUND: Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disorder that primarily affects the cerebellum and retina. SCA7 is caused by a polyglutamine expansion in the ATXN7 protein, a subunit of the transcriptional coactivator SAGA that acetylates histone H3 to deposit narrow H3K9ac mark at DNA regulatory elements of active genes. Defective histone acetylation has been presented as a possible cause for gene deregulation in SCA7 mouse models. However, the topography of acetylation defects at the whole genome level and its relationship to changes in gene expression remain to be determined. METHODS: We performed deep RNA-sequencing and chromatin immunoprecipitation coupled to high-throughput sequencing to examine the genome-wide correlation between gene deregulation and alteration of the active transcription marks, e.g. SAGA-related H3K9ac, CBP-related H3K27ac and RNA polymerase II (RNAPII), in a SCA7 mouse retinopathy model. RESULTS: Our analyses revealed that active transcription marks are reduced at most gene promoters in SCA7 retina, while a limited number of genes show changes in expression. We found that SCA7 retinopathy is caused by preferential downregulation of hundreds of highly expressed genes that define morphological and physiological identities of mature photoreceptors. We further uncovered that these photoreceptor genes harbor unusually broad H3K9ac profiles spanning the entire gene bodies and have a low RNAPII pausing. This broad H3K9ac signature co-occurs with other features that delineate superenhancers, including broad H3K27ac, binding sites for photoreceptor specific transcription factors and expression of enhancer-related non-coding RNAs (eRNAs). In SCA7 retina, downregulated photoreceptor genes show decreased H3K9 and H3K27 acetylation and eRNA expression as well as increased RNAPII pausing, suggesting that superenhancer-related features are altered. CONCLUSIONS: Our study thus provides evidence that distinctive epigenetic configurations underlying high expression of cell-type specific genes are preferentially impaired in SCA7, resulting in a defect in the maintenance of identity features of mature photoreceptors. Our results also suggest that continuous SAGA-driven acetylation plays a role in preserving post-mitotic neuronal identity.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36539812',
			'doi' => '10.1186/s12929-022-00892-1',
			'modified' => '2023-03-28 09:07:19',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 24 => 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) 25 => array(
			'id' => '4494',
			'name' => 'Cryptococcal Hsf3 controls intramitochondrial ROS homeostasis byregulating the respiratory process.',
			'authors' => 'Gao  X.et al.',
			'description' => '<p>Mitochondrial quality control prevents accumulation of intramitochondrial-derived reactive oxygen species (mtROS), thereby protecting cells against DNA damage, genome instability, and programmed cell death. However, underlying mechanisms are incompletely understood, particularly in fungal species. Here, we show that Cryptococcus neoformans heat shock factor 3 (CnHsf3) exhibits an atypical function in regulating mtROS independent of the unfolded protein response. CnHsf3 acts in nuclei and mitochondria, and nuclear- and mitochondrial-targeting signals are required for its organelle-specific functions. It represses the expression of genes involved in the tricarboxylic acid cycle while promoting expression of genes involved in electron transfer chain. In addition, CnHsf3 responds to multiple intramitochondrial stresses; this response is mediated by oxidation of the cysteine residue on its DNA binding domain, which enhances DNA binding. Our results reveal a function of HSF proteins in regulating mtROS homeostasis that is independent of the unfolded protein response.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36109512',
			'doi' => '10.1038/s41467-022-33168-1',
			'modified' => '2022-11-18 12:43:17',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 26 => array(
			'id' => '4496',
			'name' => 'Dominant role of DNA methylation over H3K9me3 for IAP silencingin endoderm.',
			'authors' => 'Wang  Z. et al.',
			'description' => '<p>Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications H3K9me3 and DNA methylation. On ERVs, these modifications are mainly deposited by the histone methyltransferase Setdb1 and by the maintenance DNA methyltransferase Dnmt1. Knock-out of either Setdb1 or Dnmt1 leads to ERV de-repression in various cell types. However, it is currently not known if H3K9me3 and DNA methylation depend on each other for ERV silencing. Here we show that conditional knock-out of Setdb1 in mouse embryonic endoderm results in ERV de-repression in visceral endoderm (VE) descendants and does not occur in definitive endoderm (DE). Deletion of Setdb1 in VE progenitors results in loss of H3K9me3 and reduced DNA methylation of Intracisternal A-particle (IAP) elements, consistent with up-regulation of this ERV family. In DE, loss of Setdb1 does not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 knock-out results in IAP de-repression in both visceral and definitive endoderm cells, while H3K9me3 is unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm cells. Our findings suggest that Setdb1-meditated H3K9me3 is not sufficient for IAP silencing, but rather critical for maintaining high DNA methylation.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36123357',
			'doi' => '10.1038/s41467-022-32978-7',
			'modified' => '2022-11-21 10:26:30',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 27 => array(
			'id' => '4415',
			'name' => 'HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependentgene repression in murine erythroleukaemia.',
			'authors' => 'Gregoricchio  S. et al.',
			'description' => '<p>Although originally described as transcriptional activator, SPI1/PU.1, a major player in haematopoiesis whose alterations are associated with haematological malignancies, has the ability to repress transcription. Here, we investigated the mechanisms underlying gene repression in the erythroid lineage, in which SPI1 exerts an oncogenic function by blocking differentiation. We show that SPI1 represses genes by binding active enhancers that are located in intergenic or gene body regions. HDAC1 acts as a cooperative mediator of SPI1-induced transcriptional repression by deacetylating SPI1-bound enhancers in a subset of genes, including those involved in erythroid differentiation. Enhancer deacetylation impacts on promoter acetylation, chromatin accessibility and RNA pol II occupancy. In addition to the activities of HDAC1, polycomb repressive complex 2 (PRC2) reinforces gene repression by depositing H3K27me3 at promoter sequences when SPI1 is located at enhancer sequences. Moreover, our study identified a synergistic relationship between PRC2 and HDAC1 complexes in mediating the transcriptional repression activity of SPI1, ultimately inducing synergistic adverse effects on leukaemic cell survival. Our results highlight the importance of the mechanism underlying transcriptional repression in leukemic cells, involving complex functional connections between SPI1 and the epigenetic regulators PRC2 and HDAC1.</p>',
			'date' => '2022-08-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35871293',
			'doi' => '10.1093/nar/gkac613',
			'modified' => '2022-09-15 08:59:26',
			'created' => '2022-09-08 16:32:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 28 => array(
			'id' => '4516',
			'name' => 'Dual role of histone variant H3.3B in spermatogenesis: positiveregulation of piRNA transcription and implication in X-chromosomeinactivation.',
			'authors' => 'Fontaine  E. et al.',
			'description' => '<p>The histone variant H3.3 is encoded by two distinct genes, H3f3a and H3f3b, exhibiting identical amino-acid sequence. H3.3 is required for spermatogenesis, but the molecular mechanism of its spermatogenic function remains obscure. Here, we have studied the role of each one of H3.3A and H3.3B proteins in spermatogenesis. We have generated transgenic conditional knock-out/knock-in (cKO/KI) epitope-tagged FLAG-FLAG-HA-H3.3B (H3.3BHA) and FLAG-FLAG-HA-H3.3A (H3.3AHA) mouse lines. We show that H3.3B, but not H3.3A, is required for spermatogenesis and male fertility. Analysis of the molecular mechanism unveils that the absence of H3.3B led to alterations in the meiotic/post-meiotic transition. Genome-wide RNA-seq reveals that the depletion of H3.3B in meiotic cells is associated with increased expression of the whole sex X and Y chromosomes as well as of both RLTR10B and RLTR10B2 retrotransposons. In contrast, the absence of H3.3B resulted in down-regulation of the expression of piRNA clusters. ChIP-seq experiments uncover that RLTR10B and RLTR10B2 retrotransposons, the whole sex chromosomes and the piRNA clusters are markedly enriched of H3.3. Taken together, our data dissect the molecular mechanism of H3.3B functions during spermatogenesis and demonstrate that H3.3B, depending on its chromatin localization, is involved in either up-regulation or down-regulation of expression of defined large chromatin regions.</p>',
			'date' => '2022-07-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35766398',
			'doi' => '10.1093/nar/gkac541',
			'modified' => '2022-11-24 08:51:34',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 29 => array(
			'id' => '4393',
			'name' => 'TBX2 acts as a potent transcriptional silencer of tumour suppressor genesthrough interaction with the CoREST complex to sustain theproliferation of breast cancers.',
			'authors' => 'McIntyre  A.J. et al.',
			'description' => '<p>Chromosome 17q23 amplification occurs in 20\% of primary breast tumours and is associated with poor outcome. The TBX2 gene is located on 17q23 and is often over-expressed in this breast tumour subset. TBX2 is an anti-senescence gene, promoting cell growth and survival through repression of Tumour Suppressor Genes (TSGs), such as NDRG1 and CST6. Previously we found that TBX2 cooperates with the PRC2 complex to repress several TSGs, and that PRC2 inhibition restored NDRG1 expression to impede cellular proliferation. Here, we now identify CoREST proteins, LSD1 and ZNF217, as novel interactors of TBX2. Genetic or pharmacological targeting of CoREST emulated TBX2 loss, inducing NDRG1 expression and abolishing breast cancer growth in vitro and in vivo. Furthermore, we uncover that TBX2/CoREST targeting of NDRG1 is achieved by recruitment of TBX2 to the NDRG1 promoter by Sp1, the abolishment of which resulted in NDRG1 upregulation and diminished cancer cell proliferation. Through ChIP-seq we reveal that 30\% of TBX2-bound promoters are shared with ZNF217 and identify novel targets repressed by TBX2/CoREST; of these targets a lncRNA, LINC00111, behaves as a negative regulator of cell proliferation. Overall, these data indicate that inhibition of CoREST proteins represents a promising therapeutic intervention for TBX2-addicted breast tumours.</p>',
			'date' => '2022-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35687133',
			'doi' => '10.1093/nar/gkac494',
			'modified' => '2022-08-11 14:23:06',
			'created' => '2022-08-11 12:14:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 30 => array(
			'id' => '4836',
			'name' => 'Caffeine intake exerts dual genome-wide effects on hippocampal metabolismand learning-dependent transcription.',
			'authors' => 'Paiva  I. et al.',
			'description' => '<p>Caffeine is the most widely consumed psychoactive substance in the world. Strikingly, the molecular pathways engaged by its regular consumption remain unclear. We herein addressed the mechanisms associated with habitual (chronic) caffeine consumption in the mouse hippocampus using untargeted orthogonal omics techniques. Our results revealed that chronic caffeine exerts concerted pleiotropic effects in the hippocampus at the epigenomic, proteomic, and metabolomic levels. Caffeine lowered metabolism-related processes (e.g., at the level of metabolomics and gene expression) in bulk tissue, while it induced neuron-specific epigenetic changes at synaptic transmission/plasticity-related genes and increased experience-driven transcriptional activity. Altogether, these findings suggest that regular caffeine intake improves the signal-to-noise ratio during information encoding, in part through fine-tuning of metabolic genes, while boosting the salience of information processing during learning in neuronal circuits.</p>',
			'date' => '2022-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35536645',
			'doi' => '10.1172/JCI149371',
			'modified' => '2023-08-01 13:52:29',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 31 => array(
			'id' => '4221',
			'name' => 'Epigenetic Mechanisms Mediating Cell State Transitions in Chondrocytes',
			'authors' => 'Wuelling M. et al.',
			'description' => '<p><span>Epigenetic modifications play critical roles in regulating cell lineage differentiation, but the epigenetic mechanisms guiding specific differentiation steps within a cell lineage have rarely been investigated. To decipher such mechanisms, we used the defined transition from proliferating (PC) into hypertrophic chondrocytes (HC) during endochondral ossification as a model. We established a map of activating and repressive histone modifications for each cell type. ChromHMM state transition analysis and Pareto-based integration of differential levels of mRNA and epigenetic marks revealed that differentiation-associated gene repression is initiated by the addition of H3K27me3 to promoters still carrying substantial levels of activating marks. Moreover, the integrative analysis identified genes specifically expressed in cells undergoing the transition into hypertrophy. Investigation of enhancer profiles detected surprising differences in enhancer number, location, and transcription factor binding sites between the two closely related cell types. Furthermore, cell type-specific upregulation of gene expression was associated with increased numbers of H3K27ac peaks. Pathway analysis identified PC-specific enhancers associated with chondrogenic genes, whereas HC-specific enhancers mainly control metabolic pathways linking epigenetic signature to biological functions. Since HC-specific enhancers show a higher conservation in postnatal tissues, the switch to metabolic pathways seems to be a hallmark of differentiated tissues. Surprisingly, the analysis of H3K27ac levels at super-enhancers revealed a rapid adaption of H3K27ac occupancy to changes in gene expression, supporting the importance of enhancer modulation for acute alterations in gene expression. &copy; 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).</span></p>',
			'date' => '2022-05-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33534175/',
			'doi' => '10.1002/jbmr.4263',
			'modified' => '2022-04-25 11:46:32',
			'created' => '2022-04-21 12:00:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 32 => array(
			'id' => '4402',
			'name' => 'The CpG Island-Binding Protein SAMD1 Contributes to anUnfavorable Gene Signature in HepG2 Hepatocellular CarcinomaCells.',
			'authors' => 'Simon  C. et al.',
			'description' => '<p>The unmethylated CpG island-binding protein SAMD1 is upregulated in many human cancer types, but its cancer-related role has not yet been investigated. Here, we used the hepatocellular carcinoma cell line HepG2 as a cancer model and investigated the cellular and transcriptional roles of SAMD1 using ChIP-Seq and RNA-Seq. SAMD1 targets several thousand gene promoters, where it acts predominantly as a transcriptional repressor. HepG2 cells with SAMD1 deletion showed slightly reduced proliferation, but strongly impaired clonogenicity. This phenotype was accompanied by the decreased expression of pro-proliferative genes, including MYC target genes. Consistently, we observed a decrease in the active H3K4me2 histone mark at most promoters, irrespective of SAMD1 binding. Conversely, we noticed an increase in interferon response pathways and a gain of H3K4me2 at a subset of enhancers that were enriched for IFN-stimulated response elements (ISREs). We identified key transcription factor genes, such as , , and , that were directly repressed by SAMD1. Moreover, SAMD1 deletion also led to the derepression of the PI3K-inhibitor , contributing to diminished mTOR signaling and ribosome biogenesis pathways. Our work suggests that SAMD1 is involved in establishing a pro-proliferative setting in hepatocellular carcinoma cells. Inhibiting SAMD1's function in liver cancer cells may therefore lead to a more favorable gene signature.</p>',
			'date' => '2022-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35453756',
			'doi' => '10.3390/biology11040557',
			'modified' => '2022-08-11 14:45:43',
			'created' => '2022-08-11 12:14:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 33 => array(
			'id' => '4524',
			'name' => 'Local euchromatin enrichment in lamina-associated domains anticipatestheir repositioning in the adipogenic lineage.',
			'authors' => 'Madsen-Østerbye  J. et al.',
			'description' => '<p>BACKGROUND: Interactions of chromatin with the nuclear lamina via lamina-associated domains (LADs) confer structural stability to the genome. The dynamics of positioning of LADs during differentiation, and how LADs impinge on developmental gene expression, remains, however, elusive. RESULTS: We examined changes in the association of lamin B1 with the genome in the first 72 h of differentiation of adipose stem cells into adipocytes. We demonstrate a repositioning of entire stand-alone LADs and of LAD edges as a prominent nuclear structural feature of early adipogenesis. Whereas adipogenic genes are released from LADs, LADs sequester downregulated or repressed genes irrelevant for the adipose lineage. However, LAD repositioning only partly concurs with gene expression changes. Differentially expressed genes in LADs, including LADs conserved throughout differentiation, reside in local euchromatic and lamin-depleted sub-domains. In these sub-domains, pre-differentiation histone modification profiles correlate with the LAD versus inter-LAD outcome of these genes during adipogenic commitment. Lastly, we link differentially expressed genes in LADs to short-range enhancers which overall co-partition with these genes in LADs versus inter-LADs during differentiation. CONCLUSIONS: We conclude that LADs are predictable structural features of adipose nuclear architecture that restrain non-adipogenic genes in a repressive environment.</p>',
			'date' => '2022-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35410387',
			'doi' => '10.1186/s13059-022-02662-6',
			'modified' => '2022-11-24 09:08:01',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 34 => array(
			'id' => '4235',
			'name' => 'NuA4 and H2A.Z control environmental responses and autotrophicgrowth in Arabidopsis',
			'authors' => 'Bieluszewski T. et al.',
			'description' => '<p>Nucleosomal acetyltransferase of H4 (NuA4) is an essential transcriptional coactivator in eukaryotes, but remains poorly characterized in plants. Here, we describe Arabidopsis homologs of the NuA4 scaffold proteins Enhancer of Polycomb-Like 1 (AtEPL1) and Esa1-Associated Factor 1 (AtEAF1). Loss of AtEAF1 results in inhibition of growth and chloroplast development. These effects are stronger in the Atepl1 mutant and are further enhanced by loss of Golden2-Like (GLK) transcription factors, suggesting that NuA4 activates nuclear plastid genes alongside GLK. We demonstrate that AtEPL1 is necessary for nucleosomal acetylation of histones H4 and H2A.Z by NuA4 in vitro. These chromatin marks are diminished genome-wide in Atepl1, while another active chromatin mark, H3K9 acetylation (H3K9ac), is locally enhanced. Expression of many chloroplast-related genes depends on NuA4, as they are downregulated with loss of H4ac and H2A.Zac. Finally, we demonstrate that NuA4 promotes H2A.Z deposition and by doing so prevents spurious activation of stress response genes.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35022409',
			'doi' => '10.1038/s41467-021-27882-5',
			'modified' => '2022-05-19 17:02:00',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 35 => array(
			'id' => '4772',
			'name' => 'Three classes of epigenomic regulators converge to hyperactivate theessential maternal gene deadhead within a heterochromatin mini-domain.',
			'authors' => 'Torres-Campana  D. et al.',
			'description' => '<p>The formation of a diploid zygote is a highly complex cellular process that is entirely controlled by maternal gene products stored in the egg cytoplasm. This highly specialized transcriptional program is tightly controlled at the chromatin level in the female germline. As an extreme case in point, the massive and specific ovarian expression of the essential thioredoxin Deadhead (DHD) is critically regulated in Drosophila by the histone demethylase Lid and its partner, the histone deacetylase complex Sin3A/Rpd3, via yet unknown mechanisms. Here, we identified Snr1 and Mod(mdg4) as essential for dhd expression and investigated how these epigenomic effectors act with Lid and Sin3A to hyperactivate dhd. Using Cut\&amp;Run chromatin profiling with a dedicated data analysis procedure, we found that dhd is intriguingly embedded in an H3K27me3/H3K9me3-enriched mini-domain flanked by DNA regulatory elements, including a dhd promoter-proximal element essential for its expression. Surprisingly, Lid, Sin3a, Snr1 and Mod(mdg4) impact H3K27me3 and this regulatory element in distinct manners. However, we show that these effectors activate dhd independently of H3K27me3/H3K9me3, and that dhd remains silent in the absence of these marks. Together, our study demonstrates an atypical and critical role for chromatin regulators Lid, Sin3A, Snr1 and Mod(mdg4) to trigger tissue-specific hyperactivation within a unique heterochromatin mini-domain.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8759638/',
			'doi' => '10.1371/journal.pgen.1009615',
			'modified' => '2023-04-17 09:46:00',
			'created' => '2023-04-14 13:41:22',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 36 => 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) 37 => array(
			'id' => '4245',
			'name' => 'Decreased PRC2 activity supports the survival of basal-like breastcancer cells to cytotoxic treatments',
			'authors' => 'Mieczkowska IK et al.',
			'description' => '<p>Breast cancer (BC) is the most common cancer occurring in women but also rarely develops in men. Recent advances in early diagnosis and development of targeted therapies have greatly improved the survival rate of BC patients. However, the basal-like BC subtype (BLBC), largely overlapping with the triple-negative BC subtype (TNBC), lacks such drug targets and conventional cytotoxic chemotherapies often remain the only treatment option. Thus, the development of resistance to cytotoxic therapies has fatal consequences. To assess the involvement of epigenetic mechanisms and their therapeutic potential increasing cytotoxic drug efficiency, we combined high-throughput RNA- and ChIP-sequencing analyses in BLBC cells. Tumor cells surviving chemotherapy upregulated transcriptional programs of epithelial-to-mesenchymal transition (EMT) and stemness. To our surprise, the same cells showed a pronounced reduction of polycomb repressive complex 2 (PRC2) activity via downregulation of its subunits Ezh2, Suz12, Rbbp7 and Mtf2. Mechanistically, loss of PRC2 activity leads to the de-repression of a set of genes through an epigenetic switch from repressive H3K27me3 to activating H3K27ac mark at regulatory regions. We identified Nfatc1 as an upregulated gene upon loss of PRC2 activity and directly implicated in the transcriptional changes happening upon survival to chemotherapy. Blocking NFATc1 activation reduced epithelial-to-mesenchymal transition, aggressiveness, and therapy resistance of BLBC cells. Our data demonstrate a previously unknown function of PRC2 maintaining low Nfatc1 expression levels and thereby repressing aggressiveness and therapy resistance in BLBC.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34845197',
			'doi' => '10.1038/s41419-021-04407-y',
			'modified' => '2022-05-20 09:21:56',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 38 => array(
			'id' => '4276',
			'name' => 'Ago1 controls myogenic differentiation by regulating eRNA-mediatedCBP-guided epigenome reprogramming.',
			'authors' => 'Fallatah Bodor et al.',
			'description' => '<p>The role of chromatin-associated RNAi components in the nucleus of mammalian cells and in particular in the context of developmental programs remains to be elucidated. Here, we investigate the function of nuclear Argonaute 1 (Ago1) in gene expression regulation during skeletal muscle differentiation. We show that Ago1 is required for activation of the myogenic program by supporting chromatin modification mediated by developmental enhancer activation. Mechanistically, we demonstrate that Ago1 directly controls global H3K27 acetylation (H3K27ac) by regulating enhancer RNA (eRNA)-CREB-binding protein (CBP) acetyltransferase interaction, a key step in enhancer-driven gene activation. In particular, we show that Ago1 is specifically required for myogenic differentiation 1 (MyoD) and downstream myogenic gene activation, whereas its depletion leads to failure of CBP acetyltransferase activation and blocking of the myogenic program. Our work establishes a role of the mammalian enhancer-associated RNAi component Ago1 in epigenome regulation and activation of developmental programs.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.celrep.2021.110066',
			'doi' => '10.1016/j.celrep.2021.110066',
			'modified' => '2022-05-23 09:53:14',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 39 => array(
			'id' => '4833',
			'name' => 'Extensive NEUROG3 occupancy in the human pancreatic endocrine generegulatory network.',
			'authors' => 'Schreiber  V. et al.',
			'description' => '<p>OBJECTIVE: Mice lacking the bHLH transcription factor (TF) Neurog3 do not form pancreatic islet cells, including insulin-secreting beta cells, the absence of which leads to diabetes. In humans, homozygous mutations of NEUROG3 manifest with neonatal or childhood diabetes. Despite this critical role in islet cell development, the precise function of and downstream genetic programs regulated directly by NEUROG3 remain elusive. Therefore, we mapped genome-wide NEUROG3 occupancy in human induced pluripotent stem cell (hiPSC)-derived endocrine progenitors and determined NEUROG3 dependency of associated genes to uncover direct targets. METHODS: We generated a novel hiPSC line (NEUROG3-HA-P2A-Venus) where NEUROG3 is HA-tagged and fused to a self-cleaving fluorescent VENUS reporter. We used the CUT\&amp;RUN technique to map NEUROG3 occupancy and epigenetic marks in pancreatic endocrine progenitors (PEP) that were differentiated from this hiPSC line. We integrated NEUROG3 occupancy data with chromatin status and gene expression in PEPs as well as their NEUROG3-dependence. In addition, we investigated whether NEUROG3 binds type 2 diabetes mellitus (T2DM)-associated variants at the PEP stage. RESULTS: CUT\&amp;RUN revealed a total of 863 NEUROG3 binding sites assigned to 1263 unique genes. NEUROG3 occupancy was found at promoters as well as at distant cis-regulatory elements that frequently overlapped within PEP active enhancers. De novo motif analyses defined a NEUROG3 consensus binding motif and suggested potential co-regulation of NEUROG3 target genes by FOXA or RFX transcription factors. We found that 22\% of the genes downregulated in NEUROG3 PEPs, and 10\% of genes enriched in NEUROG3-Venus positive endocrine cells were bound by NEUROG3 and thus likely to be directly regulated. NEUROG3 binds to 138 transcription factor genes, some with important roles in islet cell development or function, such as NEUROD1, PAX4, NKX2-2, SOX4, MLXIPL, LMX1B, RFX3, and NEUROG3 itself, and many others with unknown islet function. Unexpectedly, we uncovered that NEUROG3 targets genes critical for insulin secretion in beta cells (e.g., GCK, ABCC8/KCNJ11, CACNA1A, CHGA, SCG2, SLC30A8, and PCSK1). Thus, analysis of NEUROG3 occupancy suggests that the transient expression of NEUROG3 not only promotes islet destiny in uncommitted pancreatic progenitors, but could also initiate endocrine programs essential for beta cell function. Lastly, we identified eight T2DM risk SNPs within NEUROG3-bound regions. CONCLUSION: Mapping NEUROG3 genome occupancy in PEPs uncovered unexpectedly broad, direct control of the endocrine genes, raising novel hypotheses on how this master regulator controls islet and beta cell differentiation.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://doi.org/10.1101%2F2021.04.14.439685',
			'doi' => '10.1016/j.molmet.2021.101313',
			'modified' => '2023-08-01 13:46:35',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 40 => array(
			'id' => '4285',
			'name' => 'Alveolar macrophages from persons living with HIV show impairedepigenetic response to Mycobacterium tuberculosis.',
			'authors' => 'Correa-Macedo Wilian et al.',
			'description' => '<p>Persons living with HIV (PLWH) are at increased risk of tuberculosis (TB). HIV-associated TB is often the result of recent infection with Mycobacterium tuberculosis (Mtb) followed by rapid progression to disease. Alveolar macrophages (AM) are the first cells of the innate immune system that engage Mtb, but how HIV and antiretroviral therapy (ART) impact on the anti-mycobacterial response of AM is not known. To investigate the impact of HIV and ART on the transcriptomic and epigenetic response of AM to Mtb, we obtained AM by bronchoalveolar lavage from 20 PLWH receiving ART, 16 control subjects who were HIV-free (HC), and 14 subjects who received ART as pre-exposure prophylaxis (PrEP) to prevent HIV infection. Following in-vitro challenge with Mtb, AM from each group displayed overlapping but distinct profiles of significantly up- and down-regulated genes in response to Mtb. Comparatively, AM isolated from both PLWH and PrEP subjects presented a substantially weaker transcriptional response. In addition, AM from HC subjects challenged with Mtb responded with pronounced chromatin accessibility changes while AM obtained from PLWH and PrEP subjects displayed no significant changes in their chromatin state. Collectively, these results revealed a stronger adverse effect of ART than HIV on the epigenetic landscape and transcriptional responsiveness of AM.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473646/',
			'doi' => '10.1172/JCI148013',
			'modified' => '2022-05-24 09:08:39',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 41 => array(
			'id' => '4297',
			'name' => 'INTS11 regulates hematopoiesis by promoting PRC2 function.',
			'authors' => 'Zhang Peng et al.',
			'description' => '<p>INTS11, the catalytic subunit of the Integrator (INT) complex, is crucial for the biogenesis of small nuclear RNAs and enhancer RNAs. However, the role of INTS11 in hematopoietic stem and progenitor cell (HSPC) biology is unknown. Here, we report that INTS11 is required for normal hematopoiesis and hematopoietic-specific genetic deletion of leads to cell cycle arrest and impairment of fetal and adult HSPCs. We identified a novel INTS11-interacting protein complex, Polycomb repressive complex 2 (PRC2), that maintains HSPC functions. Loss of INTS11 destabilizes the PRC2 complex, decreases the level of histone H3 lysine 27 trimethylation (H3K27me3), and derepresses PRC2 target genes. Reexpression of INTS11 or PRC2 proteins in -deficient HSPCs restores the levels of PRC2 and H3K27me3 as well as HSPC functions. Collectively, our data demonstrate that INTS11 is an essential regulator of HSPC homeostasis through the INTS11-PRC2 axis.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34516911',
			'doi' => '10.1126/sciadv.abh1684',
			'modified' => '2022-05-30 09:31:00',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 42 => array(
			'id' => '4304',
			'name' => 'The related coactivator complexes SAGA and ATAC control embryonicstem cell self-renewal through acetyltransferase-independent mechanisms',
			'authors' => 'Fischer Veronique et al.',
			'description' => '<p>SUMMARY SAGA (Spt-Ada-Gcn5 acetyltransferase) and ATAC (Ada-two-A-containing) are two related coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development, but the role of these complexes in RNA polymerase II transcription is less understood. To determine whether SAGA and ATAC have redundant or specific functions, we compare the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC are required for complex assembly and mouse ESC growth and self-renewal. Surprisingly, depletion of HAT module subunits causes a global decrease in histone H3K9 acetylation, but does not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for self-renewal of mouse ESCs by regulating transcription through different pathways in a HAT-independent manner.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34433046',
			'doi' => '10.1016/j.celrep.2021.109598',
			'modified' => '2022-05-30 09:57:39',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 43 => array(
			'id' => '4345',
			'name' => 'Altered Chromatin States Drive Cryptic Transcription in AgingMammalian Stem Cells.',
			'authors' => 'McCauley Brenna S et al.',
			'description' => '<p>A repressive chromatin state featuring trimethylated lysine 36 on histone H3 (H3K36me3) and DNA methylation suppresses cryptic transcription in embryonic stem cells. Cryptic transcription is elevated with age in yeast and nematodes, and reducing it extends yeast lifespan, though whether this occurs in mammals is unknown. We show that cryptic transcription is elevated in aged mammalian stem cells, including murine hematopoietic stem cells (mHSCs) and neural stem cells (NSCs) and human mesenchymal stem cells (hMSCs). Precise mapping allowed quantification of age-associated cryptic transcription in hMSCs aged . Regions with significant age-associated cryptic transcription have a unique chromatin signature: decreased H3K36me3 and increased H3K4me1, H3K4me3, and H3K27ac with age. Genomic regions undergoing such changes resemble known promoter sequences and are bound by TBP even in young cells. Hence, the more permissive chromatin state at intragenic cryptic promoters likely underlies increased cryptic transcription in aged mammalian stem cells.</p>',
			'date' => '2021-08-01',
			'pmid' => 'https://doi.org/10.1038%2Fs43587-021-00091-x',
			'doi' => '10.1038/s43587-021-00091-x',
			'modified' => '2022-06-22 12:30:19',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 44 => array(
			'id' => '4333',
			'name' => 'Metabolically controlled histone H4K5 acylation/acetylation ratiodrives BRD4 genomic distribution.',
			'authors' => 'Gao M. et al.',
			'description' => '<p>In addition to acetylation, histones are modified by a series of competing longer-chain acylations. Most of these acylation marks are enriched and co-exist with acetylation on active gene regulatory elements. Their seemingly redundant functions hinder our understanding of histone acylations' specific roles. Here, by using an acute lymphoblastic leukemia (ALL) cell model and blasts from individuals with B-precusor ALL (B-ALL), we demonstrate a role of mitochondrial activity in controlling the histone acylation/acetylation ratio, especially at histone H4 lysine 5 (H4K5). An increase in the ratio of non-acetyl acylations (crotonylation or butyrylation) over acetylation on H4K5 weakens bromodomain containing protein 4 (BRD4) bromodomain-dependent chromatin interaction and enhances BRD4 nuclear mobility and availability for binding transcription start site regions of active genes. Our data suggest that the metabolism-driven control of the histone acetylation/longer-chain acylation(s) ratio could be a common mechanism regulating the bromodomain factors' functional genomic distribution.</p>',
			'date' => '2021-07-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.celrep.2021.109460',
			'doi' => '10.1016/j.celrep.2021.109460',
			'modified' => '2022-08-03 16:14:09',
			'created' => '2022-05-19 10:41:50',
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		(int) 45 => array(
			'id' => '4343',
			'name' => 'The SAM domain-containing protein 1 (SAMD1) acts as a repressivechromatin regulator at unmethylated CpG islands',
			'authors' => 'Stielow B. et al. ',
			'description' => '<p>CpG islands (CGIs) are key regulatory DNA elements at most promoters, but how they influence the chromatin status and transcription remains elusive. Here, we identify and characterize SAMD1 (SAM domain-containing protein 1) as an unmethylated CGI-binding protein. SAMD1 has an atypical winged-helix domain that directly recognizes unmethylated CpG-containing DNA via simultaneous interactions with both the major and the minor groove. The SAM domain interacts with L3MBTL3, but it can also homopolymerize into a closed pentameric ring. At a genome-wide level, SAMD1 localizes to H3K4me3-decorated CGIs, where it acts as a repressor. SAMD1 tethers L3MBTL3 to chromatin and interacts with the KDM1A histone demethylase complex to modulate H3K4me2 and H3K4me3 levels at CGIs, thereby providing a mechanism for SAMD1-mediated transcriptional repression. The absence of SAMD1 impairs ES cell differentiation processes, leading to misregulation of key biological pathways. Together, our work establishes SAMD1 as a newly identified chromatin regulator acting at unmethylated CGIs.</p>',
			'date' => '2021-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33980486',
			'doi' => '10.1126/sciadv.abf2229',
			'modified' => '2022-08-03 16:34:24',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
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		),
		(int) 46 => array(
			'id' => '4192',
			'name' => 'Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-inducedprogrammed cell death in Arabidopsis.',
			'authors' => 'Dvořák Tomaštíková E. et al.',
			'description' => '<p>The Polycomb Repressive Complex 2 (PRC2) is well-known for its role in controlling developmental transitions by suppressing the premature expression of key developmental regulators. Previous work revealed that PRC2 also controls the onset of senescence, a form of developmental programmed cell death (PCD) in plants. Whether the induction of PCD in response to stress is similarly suppressed by the PRC2 remained largely unknown. In this study, we explored whether PCD triggered in response to immunity- and disease-promoting pathogen effectors is associated with changes in the distribution of the PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) modification in Arabidopsis thaliana. We furthermore tested the distribution of the heterochromatic histone mark H3K9me2, which is established, to a large extent, by the H3K9 methyltransferase KRYPTONITE, and occupies chromatin regions generally not targeted by PRC2. We report that effector-induced PCD caused major changes in the distribution of both repressive epigenetic modifications and that both modifications have a regulatory role and impact on the onset of PCD during pathogen infection. Our work highlights that the transition to pathogen-induced PCD is epigenetically controlled, revealing striking similarities to developmental PCD.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33566101',
			'doi' => '10.1093/plphys/kiab035',
			'modified' => '2022-01-06 14:12:23',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
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			'id' => '4273',
			'name' => 'An integrated multi-omics analysis identifies prognostic molecularsubtypes of non-muscle-invasive bladder cancer',
			'authors' => 'Lindskrog Sia Viborg et al.',
			'description' => '<p>The molecular landscape in non-muscle-invasive bladder cancer (NMIBC) is characterized by large biological heterogeneity with variable clinical outcomes. Here, we perform an integrative multi-omics analysis of patients diagnosed with NMIBC (n&thinsp;=&thinsp;834). Transcriptomic analysis identifies four classes (1, 2a, 2b and 3) reflecting tumor biology and disease aggressiveness. Both transcriptome-based subtyping and the level of chromosomal instability provide independent prognostic value beyond established prognostic clinicopathological parameters. High chromosomal instability, p53-pathway disruption and APOBEC-related mutations are significantly associated with transcriptomic class 2a and poor outcome. RNA-derived immune cell infiltration is associated with chromosomally unstable tumors and enriched in class 2b. Spatial proteomics analysis confirms the higher infiltration of class 2b tumors and demonstrates an association between higher immune cell infiltration and lower recurrence rates. Finally, the independent prognostic value of the transcriptomic classes is documented in 1228 validation samples using a single sample classification tool. The classifier provides a framework for biomarker discovery and for optimizing treatment and surveillance in next-generation clinical trials.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863885',
			'doi' => '10.1038/s41467-021-22465-w',
			'modified' => '2022-05-23 09:49:43',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
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		(int) 48 => array(
			'id' => '4109',
			'name' => 'VPRBP functions downstream of the androgen receptor and OGT to restrict p53 activation in prostate cancer ',
			'authors' => 'Poulose N. et al. ',
			'description' => '<p>Androgen receptor (AR) is a major driver of prostate cancer (PCa) initiation and progression. O-GlcNAc transferase (OGT), the enzyme that catalyses the covalent addition of UDP-N-acetylglucosamine (UDP-GlcNAc) to serine and threonine residues of proteins, is often up-regulated in PCa with its expression correlated with high Gleason score. In this study we have identified an AR and OGT co-regulated factor, VPRBP/DCAF1. We show that VPRBP is regulated by the AR at the transcript level, and by OGT at the protein level. In human tissue samples, VPRBP protein expression correlated with AR amplification, OGT overexpression and poor prognosis. VPRBP knockdown in prostate cancer cells led to a significant decrease in cell proliferation, p53 stabilization, nucleolar fragmentation and increased p53 recruitment to the chromatin. In conclusion, we have shown that VPRBP/DCAF1 promotes prostate cancer cell proliferation by restraining p53 activation under the influence of the AR and OGT.</p>',
			'date' => '2021-02-21',
			'pmid' => 'https://www.biorxiv.org/content/10.1101/2021.02.28.433236v1',
			'doi' => '',
			'modified' => '2021-07-07 11:59:15',
			'created' => '2021-07-07 11:59:15',
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		),
		(int) 49 => array(
			'id' => '4124',
			'name' => 'JAZF1, A Novel p400/TIP60/NuA4 Complex Member, Regulates H2A.ZAcetylation at Regulatory Regions.',
			'authors' => 'Procida, Tara and Friedrich, Tobias and Jack, Antonia P M and Peritore,Martina and Bönisch, Clemens and Eberl, H Christian and Daus, Nadine andKletenkov, Konstantin and Nist, Andrea and Stiewe, Thorsten and Borggrefe,Tilman and Mann, Matthias and Bartk',
			'description' => '<p>Histone variants differ in amino acid sequence, expression timing and genomic localization sites from canonical histones and convey unique functions to eukaryotic cells. Their tightly controlled spatial and temporal deposition into specific chromatin regions is accomplished by dedicated chaperone and/or remodeling complexes. While quantitatively identifying the chaperone complexes of many human H2A variants by using mass spectrometry, we also found additional members of the known H2A.Z chaperone complexes p400/TIP60/NuA4 and SRCAP. We discovered JAZF1, a nuclear/nucleolar protein, as a member of a p400 sub-complex containing MBTD1 but excluding ANP32E. Depletion of JAZF1 results in transcriptome changes that affect, among other pathways, ribosome biogenesis. To identify the underlying molecular mechanism contributing to JAZF1's function in gene regulation, we performed genome-wide ChIP-seq analyses. Interestingly, depletion of JAZF1 leads to reduced H2A.Z acetylation levels at &gt; 1000 regulatory sites without affecting H2A.Z nucleosome positioning. Since JAZF1 associates with the histone acetyltransferase TIP60, whose depletion causes a correlated H2A.Z deacetylation of several JAZF1-targeted enhancer regions, we speculate that JAZF1 acts as chromatin modulator by recruiting TIP60's enzymatic activity. Altogether, this study uncovers JAZF1 as a member of a TIP60-containing p400 chaperone complex orchestrating H2A.Z acetylation at regulatory regions controlling the expression of genes, many of which are involved in ribosome biogenesis.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33445503',
			'doi' => '10.3390/ijms22020678',
			'modified' => '2021-12-07 10:00:44',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
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		(int) 50 => array(
			'id' => '4179',
			'name' => 'Histone demethylase JMJD2B/KDM4B regulates transcriptional program viadistinctive epigenetic targets and protein interactors for the maintenanceof trophoblast stem cells.',
			'authors' => 'Mak, Kylie Hin-Man et al.',
			'description' => '<p>Trophoblast stem cell (TSC) is crucial to the formation of placenta in mammals. Histone demethylase JMJD2 (also known as KDM4) family proteins have been previously shown to support self-renewal and differentiation of stem cells. However, their roles in the context of the trophoblast lineage remain unclear. Here, we find that knockdown of Jmjd2b resulted in differentiation of TSCs, suggesting an indispensable role of JMJD2B/KDM4B in maintaining the stemness. Through the integration of transcriptome and ChIP-seq profiling data, we show that JMJD2B is associated with a loss of H3K36me3 in a subset of embryonic lineage genes which are marked by H3K9me3 for stable repression. By characterizing the JMJD2B binding motifs and other transcription factor binding datasets, we discover that JMJD2B forms a protein complex with AP-2 family transcription factor TFAP2C and histone demethylase LSD1. The JMJD2B-TFAP2C-LSD1 complex predominantly occupies active gene promoters, whereas the TFAP2C-LSD1 complex is located at putative enhancers, suggesting that these proteins mediate enhancer-promoter interaction for gene regulation. We conclude that JMJD2B is vital to the TSC transcriptional program and safeguards the trophoblast cell fate via distinctive protein interactors and epigenetic targets.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33441614',
			'doi' => '10.1038/s41598-020-79601-7',
			'modified' => '2021-12-21 16:43:16',
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			'id' => '4210',
			'name' => 'Trans- and cis-acting effects of Firre on epigenetic features of theinactive X chromosome.',
			'authors' => 'Fang, He and Bonora, Giancarlo and Lewandowski, Jordan P and Thakur,Jitendra and Filippova, Galina N and Henikoff, Steven and Shendure, Jay andDuan, Zhijun and Rinn, John L and Deng, Xinxian and Noble, William S andDisteche, Christine M',
			'description' => '<p>Firre encodes a lncRNA involved in nuclear organization. Here, we show that Firre RNA expressed from the active X chromosome maintains histone H3K27me3 enrichment on the inactive X chromosome (Xi) in somatic cells. This trans-acting effect involves SUZ12, reflecting interactions between Firre RNA and components of the Polycomb repressive complexes. Without Firre RNA, H3K27me3 decreases on the Xi and the&nbsp;Xi-perinucleolar location is disrupted, possibly due to decreased CTCF binding on the Xi. We also observe widespread gene dysregulation, but not on the Xi. These effects are measurably rescued by ectopic expression of mouse or human Firre/FIRRE transgenes, supporting conserved trans-acting roles. We also find that the compact 3D structure of the Xi partly depends on the Firre locus and its RNA. In common lymphoid progenitors and T-cells Firre exerts a cis-acting effect on maintenance of H3K27me3 in a 26&thinsp;Mb region around the locus, demonstrating cell type-specific trans- and cis-acting roles of this lncRNA.</p>',
			'date' => '2020-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33247132',
			'doi' => '10.1038/s41467-020-19879-3',
			'modified' => '2022-01-13 15:03:45',
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			'name' => 'H2A.Z is dispensable for both basal and activated transcription inpost-mitotic mouse muscles.',
			'authors' => 'Belotti E. et al.',
			'description' => '<p>While the histone variant H2A.Z is known to be required for mitosis, it is also enriched in nucleosomes surrounding the transcription start site of active promoters, implicating H2A.Z in transcription. However, evidence obtained so far mainly rely on correlational data generated in actively dividing cells. We have exploited a paradigm in which transcription is uncoupled from the cell cycle by developing an in vivo system to inactivate H2A.Z in terminally differentiated post-mitotic muscle cells. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is a marker but not an active driver of transcription.</p>',
			'date' => '2020-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32266374',
			'doi' => '10.1093/nar/gkaa157',
			'modified' => '2022-01-13 13:46:38',
			'created' => '2021-12-06 15:53:19',
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	'description' => '<p>Diagenode&rsquo;s MicroPlex Library Preparation Kits v3 have been extensively validated for ChIP-seq samples and are optimized to generate DNA libraries with high molecular complexity from the lowest input amounts &ndash; down to 50 pg. The kit MicroPlex v3 includes all buffers and enzymes necessary for the library preparation. For flexibility of the choice different formats of compatible primer indexes are available separately:</p>
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<li><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns">C05010003 - 24 Dual indexes for MicroPlex Kit v3 /48 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1">C05010004 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set I /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2">C05010005 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set II /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3">C05010006 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set III /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4">C05010007 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV /96 rxns</a></li>
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<p style="padding-left: 30px;">NEW! Unique dual indexes :</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1">C05010008 - 24 UDI for MicroPlex Kit v3 - Set I</a></li>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2">C05010009 - 24 UDI for MicroPlex Kit v3 - Set II</a></li>
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<p>Read more about<span>&nbsp;</span><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">library preparation for ChIP-seq</a></p>
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<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
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<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
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<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
<div id="first" class="content">
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<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
</div>
</li>
</ul>
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			'name' => 'MicroPlex Library Preparation Kit v3 /48 rxns',
			'description' => '<p><a href="https://www.diagenode.com/files/products/kits/Microplex-library-prep-v3.pdf"><img src="https://www.diagenode.com/img/buttons/bt-manual.png" /></a></p>
<p>Diagenode&rsquo;s <strong>MicroPlex Library Preparation Kits v3</strong> have been extensively validated for ChIP-seq samples and are optimized to generate DNA libraries with high molecular complexity from the lowest input amounts &ndash; down to 50 pg. The kit MicroPlex v3 includes all buffers and enzymes necessary for the library preparation. For flexibility of the choice different formats of compatible primer indexes are available separately:</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns">C05010003 - 24 Dual indexes for MicroPlex Kit v3 /48 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1">C05010004 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set I /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2">C05010005 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set II /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3">C05010006 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set III /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4">C05010007 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV /96 rxns</a></li>
</ul>
<p style="padding-left: 30px;">NEW! Unique dual indexes :</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1">C05010008 - 24 UDI for MicroPlex Kit v3 - Set I</a></li>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2">C05010009 - 24 UDI for MicroPlex Kit v3 - Set II</a></li>
</ul>
<p>Read more about <a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">library preparation for ChIP-seq</a></p>
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<li><strong>1 tube</strong>, <strong>2 hours</strong>, <strong>3 steps</strong> protocol</li>
<li><strong>Input</strong>: 50 pg &ndash; 50 ng</li>
<li><strong>Reduce potential bias</strong> - few PCR amplification cycles needed</li>
<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
<li><strong>Great multiplexing flexibility</strong> with 24 dual indexes (8 nt)</li>
<li><strong>Validated with the IP-<a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit">Star<sup>&reg;</sup></a></strong><a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit"> Automated Platform</a></li>
</ul>
<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
<div id="first" class="content">
<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
</div>
</li>
</ul>
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			'meta_keywords' => 'MicroPlex Library Preparation Kit',
			'meta_description' => 'MicroPlex Library Preparation Kits v3 have been extensively validated for ChIP-seq samples and are optimized to generate DNA libraries with high molecular complexity from the lowest input amounts – down to 50 pg.',
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<div class="small-12 medium-12 large-12 columns">
<p><span style="font-weight: 400;">Most of the major next-generation sequencing platforms require ligation of specific adaptor oligos to </span><a href="../applications/dna-rna-shearing"><span style="font-weight: 400;">fragmented DNA or RNA</span></a><span style="font-weight: 400;"> prior to sequencing</span></p>
<p><span style="font-weight: 400;">After input DNA has been fragmented, it is end-repaired and blunt-ended</span><span style="font-weight: 400;">. The next step is a A-tailing in which dAMP is added to the 3&acute; end of the blunt phosphorylated DNA fragments to prevent concatemerization and to allow the ligation of adaptors with complementary dT overhangs. In addition, barcoded adapters can be incorporated to facilitate multiplexing prior to or during amplification.</span></p>
<center><img src="https://www.diagenode.com/img/categories/library-prep/flux.png" /></center>
<p><span style="font-weight: 400;">Diagenode offers a comprehensive product portfolio for library preparation:<br /></span></p>
<strong><a href="https://www.diagenode.com/en/categories/Library-preparation-for-RNA-seq">D-Plex&nbsp;RNA-seq Library Preparation Kits</a></strong><br />
<p><span style="font-weight: 400;">Diagenode&rsquo;s new RNA-sequencing solutions utilize the innovative c</span><span style="font-weight: 400;">apture and a</span><span style="font-weight: 400;">mplification by t</span><span style="font-weight: 400;">ailing and s</span><span style="font-weight: 400;">witching&rdquo;</span><span style="font-weight: 400;">, a ligation-free method to produce DNA libraries for next generation sequencing from low input amounts of RNA. </span><span style="font-weight: 400;"></span><a href="../categories/Library-preparation-for-RNA-seq">Learn more</a></p>
<strong><a href="../categories/library-preparation-for-ChIP-seq">ChIP-seq and DNA sequencing library preparation solutions</a></strong><br />
<p><span style="font-weight: 400;">Our kits have been optimized for DNA library preparation used for next generation sequencing for a wide range of inputs. Using a simple three-step protocols, our</span><a href="http://www.diagenode.com/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><span style="font-weight: 400;"> </span></a><span style="font-weight: 400;">kits are an optimal choice for library preparation from DNA inputs down to 50 pg.&nbsp;</span><a href="../categories/library-preparation-for-ChIP-seq">Learn more</a></p>
<a href="../p/bioruptor-pico-sonication-device"><span style="font-weight: 400;"></span><strong>Bioruptor Pico - short fragments</strong></a><a href="../categories/library-preparation-for-ChIP-seq-and-DNA-sequencing"><span style="font-weight: 400;"></span></a><br />
<p><span style="font-weight: 400;"></span><span style="font-weight: 400;">Our well-cited Bioruptor Pico is the shearing device of choice for chromatin and DNA fragmentation. Obtain uniform and tight fragment distributions &nbsp;between 150bp -2kb. </span><a href="../p/bioruptor-pico-sonication-device">Learn more</a></p>
<strong><a href="../p/megaruptor2-1-unit"><span href="../p/bioruptor-pico-sonication-device">Megaruptor</span>&reg; - long fragments</a></strong><a href="../p/bioruptor-pico-sonication-device"><span style="font-weight: 400;"></span></a><a href="../categories/library-preparation-for-ChIP-seq-and-DNA-sequencing"><span style="font-weight: 400;"></span></a><br />
<p><span style="font-weight: 400;"></span><span style="font-weight: 400;">The Megaruptor is designed to shear DNA from 3kb-75kb for long-read sequencing.&nbsp; <a href="../p/megaruptor2-1-unit">Learn more</a></span></p>
<span href="../p/bioruptor-pico-sonication-device"></span><span style="font-weight: 400;"></span></div>
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			'meta_description' => 'Diagenode offers a comprehensive product portfolio for library preparation such as CATS RNA-seq Library Preparation Kits,ChIP-seq and DNA sequencing library preparation solutions',
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			'name' => 'Library preparation for ChIP-seq',
			'description' => '<div class="row">
<div class="large-12 columns text-justify">
<p>Library preparation following ChIP can be challenging due to the limited amount of DNA recovered after ChIP. Diagenode has developed the optimal solutions for ChIP-seq using two different approaches: the ligation-based library preparation on purified DNA or the tagmentation-based ChIPmentation.</p>
</div>
</div>
<div class="row extra-spaced">
<div class="large-12 columns"><center><a href="https://www.diagenode.com/en/pages/form-microplex-promo" target="_blank"></a></center></div>
</div>
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div id="portal" class="main-portal">
<div class="portal-inner"><nav class="portal-nav">
<ul data-tab="" class="tips-menu">
<li><a href="#panel1" class="tips portal button">Ligation-based library prep</a></li>
<li><a href="#panel2" class="tips portal button">ChIPmentation</a></li>
<li><a href="#panel3" class="tips portal button">Kit choice guide</a></li>
<li><a href="#panel4" class="tips portal button">Resources</a></li>
<li><a href="#panel5" class="tips portal button">FAQs</a></li>
</ul>
</nav></div>
</div>
<div class="tabs-content">
<div class="content active" id="panel1">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v5" style="color: #13b29c;"><i class="fa fa-caret-right"></i> Standard input library prep</a>
<div id="v5" class="content">
<div class="small-12 medium-12 large-12 columns">
<p>The <strong>iDeal Library Preparation Kit</strong> reliably converts DNA into indexed libraries for next-generation sequencing, with input amounts down to <strong>5 ng</strong>. Our kit offers a simple and fast workflow, high yields, and ready-to-sequence DNA on the Illumina platform.</p>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> <strong>Sample</strong>: Fragmented dsDNA</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Input</strong>: 5 ng &ndash; 1 &micro;g</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Fast protocol</strong>: 3 hours</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Easy processing</strong>: 3 steps</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Indexing</strong>: single indexes for multiplexing up to 24 samples</li>
<li><i class="fa fa-arrow-circle-right"></i> Manual and automated protocols available</li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<ul class="square">
<li>MeDIP-seq library prep</li>
<li>Genomic DNA sequencing</li>
<li>High input ChIP-seq</li>
</ul>
</div>
<div class="extra-spaced">
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010020</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" style="color: #b21329;" target="_blank">iDeal Library Preparation Kit x24 (incl. Index Primer Set 1)</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010021</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" style="color: #b21329;" target="_blank">Index Primer Set 2 (iDeal Lib. Prep Kit x24)</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
</li>
</ul>
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v4" style="color: #13b29c;"><i class="fa fa-caret-right"></i> Low input library prep</a>
<div id="v4" class="content active"><center><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" target="_blank"><img src="https://www.diagenode.com/img/banners/banner-microplex-v3-580.jpg" class="extra-spaced" /></a></center>
<div align="center"><a href="https://www.diagenode.com/pages/form-microplex3" class="center alert radius button extra-spaced"><i class="fa fa-info"></i> Contact us</a></div>
<div class="extra-spaced">
<p>Diagenode&rsquo;s <strong>MicroPlex Library Preparation kits</strong> have been extensively validated for ChIP-seq samples. Generated libraries are compatible with single-end or paired-end sequencing. MicroPlex chemistry (using stem-loop adapters ) is specifically developed and optimized to generate DNA libraries with high molecular complexity from the lowest input amounts. Only <strong>50 pg to 50 ng</strong> of fragmented double-stranded DNA is required for library preparation. The entire <strong>three-step workflow</strong> takes place in a <strong>single tube</strong> or well in about <strong>2 hours</strong>. No intermediate purification steps and no sample transfers are necessary to prevent handling errors and loss of valuable samples.</p>
</div>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> <strong>Sample</strong>: Fragmented dsDNA</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Low input</strong>: 50 pg &ndash; 50 ng</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Fast protocol</strong>: 2 hours</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Easy processing</strong>: 3 steps in 1 tube</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>No intermediate purification</strong></li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
<li><i class="fa fa-arrow-circle-right"></i> Manual and automated protocols available</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<ul class="square">
<li>ChIP-seq library prep from ChIP-derived DNA</li>
<li>Low input DNA sequencing</li>
</ul>
</div>
<h2>Two versions are available:</h2>
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v2" style="color: #13b29c;"><i class="fa fa-caret-right"></i> MicroPlex Library Preparation Kit v2 with single indexes</a>
<div id="v2" class="content">
<p>The MicroPlex Library Preparation Kit v2 contains all necessary reagents including single indexes for multiplexing up to 48 samples using single barcoding.</p>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010012</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v2 (12 indexes)</a></td>
<td class="format">12 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</li>
<li class="accordion-navigation"><a href="#v3" style="color: #13b29c;"><i class="fa fa-caret-right"></i> MicroPlex Library Preparation Kit v3 with dual indexes &nbsp;&nbsp;<strong><span class="diacol">NEW!</span></strong></a>
<div id="v3" class="content active">
<p>In this version the library preparation reagents and the dual indexes are available separately allowing for the flexibility choosing the number of indexes. MicroPlex v3 has multiplexing capacities up to 384 samples.</p>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010001</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v3 /48 rxns</a></td>
<td class="format">48 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010002</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v3 /96 rxns</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
<h4>DUAL INDEXES</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010003</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" style="color: #b21329;" target="_blank">24 Dual indexes for MicroPlex Kit v3</a></td>
<td class="format">48 rxns</td>
<td><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010004</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set I</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010005</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set II</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010006</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set III</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010007</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</li>
</ul>
</div>
</li>
</ul>
</div>
</div>
</div>
<div class="content active" id="panel2">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<p>The TAG Kit for ChIPmentation offers an optimized ChIP-seq library preparation solution based on tagmentation. This kit includes reagents for tagmentation-based library preparation integrated in the IP and is compatible with any ChIP protocol based on magnetic beads. The primer indexes for multiplexing&nbsp;must be purchased separately and are available as a reference: <a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" target="_blank">24 SI for ChIPmentation</a>, Cat. No. C01011031. Alternatively, for histone marks, Diagenode proposes the complete solution (including all buffers for ChIP, tagmentation and multiplexing): <a href="https://www.diagenode.com/en/p/manual-chipmentation-kit-for-histones-24-rxns" target="_blank">ChIPmentation for Histones</a>.</p>
</div>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> Sample: chromatin-antibody-magnetic beads complexes</li>
<li><i class="fa fa-arrow-circle-right"></i> Input: chromatin from 5 K &ndash; 4 M cells</li>
<li><i class="fa fa-arrow-circle-right"></i> Easy and fast protocol</li>
<li><i class="fa fa-arrow-circle-right"></i> Compatible with any ChIP protocol based on magnetic beads</li>
<li><i class="fa fa-arrow-circle-right"></i> No adapter dimers</li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<p class="lead"><em><strong>TAG kit for ChIPmentation</strong></em></p>
<ul class="square">
<li>ChIPmentation library preparation</li>
</ul>
<p class="lead"><em><strong>24 SI for for ChIPmentation</strong></em></p>
<ul class="square">
<li>ChIPmentation library preparation</li>
<li>Tagmentation-based library preparation methods like ATAC-seq, CUT&amp;Tag</li>
</ul>
</div>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C01011030</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" style="color: #b21329;" target="_blank">TAG Kit for ChIPmentation</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C01011031</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" style="color: #b21329;" target="_blank">24 SI for ChIPmentation</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
<div class="content" id="panel3">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<h3 class="text-center diacol"><em>How to choose your library preparation kit?</em></h3>
</div>
<table class="noborder">
<tbody>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Sample</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Chromatin-antibody-beads complex</p>
</td>
<td colspan="2">
<p class="text-center" style="font-size: 15px;">Purified DNA</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Purified DNA</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td colspan="2"><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Application</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">ChIPmentation</p>
</td>
<td colspan="2">
<p class="text-center" style="font-size: 15px;">ChIP-seq library prep<br /> Low input DNA sequencing</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">MeDIP-seq library prep<br /> Genomic DNA sequencing<br /> High input ChIP-seq</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td colspan="2"><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Input</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Chromatin: 5 K to 4 M cells</p>
</td>
<td colspan="2&quot;">
<p class="text-center" style="font-size: 15px;">DNA: 50 pg &ndash; 50 ng</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">DNA: 5 ng &ndash; 1 &micro;g</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow-45-left.png" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow-45-right.png" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Multiplexing</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 24 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 384 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 48 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 24 samples</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Indexes</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Dual indexes (DI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Kit</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>TAG Kit for ChIPmentation</strong><br /> (indexes not included in the kit)</p>
<p class="text-center"><strong>Kit</strong><br /> <a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" target="_blank">C01011030 &ndash; 24 rxns</a></p>
<p class="text-center"><strong>Single indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" target="_blank">C01011031 &ndash; 24 SI/24 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>MicroPlex Library Preparation Kit v3</strong><br />(dual indexes not included in the kit)</p>
<p class="text-center"><strong>Kit</strong><br /> <a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" target="_blank">C05010001 - 48 rxns</a><br /> <a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" target="_blank">C05010002 - 96 rxns</a></p>
<br />
<p class="text-center"><strong>Unique dual indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1" target="_blank">C05010008 - Set I 24 UDI / 24 rxns</a><br /> <a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2" target="_blank">C05010009 - Set II 24 UDI/ 24 rxns</a></p>
<p class="text-center"><strong>Dual indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" target="_blank">C05010003 - 24 DI/ 48 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" target="_blank">C05010004 - Set I 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" target="_blank">C05010005 - Set II 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" target="_blank">C05010006 - Set III 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" target="_blank">C05010007 - Set IV 96 DI/ 96 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>MicroPlex Library Preparation Kit v2</strong><br />(single indexes included in the kit)</p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" target="_blank">C05010012 - 12 SI/ 12 rxns</a><br /> <a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x48-12-indices-48-rxns" target="_blank">C05010013 - 12 SI/ 48 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>iDeal Library Preparation Kit</strong><br />(Set 1 of indexes included in the kit)</p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" target="_blank">C05010020 - 12 SI/ 24 rxns</a></p>
<p class="text-center" style="font-size: 15px;"><strong>Index Primer Set 2</strong></p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" target="_blank">C05010021 - 12 SI/ 24 rxns</a></p>
</td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
<div class="content" id="panel4">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<p>Combined chromatin immunoprecipitation and next-generation sequencing (ChIP-seq) has become the gold standard to investigate genome-wide epigenetic profiles. However, ChIP from a limited amount of cells has been a challenge. Here we provide a complete and robust workflow solution for successful ChIP-seq from small numbers of cells using the True MicroChIP kit and MicroPlex Library Preparation kit.</p>
<blockquote><span class="label-green" style="margin-bottom: 16px; margin-left: -22px;">APPLICATION NOTE</span>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><center><img src="https://www.diagenode.com/img/categories/microplex/chip-efficiency-on-10000-cells.jpg" /></center>
<p><small><em>ChIP efficiency on 10,000 cells</em></small></p>
</div>
<div class="small-12 medium-6 large-6 columns">
<p><strong>From minuscule amounts to magnificent results:</strong><br /> reliable ChIP-seq data from 10,000 cells with the True MicroChIP&trade; and the MicroPlex Library Preparation&trade; kits.</p>
<a href="https://www.diagenode.com/files/application_notes/True_MicroChIP_and_MicroPlex_kits_Application_Note.pdf" class="details small button" target="_blank">DOWNLOAD</a></div>
</div>
</blockquote>
<blockquote><span class="label-green" style="margin-bottom: 16px; margin-left: -22px;">APPLICATION NOTE</span>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><center><img src="https://www.diagenode.com/img/categories/microplex/quality-control-check.jpg" /></center>
<p class="text-left"><small><em>Quality control check of a ChIP-seq library on the Fragment Analyzer. High Efficiency ChIP performed on 10,000 cells</em></small></p>
</div>
<div class="small-12 medium-6 large-6 columns">
<p class="text-left"><strong>Best Workflow Practices for ChIP-seq Analysis with Small Samples</strong></p>
<a href="https://www.diagenode.com/files/application_notes/Diagenode_AATI_Joint.pdf" class="details small button" target="_blank">DOWNLOAD</a></div>
</div>
</blockquote>
</div>
</div>
</div>
<div class="content" id="panel5">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<h2>TAG Kit for ChIPmentation</h2>
<ol>
<li><strong>What is the difference between tagmentation and ChIPmentation?</strong><br />Tagmentation is a reaction where an enzyme (a transposase) cleaves DNA and incorporates sequencing adaptors at the ends of the fragments in one step. In our ChIPmentation technology we combine chromatin immunoprecipitation and tagmentation in one streamlined workflow where the tagmentation step occurs directly on chromatin.<br /><br /></li>
<li><strong>What is the expected concentration of ChIPmentation libraries?</strong><br />The concentration of libraries that you need to reach will depend on the sensitivity of the machine and kits that you will use to perform the quality control and the sequencing of your libraries. Usually a concentration of 4-8 ng/&mu;l is enough for a quality control using the Qubit High Sensitivity assay (ThermoFischer Scientific) and the High Sensitivity chip for BioAnalyzer (Agilent) and for sequencing on Illumina HiSeq3000/4000.<br /><br /></li>
<li><strong>Does the ChIPmentation approach work on plants?</strong><br />Our ChIPmentation solution has been validated on human cells and we do not have any data on plants. It should be compatible. We would recommend using our Universal Plant ChIP Kit in combination with the TAG Kit for ChIPmentation and the 24 SI for ChIPmentation.<br /><br /></li>
<li><strong>What is the size of the fragments after the tagmentation?</strong><br />The size of the fragments at the end of the ChIPmentation protocol can vary depending on many parameters like the shearing efficiency, the antibody used or the tagmentation time. However, with our standard protocol we usually obtain a library peak which is around 200-300 bp (see example of results at the end of the manual). If many fragments larger than 500 bp are present , the best would be to contact your sequencing provider to ask what their requirements are, because it can vary depending on the sequencer. If you want to remove the large fragments you can use the size selection protocol described in the manual.<br /><br /></li>
<li><strong>What is the size of the adapters?</strong><br />The sum of the adapters is 128 bp.</li>
</ol>
</div>
<div class="extra-spaced">
<h2>MicroPlex Library Preparation Kit</h2>
<ol>
<li><strong>Can I use the available Illumina primers and validate them with the MicroPlex Kit v2?</strong><br /> Although the final flanking sequences of MicroPlex are the same as those used by Illumina, the PCR primers are not identical and part of them is supplied with the buffer. For this reason Illumina primers will not work as substitute.<br /><br /></li>
<li><strong>The BioAnalyzer profile of purified library shows the presence of low molecular weight peaks (primers/adaptors) in the samples. Should I re- purify the samples or they can be used directly to the sequencing? If the second purification is recommended, which ratio sample/AMPure beads should I use?</strong><br /> You can do a second round of purification using 1:1 ratio of AMPure beads to sample and this should get rid of the majority of the dimers.<br /><br /></li>
<li><strong>I am going to use the MicroPlex Library Preparation Kit v2 on ChIP samples . Our thermocycler has ramp rate 1.5&deg;/s max while the protocol recommends using a ramp rate 3 to 5&deg;/s. How would this affect the library prep?</strong><br /> We have not used a thermocycler with a ramp rate of 1.5 &deg;C, which seems faster than most of thermocyclers. Too fast of a ramp rate may affect the primer annealing and ligation steps.<br /><br /></li>
<li><strong>What is the function of the replication stop site in the adapter loops?</strong><br /> The replication stop site in the adaptor loops function to stop the polymerase from continuing to copy the rest of the stem loop.<br /><br /></li>
<li><strong>I want to do ChIP-seq. Which ChIP-seq kit can I use for sample preparation prior to Microplex Library Preparation Kit v2?</strong><br /> In our portfolio there are several ChIP-seq kits compatible with Microplex Library Preparation Kit v2. Depending on your sample type and target studied you can use the following kits: iDeal ChIP-seq Kit for Transcription Factors (Cat. No. C01010055), iDeal ChIP-seq Kit for Histones (Cat. No. C01010051), True MicroChIP kit (Cat. No. C01010130), Universal Plant ChIP-seq Kit (Cat. No. C01010152). All these kits exist in manual and automated versions.<br /><br /></li>
<li><strong>Is Microplex Library Preparation Kit v2 compatible with exome enrichment methods?</strong><br /> Microplex Library Preparation Kit v2 is compatible with major exome and target enrichment products, including Agilent SureSelect<sup>&reg;</sup>, Roche NimbleGen<sup>&reg;</sup> SeqCap<sup>&reg;</sup> EZ and custom panels.<br /><br /></li>
<li><strong>What is the nick that is mentioned in the kit method overview?</strong><br /> The nick is simply a gap between a stem adaptor and 3&rsquo; DNA end, as shown on the schema in the kit method overview.<br /><br /></li>
<li><strong>Are the indexes of the MicroPlex library preparation kit v2 located at i5 or i7?</strong><br /> The libraries generated with the MicroPlex kit v2 contain indices located at i7.<br /><br /></li>
<li><strong>Is there a need to use custom index read primers for the sequencing to read the 8nt iPCRtags?</strong><br /> There is no need for using custom Sequencing primer to sequence MicroPlex libraires. MicroPlex libraries can be sequenced using standard Illumina Sequencing kits and protocols.<br /><br /></li>
<li><strong>What is the advantage of using stem-loop adapter in the MicroPlex kit?</strong><br /> There are several advantages of using stem-loop adaptors. First of all, stem-loop adaptors prevent from self-ligation thus increases the ligation efficiency between the adapter and DNA fragment. Moreover, the background is reduced using ds adaptors with no single-stranded tails. Finally, adaptor-adaptor ligation is reduced using blocked 5&rsquo; ends.<br /><br /></li>
</ol>
</div>
<div class="extra-spaced">
<h2>IDeal Library Preparation Kit</h2>
<ol>
<li><strong>Are the index from the iDeal library Prep kit compatible with the MicroPlex library prep kit?</strong><br /> No, it is important to use only the indexes provided in the MicroPlex kit to ensure proper library preparation with this kit</li>
</ol>
</div>
</div>
</div>
</div>
</div>
</div>
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			'description' => '<p>Diagenode offers innovative DNA library preparation solutions such as a hyperactive tagmentase and the &ldquo;capture and amplification by tailing and switching&rdquo; (CATS), a ligation-free method to produce DNA libraries for next generation sequencing from low input amounts of DNA. Our powerfull ChIP-seq library preparation kits are also&nbsp;a great solution for low input DNA library preparation (discover our <a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">Diagenode MicroPlex family</a>).&nbsp;</p>
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			'meta_title' => 'Library preparation for DNA sequencing | Diagenode',
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			'id' => '1055',
			'name' => 'MicroPlex Library Preparation Kit v3',
			'description' => '<p>High Performance Library Preparation for Illumina<sup>&reg;</sup> NGS Platforms</p>',
			'image_id' => null,
			'type' => 'Manual',
			'url' => 'files/products/kits/Microplex-library-prep-v3.pdf',
			'slug' => 'microplex-library-prep-v3-manual',
			'meta_keywords' => '',
			'meta_description' => '',
			'modified' => '2019-07-18 11:50:25',
			'created' => '2019-07-18 11:50:25',
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			'id' => '1759',
			'name' => 'product/kits/chip-kit-icon.png',
			'alt' => 'chip kit icon',
			'modified' => '2018-01-18 15:26:13',
			'created' => '2018-01-18 15:08:38',
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	'Publication' => array(
		(int) 0 => array(
			'id' => '4997',
			'name' => 'ACE2 Enhances Sensitivity to PD-L1 Blockade by Inhibiting Macrophage-Induced Immunosuppression and Angiogenesis',
			'authors' => 'Peiyi Xie et al.',
			'description' => '<p><span>Anti-PD-L1-based combination immunotherapy has become the first-line treatment for unresectable hepatocellular carcinoma (HCC). However, the objective response rate is lower than 40%, highlighting the need to identify mechanisms of tolerance to immune checkpoint inhibitors and accurate biomarkers of response. Here, we employed next-generation sequencing to analyze HCC samples from 10 patients receiving anti-PD-L1 therapy. Activation of the renin-angiotensin system was elevated in nonresponders compared with responders, and ACE2 expression was significantly downregulated in nonresponders. ACE2 deficiency promoted HCC development and anti-PD-L1 resistance, whereas ACE2 overexpression inhibited HCC progression in immune competent mice. Mass cytometry by time of flight (CyTOF) revealed that ACE2 deficient murine orthotopic tumor tissues featured elevated M2-like tumor-associated macrophages (TAMs), displayed a CCR5+PD-L1+ immunosuppressive phenotype, and exhibited high VEGF&alpha; expression. ACE2 downregulated tumor intrinsic CCL5 expression by suppressing NF-&kappa;B signaling through the ACE2/angiotensin-(1&ndash;7)/Mas receptor axis. The lower CCL5 levels led to reduced activation of the JAK-STAT3 pathway and suppressed PD-L1 and VEGF&alpha; expression in macrophages, blocking macrophage infiltration and M2-like polarization. Pharmacological targeting of CCR5 using maraviroc enhanced the tumor suppressive effect of anti-PD-L1 therapy. Together, these findings suggest that activation of the ACE2 axis overcomes the immunosuppressive microenvironment of HCC and may serve as an immunotherapeutic target and predictive biomarker of response to PD-L1 blockade.</span></p>',
			'date' => '2024-11-04',
			'pmid' => 'https://aacrjournals.org/cancerres/article-abstract/doi/10.1158/0008-5472.CAN-24-0954/749696/ACE2-Enhances-Sensitivity-to-PD-L1-Blockade-by?redirectedFrom=fulltext',
			'doi' => 'https://doi.org/10.1158/0008-5472.CAN-24-0954',
			'modified' => '2024-11-07 11:22:24',
			'created' => '2024-11-07 11:22:24',
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		),
		(int) 1 => array(
			'id' => '4976',
			'name' => 'Extracellular vesicle-mediated trafficking of molecular cues during human brain development',
			'authors' => 'Forero A. et al.',
			'description' => '<p><span>Cellular crosstalk is an essential process influenced by numerous factors, including secreted vesicles that transfer nucleic acids, lipids, and proteins between cells. Extracellular vesicles (EVs) have been the center of many studies focusing on neurodegenerative disorders, but whether EVs display cell-type-specific features for cellular crosstalk during neurodevelopment is unknown. Here, using human-induced pluripotent stem cell-derived cerebral organoids, neural progenitors, neurons, and astrocytes, we identify heterogeneity in EV protein content and dynamics in a cell-type-specific and time-dependent manner. Our results support the trafficking of key molecules via EVs in neurodevelopment, such as the transcription factor YAP1, and their localization to differing cell compartments depending on the EV recipient cell type. This study sheds new light on the biology of EVs during human brain development.</span></p>',
			'date' => '2024-10-22',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01106-9',
			'doi' => '10.1016/j.celrep.2024.114755',
			'modified' => '2024-09-23 10:19:53',
			'created' => '2024-09-23 10:19:53',
			'ProductsPublication' => array(
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			)
		),
		(int) 2 => array(
			'id' => '4982',
			'name' => 'The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency',
			'authors' => 'Mathew Sheridan et al.',
			'description' => '<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Background</h3>
<p>The epigenetic factors KAT6A (MOZ/MYST3) and KMT2A (MLL/MLL1) interact in normal hematopoiesis to regulate progenitors&rsquo; self-renewal. Both proteins are recurrently translocated in AML, leading to impairment of critical differentiation pathways in these malignant cells. We evaluated the potential of different KAT6A therapeutic targeting strategies to alter the growth of KAT6A and KMT2A rearranged AMLs.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Methods</h3>
<p>We investigated the action and potential mechanisms of the first-in-class KAT6A inhibitor, WM-1119 in KAT6A and KMT2A rearranged&nbsp;(KAT6Ar and KMT2Ar) AML using cellular (flow cytometry, colony assays, cell growth) and molecular (shRNA knock-down, CRISPR knock-out, bulk and single-cell RNA-seq, ChIP-seq) assays. We also used two novel genetic murine KAT6A models combined with the most common KMT2Ar AML, KMT2A::MLLT3 AML. In these murine models, the catalytic activity of KAT6A, or the whole protein, can be conditionally abrogated or deleted. These models allowed us to compare the effects of specific KAT6A KAT activity inhibition with the complete deletion of the whole protein. Finally, we also tested these therapeutic approaches on human AML cell lines and primary patient AMLs.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Results</h3>
<p>We found that WM-1119 completely abrogated the proliferative and clonogenic potential of KAT6Ar cells<span>&nbsp;</span><i>in vitro.</i><span>&nbsp;</span>WM-1119 treatment was associated with a dramatic increase in myeloid differentiation program. The treatment also decreased stemness and leukemia pathways at the transcriptome level and led to loss of binding of the fusion protein at critical regulators of these pathways. In contrast, our pharmacologic and genetic results indicate that the catalytic activity of KAT6A plays a more limited role in KMT2Ar leukemogenicity, while targeting the whole KAT6A protein dramatically affects leukemic potential in murine KMT2A::MLLT3 AML.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Conclusion</h3>
<p>Our study indicates that inhibiting KAT6A KAT activity holds compelling promise for KAT6Ar AML patients. In contrast, targeted degradation of KAT6A, and not just its catalytic activity, may represent a more appropriate therapeutic approach for KMT2Ar AMLs.</p>',
			'date' => '2024-10-08',
			'pmid' => 'https://jhoonline.biomedcentral.com/articles/10.1186/s13045-024-01610-0',
			'doi' => 'https://doi.org/10.1186/s13045-024-01610-0',
			'modified' => '2024-10-11 10:00:42',
			'created' => '2024-10-11 10:00:42',
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		),
		(int) 3 => array(
			'id' => '4983',
			'name' => 'Integrated multi-omics analysis of PBX1 in mouse adult neural stem- and progenitor cells identifies a transcriptional module that functionally links PBX1 to TCF3/4',
			'authors' => 'Vera Laub et al.',
			'description' => '<p><span>Developmental transcription factors act in networks, but how these networks achieve cell- and tissue specificity is still poorly understood. Here, we explored pre-B cell leukemia homeobox 1 (PBX1) in adult neurogenesis combining genomic, transcriptomic, and proteomic approaches. ChIP-seq analysis uncovered PBX1 binding to numerous genomic sites. Integration of PBX1 ChIP-seq with ATAC-seq data predicted interaction partners, which were subsequently validated by mass spectrometry. Whole transcriptome spatial RNA analysis revealed shared expression dynamics of&nbsp;</span><em>Pbx1</em><span><span>&nbsp;</span>and interacting factors. Among these were class I bHLH proteins TCF3 and TCF4. RNA-seq following<span>&nbsp;</span></span><em>Pbx1</em><span>,<span>&nbsp;</span></span><em>Tcf3</em><span><span>&nbsp;</span>or<span>&nbsp;</span></span><em>Tcf4</em><span><span>&nbsp;</span>knockdown identified proliferation- and differentiation associated genes as shared targets, while sphere formation assays following knockdown argued for functional cooperativity of PBX1 and TCF3 in progenitor cell proliferation. Notably, while physiological PBX1-TCF interaction has not yet been described, chromosomal translocation resulting in genomic<span>&nbsp;</span></span><em>TCF3::PBX1</em><span><span>&nbsp;</span>fusion characterizes a subtype of acute lymphoblastic leukemia. Introducing<span>&nbsp;</span></span><em>Pbx1</em><span><span>&nbsp;</span>into Nalm6 cells, a pre-B cell line expressing<span>&nbsp;</span></span><em>TCF3</em><span><span>&nbsp;</span>but lacking<span>&nbsp;</span></span><em>PBX1</em><span>, upregulated the leukemogenic genes<span>&nbsp;</span></span><em>BLK</em><span><span>&nbsp;</span>and<span>&nbsp;</span></span><em>NOTCH3</em><span>, arguing that functional PBX1-TCF cooperativity likely extends to hematopoiesis. Our study hence uncovers a transcriptional module orchestrating the balance between progenitor cell proliferation and differentiation in adult neurogenesis with potential implications for leukemia etiology.</span></p>',
			'date' => '2024-10-08',
			'pmid' => 'https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkae864/7815639',
			'doi' => 'https://doi.org/10.1093/nar/gkae864',
			'modified' => '2024-10-11 10:02:42',
			'created' => '2024-10-11 10:02:42',
			'ProductsPublication' => array(
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			)
		),
		(int) 4 => array(
			'id' => '4985',
			'name' => 'HNF1β bookmarking involves Topoisomerase 1 activation and DNA topology relaxation in mitotic chromatin',
			'authors' => 'Alessia Bagattin et al.',
			'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HNF1&beta; mitotic site binding is preserved with a specific methanol/formaldehyde ChIP</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">BTBD2, an HNF1&beta; partner, mediates mitosis-specific interaction with TOP1</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">HNF1&beta; recruits TOP1 and induces DNA relaxation around bookmarked HNF1&beta; sites</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">An HNF1&beta; mutation, found in MODY patients, disrupts the interaction with TOP1</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">HNF1&beta; (<i>HNF1B</i>) is a transcription factor frequently mutated in patients with developmental renal disease. It binds to mitotic chromatin and reactivates gene expression after mitosis, a phenomenon referred to as bookmarking. Using a crosslinking method that circumvents the artifacts of formaldehyde, we demonstrate that&nbsp;HNF1&beta; remains associated with chromatin in a sequence-specific way in both interphase and mitosis. We identify an HNF1&beta;-interacting protein, BTBD2, that enables the interaction and activation of Topoisomerase 1 (TOP1) exclusively during mitosis. Our study identifies a shared microhomology domain between HNF1&beta; and TOP1, where a mutation, found in &ldquo;maturity onset diabetes of the young&rdquo; patients, disrupts their interaction. Importantly, HNF1&beta; recruits TOP1 and induces DNA relaxation around HNF1&beta; mitotic chromatin sites, elucidating its crucial role in chromatin remodeling and gene reactivation after mitotic exit. These findings shed light on how HNF1&beta; reactivates target gene expression after mitosis, providing insights into its crucial role in maintenance of cellular identity.</div>
</section>',
			'date' => '2024-10-08',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01156-2',
			'doi' => '10.1016/j.celrep.2024.114805',
			'modified' => '2024-10-14 09:04:44',
			'created' => '2024-10-14 09:04:44',
			'ProductsPublication' => array(
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		),
		(int) 5 => array(
			'id' => '4978',
			'name' => 'RNA polymerase II transcription initiation in holo-TFIID-depleted mouse embryonic stem cells',
			'authors' => 'Hisler V. et al.',
			'description' => '<p><span>The recognition of core promoter sequences by TFIID is the first step in RNA polymerase II (Pol II) transcription initiation. Metazoan holo-TFIID is a trilobular complex, composed of the TATA binding protein (TBP) and 13 TBP-associated factors (TAFs). Why and how TAFs are necessary for the formation of TFIID domains and how they contribute to transcription initiation remain unclear. Inducible TAF7 or TAF10 depletion, followed by comprehensive analysis of TFIID subcomplex formation, chromatin binding, and nascent transcription in mouse embryonic stem cells, result in the formation of a TAF7-lacking TFIID or a minimal core-TFIID complex, respectively. These partial complexes support TBP recruitment at promoters and nascent Pol II transcription at most genes early after depletion, but importantly, TAF10 is necessary for efficient Pol II pausing. We show that partially assembled TFIID complexes can sustain Pol II transcription initiation but cannot replace holo-TFIID over several cell divisions and/or development.</span></p>',
			'date' => '2024-09-30',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01142-2',
			'doi' => 'https://doi.org/10.1016/j.celrep.2024.114791',
			'modified' => '2024-10-04 10:18:22',
			'created' => '2024-10-04 10:18:22',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '4963',
			'name' => 'An atlas of the human liver diurnal transcriptome and its perturbation by hepatitis C virus infection',
			'authors' => 'Mukherji A. et al.',
			'description' => '<p><span>Chronic liver disease and cancer are global health challenges. The role of the circadian clock as a regulator of liver physiology and disease is well established in rodents, however, the identity and epigenetic regulation of rhythmically expressed genes in human disease is less well studied. Here we unravel the rhythmic transcriptome and epigenome of human hepatocytes using male human liver chimeric mice. We identify a large number of rhythmically expressed protein coding genes in human hepatocytes of male chimeric mice, which includes key transcription factors, chromatin modifiers, and critical enzymes. We show that hepatitis C virus (HCV) infection, a major cause of liver disease and cancer, perturbs the transcriptome by altering the rhythmicity of the expression of more than 1000 genes, and affects the epigenome, leading to an activation of critical pathways mediating metabolic alterations, fibrosis, and cancer. HCV-perturbed rhythmic pathways remain dysregulated in patients with advanced liver disease. Collectively, these data support a role for virus-induced perturbation of the hepatic rhythmic transcriptome and pathways in cancer development and may provide opportunities for cancer prevention and biomarkers to predict HCC risk.</span></p>',
			'date' => '2024-08-29',
			'pmid' => 'https://www.nature.com/articles/s41467-024-51698-8',
			'doi' => 'https://doi.org/10.1038/s41467-024-51698-8',
			'modified' => '2024-09-02 10:17:48',
			'created' => '2024-09-02 10:17:48',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '4968',
			'name' => 'Innate immune training restores pro-reparative myeloid functions to promote remyelination in the aged central nervous system',
			'authors' => 'Tiwari V. et al.',
			'description' => '<p><span>The reduced ability of the central nervous system to regenerate with increasing age limits functional recovery following demyelinating injury. Previous work has shown that myelin debris can overwhelm the metabolic capacity of microglia, thereby impeding tissue regeneration in aging, but the underlying mechanisms are unknown. In a model of demyelination, we found that a substantial number of genes that were not effectively activated in aged myeloid cells displayed epigenetic modifications associated with restricted chromatin accessibility. Ablation of two class I histone deacetylases in microglia was sufficient to restore the capacity of aged mice to remyelinate lesioned tissue. We used Bacillus Calmette-Guerin (BCG), a live-attenuated vaccine, to train the innate immune system and detected epigenetic reprogramming of brain-resident myeloid cells and functional restoration of myelin debris clearance and lesion recovery. Our results provide insight into aging-associated decline in myeloid function and how this decay can be prevented by innate immune reprogramming.</span></p>',
			'date' => '2024-07-24',
			'pmid' => 'https://www.cell.com/immunity/fulltext/S1074-7613(24)00348-0',
			'doi' => '',
			'modified' => '2024-09-02 17:05:54',
			'created' => '2024-09-02 17:05:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '4954',
			'name' => 'A multiomic atlas of the aging hippocampus reveals molecular changes in response to environmental enrichment',
			'authors' => 'Perez R. F. at al. ',
			'description' => '<p><span>Aging involves the deterioration of organismal function, leading to the emergence of multiple pathologies. Environmental stimuli, including lifestyle, can influence the trajectory of this process and may be used as tools in the pursuit of healthy aging. To evaluate the role of epigenetic mechanisms in this context, we have generated bulk tissue and single cell multi-omic maps of the male mouse dorsal hippocampus in young and old animals exposed to environmental stimulation in the form of enriched environments. We present a molecular atlas of the aging process, highlighting two distinct axes, related to inflammation and to the dysregulation of mRNA metabolism, at the functional RNA and protein level. Additionally, we report the alteration of heterochromatin domains, including the loss of bivalent chromatin and the uncovering of a heterochromatin-switch phenomenon whereby constitutive heterochromatin loss is partially mitigated through gains in facultative heterochromatin. Notably, we observed the multi-omic reversal of a great number of aging-associated alterations in the context of environmental enrichment, which was particularly linked to glial and oligodendrocyte pathways. In conclusion, our work describes the epigenomic landscape of environmental stimulation in the context of aging and reveals how lifestyle intervention can lead to the multi-layered reversal of aging-associated decline.</span></p>',
			'date' => '2024-07-16',
			'pmid' => 'https://www.nature.com/articles/s41467-024-49608-z',
			'doi' => 'https://doi.org/10.1038/s41467-024-49608-z',
			'modified' => '2024-07-29 11:33:49',
			'created' => '2024-07-29 11:33:49',
			'ProductsPublication' => array(
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			)
		),
		(int) 9 => array(
			'id' => '4952',
			'name' => 'Epigenetic alterations affecting hematopoietic regulatory networks as drivers of mixed myeloid/lymphoid leukemia',
			'authors' => 'Roger Mulet-Lazaro et al.',
			'description' => '<p><span>Leukemias with ambiguous lineage comprise several loosely defined entities, often without a clear mechanistic basis. Here, we extensively profile the epigenome and transcriptome of a subgroup of such leukemias with CpG Island Methylator Phenotype. These leukemias exhibit comparable hybrid myeloid/lymphoid epigenetic landscapes, yet heterogeneous genetic alterations, suggesting they are defined by their shared epigenetic profile rather than common genetic lesions. Gene expression enrichment reveals similarity with early T-cell precursor acute lymphoblastic leukemia and a lymphoid progenitor cell of origin. In line with this, integration of differential DNA methylation and gene expression shows widespread silencing of myeloid transcription factors. Moreover, binding sites for hematopoietic transcription factors, including CEBPA, SPI1 and LEF1, are uniquely inaccessible in these leukemias. Hypermethylation also results in loss of CTCF binding, accompanied by changes in chromatin interactions involving key transcription factors. In conclusion, epigenetic dysregulation, and not genetic lesions, explains the mixed phenotype of this group of leukemias with ambiguous lineage. The data collected here constitute a useful and comprehensive epigenomic reference for subsequent studies of acute myeloid leukemias, T-cell acute lymphoblastic leukemias and mixed-phenotype leukemias.</span></p>',
			'date' => '2024-07-07',
			'pmid' => 'https://www.nature.com/articles/s41467-024-49811-y',
			'doi' => 'https://doi.org/10.1038/s41467-024-49811-y',
			'modified' => '2024-07-10 12:21:42',
			'created' => '2024-07-10 12:21:42',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '4911',
			'name' => 'Multiomics uncovers the epigenomic and transcriptomic response to viral and bacterial stimulation in turbot',
			'authors' => 'Aramburu O. et al.',
			'description' => '<p><span>Uncovering the epigenomic regulation of immune responses is essential for a comprehensive understanding of host defence mechanisms but remains poorly described in farmed fish. Here, we report the first annotation of the innate immune regulatory response in the genome of turbot (</span><em>Scophthalmus maximus</em><span>), a farmed flatfish. We integrated RNA-Seq with ATAC-Seq and ChIP-Seq (histone marks H3K4me3, H3K27ac and H3K27me3) using samples from head kidney. Sampling was performed 24 hours post-stimulation with viral (poly I:C) and bacterial (inactivate<span>&nbsp;</span></span><em>Vibrio anguillarum</em><span>) mimics<span>&nbsp;</span></span><em>in vivo</em><span><span>&nbsp;</span>and<span>&nbsp;</span></span><em>in vitro</em><span><span>&nbsp;</span>(primary leukocyte cultures). Among the 8,797 differentially expressed genes (DEGs), we observed enrichment of transcriptional activation pathways in response to<span>&nbsp;</span></span><em>Vibrio</em><span><span>&nbsp;</span>and immune response pathways - including interferon stimulated genes - for poly I:C. Meanwhile, metabolic and cell cycle were downregulated by both mimics. We identified notable differences in chromatin accessibility (20,617<span>&nbsp;</span></span><em>in vitro</em><span>, 59,892<span>&nbsp;</span></span><em>in vivo</em><span>) and H3K4me3 bound regions (11,454<span>&nbsp;</span></span><em>in vitro</em><span>, 10,275<span>&nbsp;</span></span><em>in viv</em><span>o) - i.e. marking active promoters - between stimulations and controls. Overlaps of DEGs with promoters showing differential accessibility or histone mark binding revealed a significant coupling of the transcriptome and chromatin state. DEGs with activation marks in their promoters were enriched for similar functions to the global DEG set, but not in all cases, suggesting key regulatory genes were in poised or bivalent states. Active promoters and putative enhancers were differentially enriched in transcription factor binding motifs, many of them common to viral and bacterial responses. Finally, an in-depth analysis of immune response changes in chromatin state surrounding key DEGs encoding transcription factors was performed. This comprehensive multi-omics investigation provides an improved understanding of the epigenomic basis for the turbot immune responses and provides novel functional genomic information that can be leveraged in selective breeding towards enhanced disease resistance.</span></p>',
			'date' => '2024-02-15',
			'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.02.15.580452v1',
			'doi' => 'https://doi.org/10.1101/2024.02.15.580452',
			'modified' => '2024-02-22 11:41:27',
			'created' => '2024-02-22 11:41:27',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '4884',
			'name' => 'SMARCB1 loss activates patient-specific distal oncogenic enhancers in malignant rhabdoid tumors',
			'authors' => 'Liu, N.Q. et al.',
			'description' => '<p><span>Malignant rhabdoid tumor (MRT) is a highly malignant and often lethal childhood cancer. MRTs are genetically defined by bi-allelic inactivating mutations in&nbsp;</span><i>SMARCB1</i><span>, a member of the BRG1/BRM-associated factors (BAF) chromatin remodeling complex. Mutations in BAF complex members are common in human cancer, yet their contribution to tumorigenesis remains in many cases poorly understood. Here, we study derailed regulatory landscapes as a consequence of<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>loss in the context of MRT. Our multi-omics approach on patient-derived MRT organoids reveals a dramatic reshaping of the regulatory landscape upon<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>reconstitution. Chromosome conformation capture experiments subsequently reveal patient-specific looping of distal enhancer regions with the promoter of the<span>&nbsp;</span></span><i>MYC</i><span><span>&nbsp;</span>oncogene. This intertumoral heterogeneity in<span>&nbsp;</span></span><i>MYC</i><span><span>&nbsp;</span>enhancer utilization is also present in patient MRT tissues as shown by combined single-cell RNA-seq and ATAC-seq. We show that loss of<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>activates patient-specific epigenetic reprogramming underlying MRT tumorigenesis.</span></p>',
			'date' => '2023-12-01',
			'pmid' => 'https://www.nature.com/articles/s41467-023-43498-3#Abs1',
			'doi' => '10.1038/s41467-023-43498-3',
			'modified' => '2023-12-05 08:45:53',
			'created' => '2023-12-05 08:45:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '4885',
			'name' => 'The genetic landscape of origins of replication in P. falciparum',
			'authors' => 'Casilda Muñoz Castellano et al.',
			'description' => '<p><span>Various origin mapping approaches have enabled genome-wide identification of origins of replication (ORI) in model organisms, but only a few studies have focused on divergent organisms. By employing three complementary approaches we provide a high-resolution map of ORIs in&nbsp;</span><em>Plasmodium falciparum</em><span>, the deadliest human malaria parasite. We profiled the distribution of origin of recognition complex (ORC) binding sites by ChIP-seq of two<span>&nbsp;</span></span><em>Pf</em><span>ORC subunits and mapped active ORIs using NFS and SNS-seq. We show that ORIs lack sequence specificity but are not randomly distributed, and group in clusters. Licensing is biased towards regions of higher GC content and associated with G-quadruplex forming sequences (G4FS). While strong transcription likely enhances firing, active origins are depleted from transcription start sites. Instead, most accumulate in transcriptionally active gene bodies. Single molecule analysis of nanopore reads containing multiple initiation events, which could have only come from individual nuclei, showed a relationship between the replication fork pace and the distance to the nearest origin. While some similarities were drawn with the canonic eukaryote model, the distribution of ORIs in<span>&nbsp;</span></span><em>P. falciparum</em><span><span>&nbsp;</span>is likely shaped by unique genomic features such as extreme AT-richness&mdash;a product of evolutionary pressure imposed by the parasitic lifestyle.</span></p>',
			'date' => '2023-12-01',
			'pmid' => 'https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkad1103/7457016#428428709',
			'doi' => 'doi.org/10.1093/nar/gkad1103',
			'modified' => '2023-12-05 08:47:24',
			'created' => '2023-12-05 08:47:24',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '4843',
			'name' => 'Differentiation block in acute myeloid leukemia regulated by intronicsequences of FTO',
			'authors' => 'Camera  F. et al.',
			'description' => '<p>Iroquois transcription factor gene IRX3 is highly expressed in 20&acirc;&euro;&ldquo;30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences &acirc;&circ;&frac14;220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with the IRX3 promoter, which correlate with IRX3 expression. Deletion of these intronic elements confirms a role in positively regulating IRX3. RNAseq revealed long non-coding (lnc) transcripts arising from this locus. FTO-lncAML knockdown (KD) induced differentiation of AML cells, loss of clonogenic activity, and reduced FTO intron 8:IRX3 promoter contacts. While both FTO-lncAML KD and IRX3 KD induced differentiation, FTO-lncAML but not IRX3 KD led to HOXA downregulation suggesting transcript activity in trans. FTO-lncAMLhigh AML samples expressed higher levels of HOXA and lower levels of differentiation genes. Thus, a regulatory module in FTO intron 8 consisting of clustered enhancer elements and a long non-coding RNA is active in human AML, impeding myeloid differentiation.</p>',
			'date' => '2023-08-01',
			'pmid' => 'https://www.sciencedirect.com/science/article/pii/S2589004223013962',
			'doi' => '10.1016/j.isci.2023.107319',
			'modified' => '2023-08-01 14:14:01',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '4851',
			'name' => 'Supraphysiological Androgens Promote the Tumor Suppressive Activity of the Androgen Receptor Through cMYC Repression and Recruitment of the DREAM Complex',
			'authors' => 'Nyquist  M. et al.',
			'description' => '<p>The androgen receptor (AR) pathway regulates key cell survival programs in prostate epithelium. The AR represents a near-universal driver and therapeutic vulnerability in metastatic prostate cancer, and targeting AR has a remarkable therapeutic index. Though most approaches directed toward AR focus on inhibiting AR signaling, laboratory and now clinical data have shown that high dose, supraphysiological androgen treatment (SPA) results in growth repression and improved outcomes in subsets of prostate cancer patients. A better understanding of the mechanisms contributing to SPA response and resistance could help guide patient selection and combination therapies to improve efficacy. To characterize SPA signaling, we integrated metrics of gene expression changes induced by SPA together with cistrome data and protein-interactomes. These analyses indicated that the Dimerization partner, RB-like, E2F and Multi-vulval class B (DREAM) complex mediates growth repression and downregulation of E2F targets in response to SPA. Notably, prostate cancers with complete genomic loss of RB1 responded to SPA treatment whereas loss of DREAM complex components such as RBL1/2 promoted resistance. Overexpression of MYC resulted in complete resistance to SPA and attenuated the SPA/AR-mediated repression of E2F target genes. These findings support a model of SPA-mediated growth repression that relies on the negative regulation of MYC by AR leading to repression of E2F1 signaling via the DREAM complex. The integrity of MYC signaling and DREAM complex assembly may consequently serve as determinants of SPA responses and as pathways mediating SPA resistance.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/37352376/',
			'doi' => '10.1158/0008-5472.CAN-22-2613',
			'modified' => '2023-08-01 18:09:31',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '4852',
			'name' => 'In skeletal muscle and neural crest cells, SMCHD1 regulates biologicalpathways relevant for Bosma syndrome and facioscapulohumeral dystrophyphenotype.',
			'authors' => 'Laberthonnière  C. et al.',
			'description' => '<p>Many genetic syndromes are linked to mutations in genes encoding factors that guide chromatin organization. Among them, several distinct rare genetic diseases are linked to mutations in SMCHD1 that encodes the structural maintenance of chromosomes flexible hinge domain containing 1 chromatin-associated factor. In humans, its function as well as the impact of its mutations remains poorly defined. To fill this gap, we determined the episignature associated with heterozygous SMCHD1 variants in primary cells and cell lineages derived from induced pluripotent stem cells for Bosma arhinia and microphthalmia syndrome (BAMS) and type 2 facioscapulohumeral dystrophy (FSHD2). In human tissues, SMCHD1 regulates the distribution of methylated CpGs, H3K27 trimethylation and CTCF at repressed chromatin but also at euchromatin. Based on the exploration of tissues affected either in FSHD or in BAMS, i.e. skeletal muscle fibers and neural crest stem cells, respectively, our results emphasize multiple functions for SMCHD1, in chromatin compaction, chromatin insulation and gene regulation with variable targets or phenotypical outcomes. We concluded that in rare genetic diseases, SMCHD1 variants impact gene expression in two ways: (i) by changing the chromatin context at a number of euchromatin loci or (ii) by directly regulating some loci encoding master transcription factors required for cell fate determination and tissue differentiation.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37334829',
			'doi' => '10.1093/nar/gkad523',
			'modified' => '2023-08-01 14:35:38',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '4861',
			'name' => 'Hypomethylation and overexpression of Th17-associated genes is ahallmark of intestinal CD4+ lymphocytes in Crohn's disease.',
			'authors' => 'Sun  Z. et al.',
			'description' => '<p>BACKGROUND: The development of Crohn's disease (CD) involves immune cell signaling pathways regulated by epigenetic modifications. Aberrant DNA methylation has been identified in peripheral blood and bulk intestinal tissue from CD patients. However, the DNA methylome of disease-associated intestinal CD4 + lymphocytes has not been evaluated. MATERIALS AND METHODS: Genome-wide DNA methylation sequencing was performed from terminal ileum CD4 + cells from 21 CD patients and 12 age and sex matched controls. Data was analyzed for differentially methylated CpGs (DMCs) and methylated regions (DMRs). Integration was performed with RNA-sequencing data to evaluate the functional impact of DNA methylation changes on gene expression. DMRs were overlapped with regions of differentially open chromatin (by ATAC-seq) and CCCTC-binding factor (CTCF) binding sites (by ChIP-seq) between peripherally-derived Th17 and Treg cells. RESULTS: CD4+ cells in CD patients had significantly increased DNA methylation compared to those from the controls. A total of 119,051 DMCs and 8,113 DMRs were detected. While hyper-methylated genes were mostly related to cell metabolism and homeostasis, hypomethylated genes were significantly enriched within the Th17 signaling pathway. The differentially enriched ATAC regions in Th17 cells (compared to Tregs) were hypomethylated in CD patients, suggesting heightened Th17 activity. There was significant overlap between hypomethylated DNA regions and CTCF-associated binding sites. CONCLUSIONS: The methylome of CD patients demonstrate an overall dominant hypermethylation yet hypomethylation is more concentrated in proinflammatory pathways, including Th17 differentiation. Hypomethylation of Th17-related genes associated with areas of open chromatin and CTCF binding sites constitutes a hallmark of CD-associated intestinal CD4 + cells.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37280154',
			'doi' => '10.1093/ecco-jcc/jjad093',
			'modified' => '2023-08-01 14:52:39',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 17 => array(
			'id' => '4862',
			'name' => 'Mutant FUS induces chromatin reorganization in the hippocampus andalters memory processes.',
			'authors' => 'Tzeplaeff  L. et al.',
			'description' => '<p>Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalization to hippocampal function and memory formation are still not characterized. Herein, we show that in these mice, the hippocampus paradoxically displays nuclear FUS accumulation. Multi-omic analyses showed that FUS binds to a set of genes characterized by the presence of an ETS/ELK-binding motifs, and involved in RNA metabolism, transcription, ribosome/mitochondria and chromatin organization. Importantly, hippocampal nuclei showed a decompaction of the neuronal chromatin at highly expressed genes and an inappropriate transcriptomic response was observed after spatial training of Fus mice. Furthermore, these mice lacked precision in a hippocampal-dependent spatial memory task and displayed decreased dendritic spine density. These studies shows that mutated FUS affects epigenetic regulation of the chromatin landscape in hippocampal neurons, which could participate in FTD/ALS pathogenic events. These data call for further investigation in the neurological phenotype of FUS-related diseases and open therapeutic strategies towards epigenetic drugs.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37327984',
			'doi' => '10.1016/j.pneurobio.2023.102483',
			'modified' => '2023-08-01 14:55:49',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 18 => array(
			'id' => '4782',
			'name' => 'Transient suppression of SUMOylation in embryonic stem cells generatesembryo-like structures.',
			'authors' => 'Cossec  J-C. et al.',
			'description' => '<p>Recent advances in synthetic embryology have opened new avenues for understanding the complex events controlling mammalian peri-implantation development. Here, we show that mouse embryonic stem cells (ESCs) solely exposed to chemical inhibition of SUMOylation generate embryo-like structures comprising anterior neural and trunk-associated regions. HypoSUMOylation-instructed ESCs give rise to spheroids that self-organize into gastrulating structures containing cell types spatially and functionally related to embryonic and extraembryonic compartments. Alternatively, spheroids cultured in a droplet microfluidic device form elongated structures that undergo axial organization reminiscent of natural embryo morphogenesis. Single-cell transcriptomics reveals various cellular lineages, including properly positioned anterior neuronal cell types and paraxial mesoderm segmented into somite-like structures. Transient SUMOylation suppression gradually increases DNA methylation genome wide and repressive mark deposition at Nanog. Interestingly, cell-to-cell variations in SUMOylation levels occur during early embryogenesis. Our approach provides a proof of principle for potentially powerful strategies to explore early embryogenesis by targeting chromatin roadblocks of cell fate change.</p>',
			'date' => '2023-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37061916',
			'doi' => '10.1016/j.celrep.2023.112380',
			'modified' => '2023-06-13 09:20:06',
			'created' => '2023-05-05 12:34:24',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 19 => array(
			'id' => '4693',
			'name' => 'ZEB1 controls a lineage-specific transcriptional program essential formelanoma cell state transitions',
			'authors' => 'Tang  Y. et al.',
			'description' => '<p>Cell plasticity sustains intra-tumor heterogeneity and treatment resistance in melanoma. Deciphering the transcriptional mechanisms governing reversible phenotypic transitions between proliferative/differentiated and invasive/stem-like states is required in order to design novel therapeutic strategies. EMT-inducing transcription factors, extensively known for their role in metastasis in carcinoma, display cell-type specific functions in melanoma, with a decreased ZEB2/ZEB1 expression ratio fostering adaptive resistance to targeted therapies. While ZEB1 direct target genes have been well characterized in carcinoma models, they remain unknown in melanoma. Here, we performed a genome-wide characterization of ZEB1 transcriptional targets, by combining ChIP-sequencing and RNA-sequencing, upon phenotype switching in melanoma models. We identified and validated ZEB1 binding peaks in the promoter of key lineage-specific genes related to melanoma cell identity. Comparative analyses with breast carcinoma cells demonstrated melanoma-specific ZEB1 binding, further supporting lineage specificity. Gain- or loss-of-function of ZEB1, combined with functional analyses, further demonstrated that ZEB1 negatively regulates proliferative/melanocytic programs and positively regulates both invasive and stem-like programs. We then developed single-cell spatial multiplexed analyses to characterize melanoma cell states with respect to ZEB1/ZEB2 expression in human melanoma samples. We characterized the intra-tumoral heterogeneity of ZEB1 and ZEB2 and further validated ZEB1 increased expression in invasive cells, but also in stem-like cells, highlighting its relevance in vivo in both populations. Overall, our results define ZEB1 as a major transcriptional regulator of cell states transitions and provide a better understanding of lineage-specific transcriptional programs sustaining intra-tumor heterogeneity in melanoma.</p>',
			'date' => '2023-02-01',
			'pmid' => 'https://doi.org/10.1101%2F2023.02.10.526467',
			'doi' => '10.1101/2023.02.10.526467',
			'modified' => '2023-04-14 09:11:23',
			'created' => '2023-02-28 12:19:11',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 20 => 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) 21 => array(
			'id' => '4651',
			'name' => 'TCDD induces multigenerational alterations in the expression ofmicroRNA in the thymus through epigenetic modifications',
			'authors' => 'Singh  Narendra P et al.',
			'description' => '<p>2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a potent AhR ligand, is an environmental contaminant that is known for mediating toxicity across generations. However, whether TCDD can induce multigenerational changes in the expression of miRNAs (miRs) has not been previously studied. In the current study, we investigated the effect of administration of TCDD in pregnant mice (F0) on gestational day 14, on the expression of miRs in the thymus of F0 and subsequent generations (F1 and F2). Of the 3200 miRs screened, 160 miRs were dysregulated similarly in F0, F1, and F2 generations while 46 miRs were differentially altered in F0-F2 generations. Pathway analysis revealed that the changes in miR signature profile mediated by TCDD affected the genes that regulate cell signaling, apoptosis, thymic atrophy, cancer, immunosuppression, and other physiological pathways. A significant number of miRs that showed altered expression exhibited dioxin response elements (DRE) on their promoters. Focusing on one such miR, namely miR-203 that expressed DREs and was induced across F0-F2 by TCDD, promoter analysis showed that one of the DREs expressed by miR-203 was functional to TCDD-mediated upregulation. Also, the histone methylation status of H3K4me3 in the miR-203 promoter was significantly increased near the transcriptional start site (TSS) in TCDD-treated thymocytes across F0-F2 generations. Genome-wide ChIP-seq study suggested that TCDD may cause alterations in histone methylation in certain genes across the three generations. Together, the current study demonstrates that gestational exposure to TCDD can alter the expression of miRs in F0 through direct activation of DREs as well as across F0, F1, and F2 generations through epigenetic pathways.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://academic.oup.com/pnasnexus/advance-article/doi/10.1093/pnasnexus/pgac290/6886578',
			'doi' => 'https://doi.org/10.1093/pnasnexus/pgac290',
			'modified' => '2023-03-13 10:55:36',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 22 => array(
			'id' => '4632',
			'name' => 'The histone acetyltransferase KAT6A is recruited to unmethylatedCpG islands via a DNA binding winged helix domain.',
			'authors' => 'Weber  L.M. et al.',
			'description' => '<p>The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrate that a winged helix (WH) domain at the very N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A with unmethylated CpG islands (CGIs) genome-wide. Mutation of the essential amino acids for DNA binding completely abrogates the enrichment of KAT6A at CGIs. In contrast, deletion of a second WH domain or the histone tail binding PHD fingers only subtly influences the binding of KAT6A to CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36537216',
			'doi' => '10.1093/nar/gkac1188',
			'modified' => '2023-03-28 09:01:38',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 23 => array(
			'id' => '4629',
			'name' => 'Polyglutamine-expanded ATXN7 alters a specific epigenetic signatureunderlying photoreceptor identity gene expression in SCA7 mouseretinopathy.',
			'authors' => 'Niewiadomska-Cimicka  A.et al.',
			'description' => '<p>BACKGROUND: Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disorder that primarily affects the cerebellum and retina. SCA7 is caused by a polyglutamine expansion in the ATXN7 protein, a subunit of the transcriptional coactivator SAGA that acetylates histone H3 to deposit narrow H3K9ac mark at DNA regulatory elements of active genes. Defective histone acetylation has been presented as a possible cause for gene deregulation in SCA7 mouse models. However, the topography of acetylation defects at the whole genome level and its relationship to changes in gene expression remain to be determined. METHODS: We performed deep RNA-sequencing and chromatin immunoprecipitation coupled to high-throughput sequencing to examine the genome-wide correlation between gene deregulation and alteration of the active transcription marks, e.g. SAGA-related H3K9ac, CBP-related H3K27ac and RNA polymerase II (RNAPII), in a SCA7 mouse retinopathy model. RESULTS: Our analyses revealed that active transcription marks are reduced at most gene promoters in SCA7 retina, while a limited number of genes show changes in expression. We found that SCA7 retinopathy is caused by preferential downregulation of hundreds of highly expressed genes that define morphological and physiological identities of mature photoreceptors. We further uncovered that these photoreceptor genes harbor unusually broad H3K9ac profiles spanning the entire gene bodies and have a low RNAPII pausing. This broad H3K9ac signature co-occurs with other features that delineate superenhancers, including broad H3K27ac, binding sites for photoreceptor specific transcription factors and expression of enhancer-related non-coding RNAs (eRNAs). In SCA7 retina, downregulated photoreceptor genes show decreased H3K9 and H3K27 acetylation and eRNA expression as well as increased RNAPII pausing, suggesting that superenhancer-related features are altered. CONCLUSIONS: Our study thus provides evidence that distinctive epigenetic configurations underlying high expression of cell-type specific genes are preferentially impaired in SCA7, resulting in a defect in the maintenance of identity features of mature photoreceptors. Our results also suggest that continuous SAGA-driven acetylation plays a role in preserving post-mitotic neuronal identity.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36539812',
			'doi' => '10.1186/s12929-022-00892-1',
			'modified' => '2023-03-28 09:07:19',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 24 => 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) 25 => array(
			'id' => '4494',
			'name' => 'Cryptococcal Hsf3 controls intramitochondrial ROS homeostasis byregulating the respiratory process.',
			'authors' => 'Gao  X.et al.',
			'description' => '<p>Mitochondrial quality control prevents accumulation of intramitochondrial-derived reactive oxygen species (mtROS), thereby protecting cells against DNA damage, genome instability, and programmed cell death. However, underlying mechanisms are incompletely understood, particularly in fungal species. Here, we show that Cryptococcus neoformans heat shock factor 3 (CnHsf3) exhibits an atypical function in regulating mtROS independent of the unfolded protein response. CnHsf3 acts in nuclei and mitochondria, and nuclear- and mitochondrial-targeting signals are required for its organelle-specific functions. It represses the expression of genes involved in the tricarboxylic acid cycle while promoting expression of genes involved in electron transfer chain. In addition, CnHsf3 responds to multiple intramitochondrial stresses; this response is mediated by oxidation of the cysteine residue on its DNA binding domain, which enhances DNA binding. Our results reveal a function of HSF proteins in regulating mtROS homeostasis that is independent of the unfolded protein response.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36109512',
			'doi' => '10.1038/s41467-022-33168-1',
			'modified' => '2022-11-18 12:43:17',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 26 => array(
			'id' => '4496',
			'name' => 'Dominant role of DNA methylation over H3K9me3 for IAP silencingin endoderm.',
			'authors' => 'Wang  Z. et al.',
			'description' => '<p>Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications H3K9me3 and DNA methylation. On ERVs, these modifications are mainly deposited by the histone methyltransferase Setdb1 and by the maintenance DNA methyltransferase Dnmt1. Knock-out of either Setdb1 or Dnmt1 leads to ERV de-repression in various cell types. However, it is currently not known if H3K9me3 and DNA methylation depend on each other for ERV silencing. Here we show that conditional knock-out of Setdb1 in mouse embryonic endoderm results in ERV de-repression in visceral endoderm (VE) descendants and does not occur in definitive endoderm (DE). Deletion of Setdb1 in VE progenitors results in loss of H3K9me3 and reduced DNA methylation of Intracisternal A-particle (IAP) elements, consistent with up-regulation of this ERV family. In DE, loss of Setdb1 does not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 knock-out results in IAP de-repression in both visceral and definitive endoderm cells, while H3K9me3 is unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm cells. Our findings suggest that Setdb1-meditated H3K9me3 is not sufficient for IAP silencing, but rather critical for maintaining high DNA methylation.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36123357',
			'doi' => '10.1038/s41467-022-32978-7',
			'modified' => '2022-11-21 10:26:30',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 27 => array(
			'id' => '4415',
			'name' => 'HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependentgene repression in murine erythroleukaemia.',
			'authors' => 'Gregoricchio  S. et al.',
			'description' => '<p>Although originally described as transcriptional activator, SPI1/PU.1, a major player in haematopoiesis whose alterations are associated with haematological malignancies, has the ability to repress transcription. Here, we investigated the mechanisms underlying gene repression in the erythroid lineage, in which SPI1 exerts an oncogenic function by blocking differentiation. We show that SPI1 represses genes by binding active enhancers that are located in intergenic or gene body regions. HDAC1 acts as a cooperative mediator of SPI1-induced transcriptional repression by deacetylating SPI1-bound enhancers in a subset of genes, including those involved in erythroid differentiation. Enhancer deacetylation impacts on promoter acetylation, chromatin accessibility and RNA pol II occupancy. In addition to the activities of HDAC1, polycomb repressive complex 2 (PRC2) reinforces gene repression by depositing H3K27me3 at promoter sequences when SPI1 is located at enhancer sequences. Moreover, our study identified a synergistic relationship between PRC2 and HDAC1 complexes in mediating the transcriptional repression activity of SPI1, ultimately inducing synergistic adverse effects on leukaemic cell survival. Our results highlight the importance of the mechanism underlying transcriptional repression in leukemic cells, involving complex functional connections between SPI1 and the epigenetic regulators PRC2 and HDAC1.</p>',
			'date' => '2022-08-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35871293',
			'doi' => '10.1093/nar/gkac613',
			'modified' => '2022-09-15 08:59:26',
			'created' => '2022-09-08 16:32:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 28 => array(
			'id' => '4516',
			'name' => 'Dual role of histone variant H3.3B in spermatogenesis: positiveregulation of piRNA transcription and implication in X-chromosomeinactivation.',
			'authors' => 'Fontaine  E. et al.',
			'description' => '<p>The histone variant H3.3 is encoded by two distinct genes, H3f3a and H3f3b, exhibiting identical amino-acid sequence. H3.3 is required for spermatogenesis, but the molecular mechanism of its spermatogenic function remains obscure. Here, we have studied the role of each one of H3.3A and H3.3B proteins in spermatogenesis. We have generated transgenic conditional knock-out/knock-in (cKO/KI) epitope-tagged FLAG-FLAG-HA-H3.3B (H3.3BHA) and FLAG-FLAG-HA-H3.3A (H3.3AHA) mouse lines. We show that H3.3B, but not H3.3A, is required for spermatogenesis and male fertility. Analysis of the molecular mechanism unveils that the absence of H3.3B led to alterations in the meiotic/post-meiotic transition. Genome-wide RNA-seq reveals that the depletion of H3.3B in meiotic cells is associated with increased expression of the whole sex X and Y chromosomes as well as of both RLTR10B and RLTR10B2 retrotransposons. In contrast, the absence of H3.3B resulted in down-regulation of the expression of piRNA clusters. ChIP-seq experiments uncover that RLTR10B and RLTR10B2 retrotransposons, the whole sex chromosomes and the piRNA clusters are markedly enriched of H3.3. Taken together, our data dissect the molecular mechanism of H3.3B functions during spermatogenesis and demonstrate that H3.3B, depending on its chromatin localization, is involved in either up-regulation or down-regulation of expression of defined large chromatin regions.</p>',
			'date' => '2022-07-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35766398',
			'doi' => '10.1093/nar/gkac541',
			'modified' => '2022-11-24 08:51:34',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 29 => array(
			'id' => '4393',
			'name' => 'TBX2 acts as a potent transcriptional silencer of tumour suppressor genesthrough interaction with the CoREST complex to sustain theproliferation of breast cancers.',
			'authors' => 'McIntyre  A.J. et al.',
			'description' => '<p>Chromosome 17q23 amplification occurs in 20\% of primary breast tumours and is associated with poor outcome. The TBX2 gene is located on 17q23 and is often over-expressed in this breast tumour subset. TBX2 is an anti-senescence gene, promoting cell growth and survival through repression of Tumour Suppressor Genes (TSGs), such as NDRG1 and CST6. Previously we found that TBX2 cooperates with the PRC2 complex to repress several TSGs, and that PRC2 inhibition restored NDRG1 expression to impede cellular proliferation. Here, we now identify CoREST proteins, LSD1 and ZNF217, as novel interactors of TBX2. Genetic or pharmacological targeting of CoREST emulated TBX2 loss, inducing NDRG1 expression and abolishing breast cancer growth in vitro and in vivo. Furthermore, we uncover that TBX2/CoREST targeting of NDRG1 is achieved by recruitment of TBX2 to the NDRG1 promoter by Sp1, the abolishment of which resulted in NDRG1 upregulation and diminished cancer cell proliferation. Through ChIP-seq we reveal that 30\% of TBX2-bound promoters are shared with ZNF217 and identify novel targets repressed by TBX2/CoREST; of these targets a lncRNA, LINC00111, behaves as a negative regulator of cell proliferation. Overall, these data indicate that inhibition of CoREST proteins represents a promising therapeutic intervention for TBX2-addicted breast tumours.</p>',
			'date' => '2022-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35687133',
			'doi' => '10.1093/nar/gkac494',
			'modified' => '2022-08-11 14:23:06',
			'created' => '2022-08-11 12:14:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 30 => array(
			'id' => '4836',
			'name' => 'Caffeine intake exerts dual genome-wide effects on hippocampal metabolismand learning-dependent transcription.',
			'authors' => 'Paiva  I. et al.',
			'description' => '<p>Caffeine is the most widely consumed psychoactive substance in the world. Strikingly, the molecular pathways engaged by its regular consumption remain unclear. We herein addressed the mechanisms associated with habitual (chronic) caffeine consumption in the mouse hippocampus using untargeted orthogonal omics techniques. Our results revealed that chronic caffeine exerts concerted pleiotropic effects in the hippocampus at the epigenomic, proteomic, and metabolomic levels. Caffeine lowered metabolism-related processes (e.g., at the level of metabolomics and gene expression) in bulk tissue, while it induced neuron-specific epigenetic changes at synaptic transmission/plasticity-related genes and increased experience-driven transcriptional activity. Altogether, these findings suggest that regular caffeine intake improves the signal-to-noise ratio during information encoding, in part through fine-tuning of metabolic genes, while boosting the salience of information processing during learning in neuronal circuits.</p>',
			'date' => '2022-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35536645',
			'doi' => '10.1172/JCI149371',
			'modified' => '2023-08-01 13:52:29',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 31 => array(
			'id' => '4221',
			'name' => 'Epigenetic Mechanisms Mediating Cell State Transitions in Chondrocytes',
			'authors' => 'Wuelling M. et al.',
			'description' => '<p><span>Epigenetic modifications play critical roles in regulating cell lineage differentiation, but the epigenetic mechanisms guiding specific differentiation steps within a cell lineage have rarely been investigated. To decipher such mechanisms, we used the defined transition from proliferating (PC) into hypertrophic chondrocytes (HC) during endochondral ossification as a model. We established a map of activating and repressive histone modifications for each cell type. ChromHMM state transition analysis and Pareto-based integration of differential levels of mRNA and epigenetic marks revealed that differentiation-associated gene repression is initiated by the addition of H3K27me3 to promoters still carrying substantial levels of activating marks. Moreover, the integrative analysis identified genes specifically expressed in cells undergoing the transition into hypertrophy. Investigation of enhancer profiles detected surprising differences in enhancer number, location, and transcription factor binding sites between the two closely related cell types. Furthermore, cell type-specific upregulation of gene expression was associated with increased numbers of H3K27ac peaks. Pathway analysis identified PC-specific enhancers associated with chondrogenic genes, whereas HC-specific enhancers mainly control metabolic pathways linking epigenetic signature to biological functions. Since HC-specific enhancers show a higher conservation in postnatal tissues, the switch to metabolic pathways seems to be a hallmark of differentiated tissues. Surprisingly, the analysis of H3K27ac levels at super-enhancers revealed a rapid adaption of H3K27ac occupancy to changes in gene expression, supporting the importance of enhancer modulation for acute alterations in gene expression. &copy; 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).</span></p>',
			'date' => '2022-05-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33534175/',
			'doi' => '10.1002/jbmr.4263',
			'modified' => '2022-04-25 11:46:32',
			'created' => '2022-04-21 12:00:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 32 => array(
			'id' => '4402',
			'name' => 'The CpG Island-Binding Protein SAMD1 Contributes to anUnfavorable Gene Signature in HepG2 Hepatocellular CarcinomaCells.',
			'authors' => 'Simon  C. et al.',
			'description' => '<p>The unmethylated CpG island-binding protein SAMD1 is upregulated in many human cancer types, but its cancer-related role has not yet been investigated. Here, we used the hepatocellular carcinoma cell line HepG2 as a cancer model and investigated the cellular and transcriptional roles of SAMD1 using ChIP-Seq and RNA-Seq. SAMD1 targets several thousand gene promoters, where it acts predominantly as a transcriptional repressor. HepG2 cells with SAMD1 deletion showed slightly reduced proliferation, but strongly impaired clonogenicity. This phenotype was accompanied by the decreased expression of pro-proliferative genes, including MYC target genes. Consistently, we observed a decrease in the active H3K4me2 histone mark at most promoters, irrespective of SAMD1 binding. Conversely, we noticed an increase in interferon response pathways and a gain of H3K4me2 at a subset of enhancers that were enriched for IFN-stimulated response elements (ISREs). We identified key transcription factor genes, such as , , and , that were directly repressed by SAMD1. Moreover, SAMD1 deletion also led to the derepression of the PI3K-inhibitor , contributing to diminished mTOR signaling and ribosome biogenesis pathways. Our work suggests that SAMD1 is involved in establishing a pro-proliferative setting in hepatocellular carcinoma cells. Inhibiting SAMD1's function in liver cancer cells may therefore lead to a more favorable gene signature.</p>',
			'date' => '2022-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35453756',
			'doi' => '10.3390/biology11040557',
			'modified' => '2022-08-11 14:45:43',
			'created' => '2022-08-11 12:14:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 33 => array(
			'id' => '4524',
			'name' => 'Local euchromatin enrichment in lamina-associated domains anticipatestheir repositioning in the adipogenic lineage.',
			'authors' => 'Madsen-Østerbye  J. et al.',
			'description' => '<p>BACKGROUND: Interactions of chromatin with the nuclear lamina via lamina-associated domains (LADs) confer structural stability to the genome. The dynamics of positioning of LADs during differentiation, and how LADs impinge on developmental gene expression, remains, however, elusive. RESULTS: We examined changes in the association of lamin B1 with the genome in the first 72 h of differentiation of adipose stem cells into adipocytes. We demonstrate a repositioning of entire stand-alone LADs and of LAD edges as a prominent nuclear structural feature of early adipogenesis. Whereas adipogenic genes are released from LADs, LADs sequester downregulated or repressed genes irrelevant for the adipose lineage. However, LAD repositioning only partly concurs with gene expression changes. Differentially expressed genes in LADs, including LADs conserved throughout differentiation, reside in local euchromatic and lamin-depleted sub-domains. In these sub-domains, pre-differentiation histone modification profiles correlate with the LAD versus inter-LAD outcome of these genes during adipogenic commitment. Lastly, we link differentially expressed genes in LADs to short-range enhancers which overall co-partition with these genes in LADs versus inter-LADs during differentiation. CONCLUSIONS: We conclude that LADs are predictable structural features of adipose nuclear architecture that restrain non-adipogenic genes in a repressive environment.</p>',
			'date' => '2022-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35410387',
			'doi' => '10.1186/s13059-022-02662-6',
			'modified' => '2022-11-24 09:08:01',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 34 => array(
			'id' => '4235',
			'name' => 'NuA4 and H2A.Z control environmental responses and autotrophicgrowth in Arabidopsis',
			'authors' => 'Bieluszewski T. et al.',
			'description' => '<p>Nucleosomal acetyltransferase of H4 (NuA4) is an essential transcriptional coactivator in eukaryotes, but remains poorly characterized in plants. Here, we describe Arabidopsis homologs of the NuA4 scaffold proteins Enhancer of Polycomb-Like 1 (AtEPL1) and Esa1-Associated Factor 1 (AtEAF1). Loss of AtEAF1 results in inhibition of growth and chloroplast development. These effects are stronger in the Atepl1 mutant and are further enhanced by loss of Golden2-Like (GLK) transcription factors, suggesting that NuA4 activates nuclear plastid genes alongside GLK. We demonstrate that AtEPL1 is necessary for nucleosomal acetylation of histones H4 and H2A.Z by NuA4 in vitro. These chromatin marks are diminished genome-wide in Atepl1, while another active chromatin mark, H3K9 acetylation (H3K9ac), is locally enhanced. Expression of many chloroplast-related genes depends on NuA4, as they are downregulated with loss of H4ac and H2A.Zac. Finally, we demonstrate that NuA4 promotes H2A.Z deposition and by doing so prevents spurious activation of stress response genes.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35022409',
			'doi' => '10.1038/s41467-021-27882-5',
			'modified' => '2022-05-19 17:02:00',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 35 => array(
			'id' => '4772',
			'name' => 'Three classes of epigenomic regulators converge to hyperactivate theessential maternal gene deadhead within a heterochromatin mini-domain.',
			'authors' => 'Torres-Campana  D. et al.',
			'description' => '<p>The formation of a diploid zygote is a highly complex cellular process that is entirely controlled by maternal gene products stored in the egg cytoplasm. This highly specialized transcriptional program is tightly controlled at the chromatin level in the female germline. As an extreme case in point, the massive and specific ovarian expression of the essential thioredoxin Deadhead (DHD) is critically regulated in Drosophila by the histone demethylase Lid and its partner, the histone deacetylase complex Sin3A/Rpd3, via yet unknown mechanisms. Here, we identified Snr1 and Mod(mdg4) as essential for dhd expression and investigated how these epigenomic effectors act with Lid and Sin3A to hyperactivate dhd. Using Cut\&amp;Run chromatin profiling with a dedicated data analysis procedure, we found that dhd is intriguingly embedded in an H3K27me3/H3K9me3-enriched mini-domain flanked by DNA regulatory elements, including a dhd promoter-proximal element essential for its expression. Surprisingly, Lid, Sin3a, Snr1 and Mod(mdg4) impact H3K27me3 and this regulatory element in distinct manners. However, we show that these effectors activate dhd independently of H3K27me3/H3K9me3, and that dhd remains silent in the absence of these marks. Together, our study demonstrates an atypical and critical role for chromatin regulators Lid, Sin3A, Snr1 and Mod(mdg4) to trigger tissue-specific hyperactivation within a unique heterochromatin mini-domain.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8759638/',
			'doi' => '10.1371/journal.pgen.1009615',
			'modified' => '2023-04-17 09:46:00',
			'created' => '2023-04-14 13:41:22',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 36 => 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) 37 => array(
			'id' => '4245',
			'name' => 'Decreased PRC2 activity supports the survival of basal-like breastcancer cells to cytotoxic treatments',
			'authors' => 'Mieczkowska IK et al.',
			'description' => '<p>Breast cancer (BC) is the most common cancer occurring in women but also rarely develops in men. Recent advances in early diagnosis and development of targeted therapies have greatly improved the survival rate of BC patients. However, the basal-like BC subtype (BLBC), largely overlapping with the triple-negative BC subtype (TNBC), lacks such drug targets and conventional cytotoxic chemotherapies often remain the only treatment option. Thus, the development of resistance to cytotoxic therapies has fatal consequences. To assess the involvement of epigenetic mechanisms and their therapeutic potential increasing cytotoxic drug efficiency, we combined high-throughput RNA- and ChIP-sequencing analyses in BLBC cells. Tumor cells surviving chemotherapy upregulated transcriptional programs of epithelial-to-mesenchymal transition (EMT) and stemness. To our surprise, the same cells showed a pronounced reduction of polycomb repressive complex 2 (PRC2) activity via downregulation of its subunits Ezh2, Suz12, Rbbp7 and Mtf2. Mechanistically, loss of PRC2 activity leads to the de-repression of a set of genes through an epigenetic switch from repressive H3K27me3 to activating H3K27ac mark at regulatory regions. We identified Nfatc1 as an upregulated gene upon loss of PRC2 activity and directly implicated in the transcriptional changes happening upon survival to chemotherapy. Blocking NFATc1 activation reduced epithelial-to-mesenchymal transition, aggressiveness, and therapy resistance of BLBC cells. Our data demonstrate a previously unknown function of PRC2 maintaining low Nfatc1 expression levels and thereby repressing aggressiveness and therapy resistance in BLBC.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34845197',
			'doi' => '10.1038/s41419-021-04407-y',
			'modified' => '2022-05-20 09:21:56',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 38 => array(
			'id' => '4276',
			'name' => 'Ago1 controls myogenic differentiation by regulating eRNA-mediatedCBP-guided epigenome reprogramming.',
			'authors' => 'Fallatah Bodor et al.',
			'description' => '<p>The role of chromatin-associated RNAi components in the nucleus of mammalian cells and in particular in the context of developmental programs remains to be elucidated. Here, we investigate the function of nuclear Argonaute 1 (Ago1) in gene expression regulation during skeletal muscle differentiation. We show that Ago1 is required for activation of the myogenic program by supporting chromatin modification mediated by developmental enhancer activation. Mechanistically, we demonstrate that Ago1 directly controls global H3K27 acetylation (H3K27ac) by regulating enhancer RNA (eRNA)-CREB-binding protein (CBP) acetyltransferase interaction, a key step in enhancer-driven gene activation. In particular, we show that Ago1 is specifically required for myogenic differentiation 1 (MyoD) and downstream myogenic gene activation, whereas its depletion leads to failure of CBP acetyltransferase activation and blocking of the myogenic program. Our work establishes a role of the mammalian enhancer-associated RNAi component Ago1 in epigenome regulation and activation of developmental programs.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.celrep.2021.110066',
			'doi' => '10.1016/j.celrep.2021.110066',
			'modified' => '2022-05-23 09:53:14',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 39 => array(
			'id' => '4833',
			'name' => 'Extensive NEUROG3 occupancy in the human pancreatic endocrine generegulatory network.',
			'authors' => 'Schreiber  V. et al.',
			'description' => '<p>OBJECTIVE: Mice lacking the bHLH transcription factor (TF) Neurog3 do not form pancreatic islet cells, including insulin-secreting beta cells, the absence of which leads to diabetes. In humans, homozygous mutations of NEUROG3 manifest with neonatal or childhood diabetes. Despite this critical role in islet cell development, the precise function of and downstream genetic programs regulated directly by NEUROG3 remain elusive. Therefore, we mapped genome-wide NEUROG3 occupancy in human induced pluripotent stem cell (hiPSC)-derived endocrine progenitors and determined NEUROG3 dependency of associated genes to uncover direct targets. METHODS: We generated a novel hiPSC line (NEUROG3-HA-P2A-Venus) where NEUROG3 is HA-tagged and fused to a self-cleaving fluorescent VENUS reporter. We used the CUT\&amp;RUN technique to map NEUROG3 occupancy and epigenetic marks in pancreatic endocrine progenitors (PEP) that were differentiated from this hiPSC line. We integrated NEUROG3 occupancy data with chromatin status and gene expression in PEPs as well as their NEUROG3-dependence. In addition, we investigated whether NEUROG3 binds type 2 diabetes mellitus (T2DM)-associated variants at the PEP stage. RESULTS: CUT\&amp;RUN revealed a total of 863 NEUROG3 binding sites assigned to 1263 unique genes. NEUROG3 occupancy was found at promoters as well as at distant cis-regulatory elements that frequently overlapped within PEP active enhancers. De novo motif analyses defined a NEUROG3 consensus binding motif and suggested potential co-regulation of NEUROG3 target genes by FOXA or RFX transcription factors. We found that 22\% of the genes downregulated in NEUROG3 PEPs, and 10\% of genes enriched in NEUROG3-Venus positive endocrine cells were bound by NEUROG3 and thus likely to be directly regulated. NEUROG3 binds to 138 transcription factor genes, some with important roles in islet cell development or function, such as NEUROD1, PAX4, NKX2-2, SOX4, MLXIPL, LMX1B, RFX3, and NEUROG3 itself, and many others with unknown islet function. Unexpectedly, we uncovered that NEUROG3 targets genes critical for insulin secretion in beta cells (e.g., GCK, ABCC8/KCNJ11, CACNA1A, CHGA, SCG2, SLC30A8, and PCSK1). Thus, analysis of NEUROG3 occupancy suggests that the transient expression of NEUROG3 not only promotes islet destiny in uncommitted pancreatic progenitors, but could also initiate endocrine programs essential for beta cell function. Lastly, we identified eight T2DM risk SNPs within NEUROG3-bound regions. CONCLUSION: Mapping NEUROG3 genome occupancy in PEPs uncovered unexpectedly broad, direct control of the endocrine genes, raising novel hypotheses on how this master regulator controls islet and beta cell differentiation.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://doi.org/10.1101%2F2021.04.14.439685',
			'doi' => '10.1016/j.molmet.2021.101313',
			'modified' => '2023-08-01 13:46:35',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 40 => array(
			'id' => '4285',
			'name' => 'Alveolar macrophages from persons living with HIV show impairedepigenetic response to Mycobacterium tuberculosis.',
			'authors' => 'Correa-Macedo Wilian et al.',
			'description' => '<p>Persons living with HIV (PLWH) are at increased risk of tuberculosis (TB). HIV-associated TB is often the result of recent infection with Mycobacterium tuberculosis (Mtb) followed by rapid progression to disease. Alveolar macrophages (AM) are the first cells of the innate immune system that engage Mtb, but how HIV and antiretroviral therapy (ART) impact on the anti-mycobacterial response of AM is not known. To investigate the impact of HIV and ART on the transcriptomic and epigenetic response of AM to Mtb, we obtained AM by bronchoalveolar lavage from 20 PLWH receiving ART, 16 control subjects who were HIV-free (HC), and 14 subjects who received ART as pre-exposure prophylaxis (PrEP) to prevent HIV infection. Following in-vitro challenge with Mtb, AM from each group displayed overlapping but distinct profiles of significantly up- and down-regulated genes in response to Mtb. Comparatively, AM isolated from both PLWH and PrEP subjects presented a substantially weaker transcriptional response. In addition, AM from HC subjects challenged with Mtb responded with pronounced chromatin accessibility changes while AM obtained from PLWH and PrEP subjects displayed no significant changes in their chromatin state. Collectively, these results revealed a stronger adverse effect of ART than HIV on the epigenetic landscape and transcriptional responsiveness of AM.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473646/',
			'doi' => '10.1172/JCI148013',
			'modified' => '2022-05-24 09:08:39',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 41 => array(
			'id' => '4297',
			'name' => 'INTS11 regulates hematopoiesis by promoting PRC2 function.',
			'authors' => 'Zhang Peng et al.',
			'description' => '<p>INTS11, the catalytic subunit of the Integrator (INT) complex, is crucial for the biogenesis of small nuclear RNAs and enhancer RNAs. However, the role of INTS11 in hematopoietic stem and progenitor cell (HSPC) biology is unknown. Here, we report that INTS11 is required for normal hematopoiesis and hematopoietic-specific genetic deletion of leads to cell cycle arrest and impairment of fetal and adult HSPCs. We identified a novel INTS11-interacting protein complex, Polycomb repressive complex 2 (PRC2), that maintains HSPC functions. Loss of INTS11 destabilizes the PRC2 complex, decreases the level of histone H3 lysine 27 trimethylation (H3K27me3), and derepresses PRC2 target genes. Reexpression of INTS11 or PRC2 proteins in -deficient HSPCs restores the levels of PRC2 and H3K27me3 as well as HSPC functions. Collectively, our data demonstrate that INTS11 is an essential regulator of HSPC homeostasis through the INTS11-PRC2 axis.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34516911',
			'doi' => '10.1126/sciadv.abh1684',
			'modified' => '2022-05-30 09:31:00',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 42 => array(
			'id' => '4304',
			'name' => 'The related coactivator complexes SAGA and ATAC control embryonicstem cell self-renewal through acetyltransferase-independent mechanisms',
			'authors' => 'Fischer Veronique et al.',
			'description' => '<p>SUMMARY SAGA (Spt-Ada-Gcn5 acetyltransferase) and ATAC (Ada-two-A-containing) are two related coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development, but the role of these complexes in RNA polymerase II transcription is less understood. To determine whether SAGA and ATAC have redundant or specific functions, we compare the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC are required for complex assembly and mouse ESC growth and self-renewal. Surprisingly, depletion of HAT module subunits causes a global decrease in histone H3K9 acetylation, but does not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for self-renewal of mouse ESCs by regulating transcription through different pathways in a HAT-independent manner.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34433046',
			'doi' => '10.1016/j.celrep.2021.109598',
			'modified' => '2022-05-30 09:57:39',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 43 => array(
			'id' => '4345',
			'name' => 'Altered Chromatin States Drive Cryptic Transcription in AgingMammalian Stem Cells.',
			'authors' => 'McCauley Brenna S et al.',
			'description' => '<p>A repressive chromatin state featuring trimethylated lysine 36 on histone H3 (H3K36me3) and DNA methylation suppresses cryptic transcription in embryonic stem cells. Cryptic transcription is elevated with age in yeast and nematodes, and reducing it extends yeast lifespan, though whether this occurs in mammals is unknown. We show that cryptic transcription is elevated in aged mammalian stem cells, including murine hematopoietic stem cells (mHSCs) and neural stem cells (NSCs) and human mesenchymal stem cells (hMSCs). Precise mapping allowed quantification of age-associated cryptic transcription in hMSCs aged . Regions with significant age-associated cryptic transcription have a unique chromatin signature: decreased H3K36me3 and increased H3K4me1, H3K4me3, and H3K27ac with age. Genomic regions undergoing such changes resemble known promoter sequences and are bound by TBP even in young cells. Hence, the more permissive chromatin state at intragenic cryptic promoters likely underlies increased cryptic transcription in aged mammalian stem cells.</p>',
			'date' => '2021-08-01',
			'pmid' => 'https://doi.org/10.1038%2Fs43587-021-00091-x',
			'doi' => '10.1038/s43587-021-00091-x',
			'modified' => '2022-06-22 12:30:19',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 44 => array(
			'id' => '4333',
			'name' => 'Metabolically controlled histone H4K5 acylation/acetylation ratiodrives BRD4 genomic distribution.',
			'authors' => 'Gao M. et al.',
			'description' => '<p>In addition to acetylation, histones are modified by a series of competing longer-chain acylations. Most of these acylation marks are enriched and co-exist with acetylation on active gene regulatory elements. Their seemingly redundant functions hinder our understanding of histone acylations' specific roles. Here, by using an acute lymphoblastic leukemia (ALL) cell model and blasts from individuals with B-precusor ALL (B-ALL), we demonstrate a role of mitochondrial activity in controlling the histone acylation/acetylation ratio, especially at histone H4 lysine 5 (H4K5). An increase in the ratio of non-acetyl acylations (crotonylation or butyrylation) over acetylation on H4K5 weakens bromodomain containing protein 4 (BRD4) bromodomain-dependent chromatin interaction and enhances BRD4 nuclear mobility and availability for binding transcription start site regions of active genes. Our data suggest that the metabolism-driven control of the histone acetylation/longer-chain acylation(s) ratio could be a common mechanism regulating the bromodomain factors' functional genomic distribution.</p>',
			'date' => '2021-07-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.celrep.2021.109460',
			'doi' => '10.1016/j.celrep.2021.109460',
			'modified' => '2022-08-03 16:14:09',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 45 => array(
			'id' => '4343',
			'name' => 'The SAM domain-containing protein 1 (SAMD1) acts as a repressivechromatin regulator at unmethylated CpG islands',
			'authors' => 'Stielow B. et al. ',
			'description' => '<p>CpG islands (CGIs) are key regulatory DNA elements at most promoters, but how they influence the chromatin status and transcription remains elusive. Here, we identify and characterize SAMD1 (SAM domain-containing protein 1) as an unmethylated CGI-binding protein. SAMD1 has an atypical winged-helix domain that directly recognizes unmethylated CpG-containing DNA via simultaneous interactions with both the major and the minor groove. The SAM domain interacts with L3MBTL3, but it can also homopolymerize into a closed pentameric ring. At a genome-wide level, SAMD1 localizes to H3K4me3-decorated CGIs, where it acts as a repressor. SAMD1 tethers L3MBTL3 to chromatin and interacts with the KDM1A histone demethylase complex to modulate H3K4me2 and H3K4me3 levels at CGIs, thereby providing a mechanism for SAMD1-mediated transcriptional repression. The absence of SAMD1 impairs ES cell differentiation processes, leading to misregulation of key biological pathways. Together, our work establishes SAMD1 as a newly identified chromatin regulator acting at unmethylated CGIs.</p>',
			'date' => '2021-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33980486',
			'doi' => '10.1126/sciadv.abf2229',
			'modified' => '2022-08-03 16:34:24',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 46 => array(
			'id' => '4192',
			'name' => 'Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-inducedprogrammed cell death in Arabidopsis.',
			'authors' => 'Dvořák Tomaštíková E. et al.',
			'description' => '<p>The Polycomb Repressive Complex 2 (PRC2) is well-known for its role in controlling developmental transitions by suppressing the premature expression of key developmental regulators. Previous work revealed that PRC2 also controls the onset of senescence, a form of developmental programmed cell death (PCD) in plants. Whether the induction of PCD in response to stress is similarly suppressed by the PRC2 remained largely unknown. In this study, we explored whether PCD triggered in response to immunity- and disease-promoting pathogen effectors is associated with changes in the distribution of the PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) modification in Arabidopsis thaliana. We furthermore tested the distribution of the heterochromatic histone mark H3K9me2, which is established, to a large extent, by the H3K9 methyltransferase KRYPTONITE, and occupies chromatin regions generally not targeted by PRC2. We report that effector-induced PCD caused major changes in the distribution of both repressive epigenetic modifications and that both modifications have a regulatory role and impact on the onset of PCD during pathogen infection. Our work highlights that the transition to pathogen-induced PCD is epigenetically controlled, revealing striking similarities to developmental PCD.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33566101',
			'doi' => '10.1093/plphys/kiab035',
			'modified' => '2022-01-06 14:12:23',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 47 => array(
			'id' => '4273',
			'name' => 'An integrated multi-omics analysis identifies prognostic molecularsubtypes of non-muscle-invasive bladder cancer',
			'authors' => 'Lindskrog Sia Viborg et al.',
			'description' => '<p>The molecular landscape in non-muscle-invasive bladder cancer (NMIBC) is characterized by large biological heterogeneity with variable clinical outcomes. Here, we perform an integrative multi-omics analysis of patients diagnosed with NMIBC (n&thinsp;=&thinsp;834). Transcriptomic analysis identifies four classes (1, 2a, 2b and 3) reflecting tumor biology and disease aggressiveness. Both transcriptome-based subtyping and the level of chromosomal instability provide independent prognostic value beyond established prognostic clinicopathological parameters. High chromosomal instability, p53-pathway disruption and APOBEC-related mutations are significantly associated with transcriptomic class 2a and poor outcome. RNA-derived immune cell infiltration is associated with chromosomally unstable tumors and enriched in class 2b. Spatial proteomics analysis confirms the higher infiltration of class 2b tumors and demonstrates an association between higher immune cell infiltration and lower recurrence rates. Finally, the independent prognostic value of the transcriptomic classes is documented in 1228 validation samples using a single sample classification tool. The classifier provides a framework for biomarker discovery and for optimizing treatment and surveillance in next-generation clinical trials.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863885',
			'doi' => '10.1038/s41467-021-22465-w',
			'modified' => '2022-05-23 09:49:43',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 48 => array(
			'id' => '4109',
			'name' => 'VPRBP functions downstream of the androgen receptor and OGT to restrict p53 activation in prostate cancer ',
			'authors' => 'Poulose N. et al. ',
			'description' => '<p>Androgen receptor (AR) is a major driver of prostate cancer (PCa) initiation and progression. O-GlcNAc transferase (OGT), the enzyme that catalyses the covalent addition of UDP-N-acetylglucosamine (UDP-GlcNAc) to serine and threonine residues of proteins, is often up-regulated in PCa with its expression correlated with high Gleason score. In this study we have identified an AR and OGT co-regulated factor, VPRBP/DCAF1. We show that VPRBP is regulated by the AR at the transcript level, and by OGT at the protein level. In human tissue samples, VPRBP protein expression correlated with AR amplification, OGT overexpression and poor prognosis. VPRBP knockdown in prostate cancer cells led to a significant decrease in cell proliferation, p53 stabilization, nucleolar fragmentation and increased p53 recruitment to the chromatin. In conclusion, we have shown that VPRBP/DCAF1 promotes prostate cancer cell proliferation by restraining p53 activation under the influence of the AR and OGT.</p>',
			'date' => '2021-02-21',
			'pmid' => 'https://www.biorxiv.org/content/10.1101/2021.02.28.433236v1',
			'doi' => '',
			'modified' => '2021-07-07 11:59:15',
			'created' => '2021-07-07 11:59:15',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 49 => array(
			'id' => '4124',
			'name' => 'JAZF1, A Novel p400/TIP60/NuA4 Complex Member, Regulates H2A.ZAcetylation at Regulatory Regions.',
			'authors' => 'Procida, Tara and Friedrich, Tobias and Jack, Antonia P M and Peritore,Martina and Bönisch, Clemens and Eberl, H Christian and Daus, Nadine andKletenkov, Konstantin and Nist, Andrea and Stiewe, Thorsten and Borggrefe,Tilman and Mann, Matthias and Bartk',
			'description' => '<p>Histone variants differ in amino acid sequence, expression timing and genomic localization sites from canonical histones and convey unique functions to eukaryotic cells. Their tightly controlled spatial and temporal deposition into specific chromatin regions is accomplished by dedicated chaperone and/or remodeling complexes. While quantitatively identifying the chaperone complexes of many human H2A variants by using mass spectrometry, we also found additional members of the known H2A.Z chaperone complexes p400/TIP60/NuA4 and SRCAP. We discovered JAZF1, a nuclear/nucleolar protein, as a member of a p400 sub-complex containing MBTD1 but excluding ANP32E. Depletion of JAZF1 results in transcriptome changes that affect, among other pathways, ribosome biogenesis. To identify the underlying molecular mechanism contributing to JAZF1's function in gene regulation, we performed genome-wide ChIP-seq analyses. Interestingly, depletion of JAZF1 leads to reduced H2A.Z acetylation levels at &gt; 1000 regulatory sites without affecting H2A.Z nucleosome positioning. Since JAZF1 associates with the histone acetyltransferase TIP60, whose depletion causes a correlated H2A.Z deacetylation of several JAZF1-targeted enhancer regions, we speculate that JAZF1 acts as chromatin modulator by recruiting TIP60's enzymatic activity. Altogether, this study uncovers JAZF1 as a member of a TIP60-containing p400 chaperone complex orchestrating H2A.Z acetylation at regulatory regions controlling the expression of genes, many of which are involved in ribosome biogenesis.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33445503',
			'doi' => '10.3390/ijms22020678',
			'modified' => '2021-12-07 10:00:44',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 50 => array(
			'id' => '4179',
			'name' => 'Histone demethylase JMJD2B/KDM4B regulates transcriptional program viadistinctive epigenetic targets and protein interactors for the maintenanceof trophoblast stem cells.',
			'authors' => 'Mak, Kylie Hin-Man et al.',
			'description' => '<p>Trophoblast stem cell (TSC) is crucial to the formation of placenta in mammals. Histone demethylase JMJD2 (also known as KDM4) family proteins have been previously shown to support self-renewal and differentiation of stem cells. However, their roles in the context of the trophoblast lineage remain unclear. Here, we find that knockdown of Jmjd2b resulted in differentiation of TSCs, suggesting an indispensable role of JMJD2B/KDM4B in maintaining the stemness. Through the integration of transcriptome and ChIP-seq profiling data, we show that JMJD2B is associated with a loss of H3K36me3 in a subset of embryonic lineage genes which are marked by H3K9me3 for stable repression. By characterizing the JMJD2B binding motifs and other transcription factor binding datasets, we discover that JMJD2B forms a protein complex with AP-2 family transcription factor TFAP2C and histone demethylase LSD1. The JMJD2B-TFAP2C-LSD1 complex predominantly occupies active gene promoters, whereas the TFAP2C-LSD1 complex is located at putative enhancers, suggesting that these proteins mediate enhancer-promoter interaction for gene regulation. We conclude that JMJD2B is vital to the TSC transcriptional program and safeguards the trophoblast cell fate via distinctive protein interactors and epigenetic targets.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33441614',
			'doi' => '10.1038/s41598-020-79601-7',
			'modified' => '2021-12-21 16:43:16',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 51 => array(
			'id' => '4210',
			'name' => 'Trans- and cis-acting effects of Firre on epigenetic features of theinactive X chromosome.',
			'authors' => 'Fang, He and Bonora, Giancarlo and Lewandowski, Jordan P and Thakur,Jitendra and Filippova, Galina N and Henikoff, Steven and Shendure, Jay andDuan, Zhijun and Rinn, John L and Deng, Xinxian and Noble, William S andDisteche, Christine M',
			'description' => '<p>Firre encodes a lncRNA involved in nuclear organization. Here, we show that Firre RNA expressed from the active X chromosome maintains histone H3K27me3 enrichment on the inactive X chromosome (Xi) in somatic cells. This trans-acting effect involves SUZ12, reflecting interactions between Firre RNA and components of the Polycomb repressive complexes. Without Firre RNA, H3K27me3 decreases on the Xi and the&nbsp;Xi-perinucleolar location is disrupted, possibly due to decreased CTCF binding on the Xi. We also observe widespread gene dysregulation, but not on the Xi. These effects are measurably rescued by ectopic expression of mouse or human Firre/FIRRE transgenes, supporting conserved trans-acting roles. We also find that the compact 3D structure of the Xi partly depends on the Firre locus and its RNA. In common lymphoid progenitors and T-cells Firre exerts a cis-acting effect on maintenance of H3K27me3 in a 26&thinsp;Mb region around the locus, demonstrating cell type-specific trans- and cis-acting roles of this lncRNA.</p>',
			'date' => '2020-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33247132',
			'doi' => '10.1038/s41467-020-19879-3',
			'modified' => '2022-01-13 15:03:45',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
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		),
		(int) 52 => array(
			'id' => '4206',
			'name' => 'H2A.Z is dispensable for both basal and activated transcription inpost-mitotic mouse muscles.',
			'authors' => 'Belotti E. et al.',
			'description' => '<p>While the histone variant H2A.Z is known to be required for mitosis, it is also enriched in nucleosomes surrounding the transcription start site of active promoters, implicating H2A.Z in transcription. However, evidence obtained so far mainly rely on correlational data generated in actively dividing cells. We have exploited a paradigm in which transcription is uncoupled from the cell cycle by developing an in vivo system to inactivate H2A.Z in terminally differentiated post-mitotic muscle cells. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is a marker but not an active driver of transcription.</p>',
			'date' => '2020-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32266374',
			'doi' => '10.1093/nar/gkaa157',
			'modified' => '2022-01-13 13:46:38',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		)
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	'name' => 'MicroPlex Library Preparation Kit v3 /96 rxns',
	'description' => '<p>Diagenode&rsquo;s MicroPlex Library Preparation Kits v3 have been extensively validated for ChIP-seq samples and are optimized to generate DNA libraries with high molecular complexity from the lowest input amounts &ndash; down to 50 pg. The kit MicroPlex v3 includes all buffers and enzymes necessary for the library preparation. For flexibility of the choice different formats of compatible primer indexes are available separately:</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns">C05010003 - 24 Dual indexes for MicroPlex Kit v3 /48 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1">C05010004 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set I /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2">C05010005 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set II /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3">C05010006 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set III /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4">C05010007 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV /96 rxns</a></li>
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<p style="padding-left: 30px;">NEW! Unique dual indexes :</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1">C05010008 - 24 UDI for MicroPlex Kit v3 - Set I</a></li>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2">C05010009 - 24 UDI for MicroPlex Kit v3 - Set II</a></li>
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<p>Read more about<span>&nbsp;</span><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">library preparation for ChIP-seq</a></p>
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<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
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<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
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<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
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<li><strong>Reduce potential bias</strong> - few PCR amplification cycles needed</li>
<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
<li><strong>Great multiplexing flexibility</strong> with 24 dual indexes (8 nt)</li>
<li><strong>Validated with the IP-<a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit">Star<sup>&reg;</sup></a></strong><a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit"> Automated Platform</a></li>
</ul>
<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
<div id="first" class="content">
<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
</div>
</li>
</ul>
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			'name' => 'MicroPlex Library Preparation Kit v3 /48 rxns',
			'description' => '<p><a href="https://www.diagenode.com/files/products/kits/Microplex-library-prep-v3.pdf"><img src="https://www.diagenode.com/img/buttons/bt-manual.png" /></a></p>
<p>Diagenode&rsquo;s <strong>MicroPlex Library Preparation Kits v3</strong> have been extensively validated for ChIP-seq samples and are optimized to generate DNA libraries with high molecular complexity from the lowest input amounts &ndash; down to 50 pg. The kit MicroPlex v3 includes all buffers and enzymes necessary for the library preparation. For flexibility of the choice different formats of compatible primer indexes are available separately:</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns">C05010003 - 24 Dual indexes for MicroPlex Kit v3 /48 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1">C05010004 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set I /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2">C05010005 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set II /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3">C05010006 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set III /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4">C05010007 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV /96 rxns</a></li>
</ul>
<p style="padding-left: 30px;">NEW! Unique dual indexes :</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1">C05010008 - 24 UDI for MicroPlex Kit v3 - Set I</a></li>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2">C05010009 - 24 UDI for MicroPlex Kit v3 - Set II</a></li>
</ul>
<p>Read more about <a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">library preparation for ChIP-seq</a></p>
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<li><strong>1 tube</strong>, <strong>2 hours</strong>, <strong>3 steps</strong> protocol</li>
<li><strong>Input</strong>: 50 pg &ndash; 50 ng</li>
<li><strong>Reduce potential bias</strong> - few PCR amplification cycles needed</li>
<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
<li><strong>Great multiplexing flexibility</strong> with 24 dual indexes (8 nt)</li>
<li><strong>Validated with the IP-<a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit">Star<sup>&reg;</sup></a></strong><a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit"> Automated Platform</a></li>
</ul>
<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
<div id="first" class="content">
<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
</div>
</li>
</ul>
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<div class="small-12 medium-12 large-12 columns">
<p><span style="font-weight: 400;">Most of the major next-generation sequencing platforms require ligation of specific adaptor oligos to </span><a href="../applications/dna-rna-shearing"><span style="font-weight: 400;">fragmented DNA or RNA</span></a><span style="font-weight: 400;"> prior to sequencing</span></p>
<p><span style="font-weight: 400;">After input DNA has been fragmented, it is end-repaired and blunt-ended</span><span style="font-weight: 400;">. The next step is a A-tailing in which dAMP is added to the 3&acute; end of the blunt phosphorylated DNA fragments to prevent concatemerization and to allow the ligation of adaptors with complementary dT overhangs. In addition, barcoded adapters can be incorporated to facilitate multiplexing prior to or during amplification.</span></p>
<center><img src="https://www.diagenode.com/img/categories/library-prep/flux.png" /></center>
<p><span style="font-weight: 400;">Diagenode offers a comprehensive product portfolio for library preparation:<br /></span></p>
<strong><a href="https://www.diagenode.com/en/categories/Library-preparation-for-RNA-seq">D-Plex&nbsp;RNA-seq Library Preparation Kits</a></strong><br />
<p><span style="font-weight: 400;">Diagenode&rsquo;s new RNA-sequencing solutions utilize the innovative c</span><span style="font-weight: 400;">apture and a</span><span style="font-weight: 400;">mplification by t</span><span style="font-weight: 400;">ailing and s</span><span style="font-weight: 400;">witching&rdquo;</span><span style="font-weight: 400;">, a ligation-free method to produce DNA libraries for next generation sequencing from low input amounts of RNA. </span><span style="font-weight: 400;"></span><a href="../categories/Library-preparation-for-RNA-seq">Learn more</a></p>
<strong><a href="../categories/library-preparation-for-ChIP-seq">ChIP-seq and DNA sequencing library preparation solutions</a></strong><br />
<p><span style="font-weight: 400;">Our kits have been optimized for DNA library preparation used for next generation sequencing for a wide range of inputs. Using a simple three-step protocols, our</span><a href="http://www.diagenode.com/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><span style="font-weight: 400;"> </span></a><span style="font-weight: 400;">kits are an optimal choice for library preparation from DNA inputs down to 50 pg.&nbsp;</span><a href="../categories/library-preparation-for-ChIP-seq">Learn more</a></p>
<a href="../p/bioruptor-pico-sonication-device"><span style="font-weight: 400;"></span><strong>Bioruptor Pico - short fragments</strong></a><a href="../categories/library-preparation-for-ChIP-seq-and-DNA-sequencing"><span style="font-weight: 400;"></span></a><br />
<p><span style="font-weight: 400;"></span><span style="font-weight: 400;">Our well-cited Bioruptor Pico is the shearing device of choice for chromatin and DNA fragmentation. Obtain uniform and tight fragment distributions &nbsp;between 150bp -2kb. </span><a href="../p/bioruptor-pico-sonication-device">Learn more</a></p>
<strong><a href="../p/megaruptor2-1-unit"><span href="../p/bioruptor-pico-sonication-device">Megaruptor</span>&reg; - long fragments</a></strong><a href="../p/bioruptor-pico-sonication-device"><span style="font-weight: 400;"></span></a><a href="../categories/library-preparation-for-ChIP-seq-and-DNA-sequencing"><span style="font-weight: 400;"></span></a><br />
<p><span style="font-weight: 400;"></span><span style="font-weight: 400;">The Megaruptor is designed to shear DNA from 3kb-75kb for long-read sequencing.&nbsp; <a href="../p/megaruptor2-1-unit">Learn more</a></span></p>
<span href="../p/bioruptor-pico-sonication-device"></span><span style="font-weight: 400;"></span></div>
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<div class="large-12 columns text-justify">
<p>Library preparation following ChIP can be challenging due to the limited amount of DNA recovered after ChIP. Diagenode has developed the optimal solutions for ChIP-seq using two different approaches: the ligation-based library preparation on purified DNA or the tagmentation-based ChIPmentation.</p>
</div>
</div>
<div class="row extra-spaced">
<div class="large-12 columns"><center><a href="https://www.diagenode.com/en/pages/form-microplex-promo" target="_blank"></a></center></div>
</div>
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div id="portal" class="main-portal">
<div class="portal-inner"><nav class="portal-nav">
<ul data-tab="" class="tips-menu">
<li><a href="#panel1" class="tips portal button">Ligation-based library prep</a></li>
<li><a href="#panel2" class="tips portal button">ChIPmentation</a></li>
<li><a href="#panel3" class="tips portal button">Kit choice guide</a></li>
<li><a href="#panel4" class="tips portal button">Resources</a></li>
<li><a href="#panel5" class="tips portal button">FAQs</a></li>
</ul>
</nav></div>
</div>
<div class="tabs-content">
<div class="content active" id="panel1">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v5" style="color: #13b29c;"><i class="fa fa-caret-right"></i> Standard input library prep</a>
<div id="v5" class="content">
<div class="small-12 medium-12 large-12 columns">
<p>The <strong>iDeal Library Preparation Kit</strong> reliably converts DNA into indexed libraries for next-generation sequencing, with input amounts down to <strong>5 ng</strong>. Our kit offers a simple and fast workflow, high yields, and ready-to-sequence DNA on the Illumina platform.</p>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> <strong>Sample</strong>: Fragmented dsDNA</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Input</strong>: 5 ng &ndash; 1 &micro;g</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Fast protocol</strong>: 3 hours</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Easy processing</strong>: 3 steps</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Indexing</strong>: single indexes for multiplexing up to 24 samples</li>
<li><i class="fa fa-arrow-circle-right"></i> Manual and automated protocols available</li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<ul class="square">
<li>MeDIP-seq library prep</li>
<li>Genomic DNA sequencing</li>
<li>High input ChIP-seq</li>
</ul>
</div>
<div class="extra-spaced">
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010020</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" style="color: #b21329;" target="_blank">iDeal Library Preparation Kit x24 (incl. Index Primer Set 1)</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010021</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" style="color: #b21329;" target="_blank">Index Primer Set 2 (iDeal Lib. Prep Kit x24)</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
</li>
</ul>
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v4" style="color: #13b29c;"><i class="fa fa-caret-right"></i> Low input library prep</a>
<div id="v4" class="content active"><center><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" target="_blank"><img src="https://www.diagenode.com/img/banners/banner-microplex-v3-580.jpg" class="extra-spaced" /></a></center>
<div align="center"><a href="https://www.diagenode.com/pages/form-microplex3" class="center alert radius button extra-spaced"><i class="fa fa-info"></i> Contact us</a></div>
<div class="extra-spaced">
<p>Diagenode&rsquo;s <strong>MicroPlex Library Preparation kits</strong> have been extensively validated for ChIP-seq samples. Generated libraries are compatible with single-end or paired-end sequencing. MicroPlex chemistry (using stem-loop adapters ) is specifically developed and optimized to generate DNA libraries with high molecular complexity from the lowest input amounts. Only <strong>50 pg to 50 ng</strong> of fragmented double-stranded DNA is required for library preparation. The entire <strong>three-step workflow</strong> takes place in a <strong>single tube</strong> or well in about <strong>2 hours</strong>. No intermediate purification steps and no sample transfers are necessary to prevent handling errors and loss of valuable samples.</p>
</div>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> <strong>Sample</strong>: Fragmented dsDNA</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Low input</strong>: 50 pg &ndash; 50 ng</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Fast protocol</strong>: 2 hours</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Easy processing</strong>: 3 steps in 1 tube</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>No intermediate purification</strong></li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
<li><i class="fa fa-arrow-circle-right"></i> Manual and automated protocols available</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<ul class="square">
<li>ChIP-seq library prep from ChIP-derived DNA</li>
<li>Low input DNA sequencing</li>
</ul>
</div>
<h2>Two versions are available:</h2>
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v2" style="color: #13b29c;"><i class="fa fa-caret-right"></i> MicroPlex Library Preparation Kit v2 with single indexes</a>
<div id="v2" class="content">
<p>The MicroPlex Library Preparation Kit v2 contains all necessary reagents including single indexes for multiplexing up to 48 samples using single barcoding.</p>
<h4>KITS</h4>
<table>
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<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
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<tr>
<td class="catalog_number"><span class="success label">C05010012</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v2 (12 indexes)</a></td>
<td class="format">12 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
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</tbody>
</table>
</div>
</li>
<li class="accordion-navigation"><a href="#v3" style="color: #13b29c;"><i class="fa fa-caret-right"></i> MicroPlex Library Preparation Kit v3 with dual indexes &nbsp;&nbsp;<strong><span class="diacol">NEW!</span></strong></a>
<div id="v3" class="content active">
<p>In this version the library preparation reagents and the dual indexes are available separately allowing for the flexibility choosing the number of indexes. MicroPlex v3 has multiplexing capacities up to 384 samples.</p>
<h4>KITS</h4>
<table>
<thead>
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<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
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</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010001</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v3 /48 rxns</a></td>
<td class="format">48 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
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<td class="catalog_number"><span class="success label">C05010002</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v3 /96 rxns</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
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</tbody>
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<h4>DUAL INDEXES</h4>
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<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
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<td class="catalog_number"><span class="success label">C05010003</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" style="color: #b21329;" target="_blank">24 Dual indexes for MicroPlex Kit v3</a></td>
<td class="format">48 rxns</td>
<td><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
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<td class="catalog_number"><span class="success label">C05010004</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set I</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010005</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set II</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010006</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set III</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010007</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
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</tbody>
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</li>
</ul>
</div>
</li>
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<div class="content active" id="panel2">
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<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<p>The TAG Kit for ChIPmentation offers an optimized ChIP-seq library preparation solution based on tagmentation. This kit includes reagents for tagmentation-based library preparation integrated in the IP and is compatible with any ChIP protocol based on magnetic beads. The primer indexes for multiplexing&nbsp;must be purchased separately and are available as a reference: <a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" target="_blank">24 SI for ChIPmentation</a>, Cat. No. C01011031. Alternatively, for histone marks, Diagenode proposes the complete solution (including all buffers for ChIP, tagmentation and multiplexing): <a href="https://www.diagenode.com/en/p/manual-chipmentation-kit-for-histones-24-rxns" target="_blank">ChIPmentation for Histones</a>.</p>
</div>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> Sample: chromatin-antibody-magnetic beads complexes</li>
<li><i class="fa fa-arrow-circle-right"></i> Input: chromatin from 5 K &ndash; 4 M cells</li>
<li><i class="fa fa-arrow-circle-right"></i> Easy and fast protocol</li>
<li><i class="fa fa-arrow-circle-right"></i> Compatible with any ChIP protocol based on magnetic beads</li>
<li><i class="fa fa-arrow-circle-right"></i> No adapter dimers</li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<p class="lead"><em><strong>TAG kit for ChIPmentation</strong></em></p>
<ul class="square">
<li>ChIPmentation library preparation</li>
</ul>
<p class="lead"><em><strong>24 SI for for ChIPmentation</strong></em></p>
<ul class="square">
<li>ChIPmentation library preparation</li>
<li>Tagmentation-based library preparation methods like ATAC-seq, CUT&amp;Tag</li>
</ul>
</div>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C01011030</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" style="color: #b21329;" target="_blank">TAG Kit for ChIPmentation</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C01011031</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" style="color: #b21329;" target="_blank">24 SI for ChIPmentation</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
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<div class="content" id="panel3">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<h3 class="text-center diacol"><em>How to choose your library preparation kit?</em></h3>
</div>
<table class="noborder">
<tbody>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Sample</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Chromatin-antibody-beads complex</p>
</td>
<td colspan="2">
<p class="text-center" style="font-size: 15px;">Purified DNA</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Purified DNA</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td colspan="2"><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
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<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Application</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">ChIPmentation</p>
</td>
<td colspan="2">
<p class="text-center" style="font-size: 15px;">ChIP-seq library prep<br /> Low input DNA sequencing</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">MeDIP-seq library prep<br /> Genomic DNA sequencing<br /> High input ChIP-seq</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td colspan="2"><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Input</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Chromatin: 5 K to 4 M cells</p>
</td>
<td colspan="2&quot;">
<p class="text-center" style="font-size: 15px;">DNA: 50 pg &ndash; 50 ng</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">DNA: 5 ng &ndash; 1 &micro;g</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow-45-left.png" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow-45-right.png" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Multiplexing</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 24 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 384 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 48 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 24 samples</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
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<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Indexes</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Dual indexes (DI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Kit</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>TAG Kit for ChIPmentation</strong><br /> (indexes not included in the kit)</p>
<p class="text-center"><strong>Kit</strong><br /> <a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" target="_blank">C01011030 &ndash; 24 rxns</a></p>
<p class="text-center"><strong>Single indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" target="_blank">C01011031 &ndash; 24 SI/24 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>MicroPlex Library Preparation Kit v3</strong><br />(dual indexes not included in the kit)</p>
<p class="text-center"><strong>Kit</strong><br /> <a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" target="_blank">C05010001 - 48 rxns</a><br /> <a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" target="_blank">C05010002 - 96 rxns</a></p>
<br />
<p class="text-center"><strong>Unique dual indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1" target="_blank">C05010008 - Set I 24 UDI / 24 rxns</a><br /> <a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2" target="_blank">C05010009 - Set II 24 UDI/ 24 rxns</a></p>
<p class="text-center"><strong>Dual indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" target="_blank">C05010003 - 24 DI/ 48 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" target="_blank">C05010004 - Set I 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" target="_blank">C05010005 - Set II 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" target="_blank">C05010006 - Set III 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" target="_blank">C05010007 - Set IV 96 DI/ 96 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>MicroPlex Library Preparation Kit v2</strong><br />(single indexes included in the kit)</p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" target="_blank">C05010012 - 12 SI/ 12 rxns</a><br /> <a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x48-12-indices-48-rxns" target="_blank">C05010013 - 12 SI/ 48 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>iDeal Library Preparation Kit</strong><br />(Set 1 of indexes included in the kit)</p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" target="_blank">C05010020 - 12 SI/ 24 rxns</a></p>
<p class="text-center" style="font-size: 15px;"><strong>Index Primer Set 2</strong></p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" target="_blank">C05010021 - 12 SI/ 24 rxns</a></p>
</td>
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<div class="content" id="panel4">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<p>Combined chromatin immunoprecipitation and next-generation sequencing (ChIP-seq) has become the gold standard to investigate genome-wide epigenetic profiles. However, ChIP from a limited amount of cells has been a challenge. Here we provide a complete and robust workflow solution for successful ChIP-seq from small numbers of cells using the True MicroChIP kit and MicroPlex Library Preparation kit.</p>
<blockquote><span class="label-green" style="margin-bottom: 16px; margin-left: -22px;">APPLICATION NOTE</span>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><center><img src="https://www.diagenode.com/img/categories/microplex/chip-efficiency-on-10000-cells.jpg" /></center>
<p><small><em>ChIP efficiency on 10,000 cells</em></small></p>
</div>
<div class="small-12 medium-6 large-6 columns">
<p><strong>From minuscule amounts to magnificent results:</strong><br /> reliable ChIP-seq data from 10,000 cells with the True MicroChIP&trade; and the MicroPlex Library Preparation&trade; kits.</p>
<a href="https://www.diagenode.com/files/application_notes/True_MicroChIP_and_MicroPlex_kits_Application_Note.pdf" class="details small button" target="_blank">DOWNLOAD</a></div>
</div>
</blockquote>
<blockquote><span class="label-green" style="margin-bottom: 16px; margin-left: -22px;">APPLICATION NOTE</span>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><center><img src="https://www.diagenode.com/img/categories/microplex/quality-control-check.jpg" /></center>
<p class="text-left"><small><em>Quality control check of a ChIP-seq library on the Fragment Analyzer. High Efficiency ChIP performed on 10,000 cells</em></small></p>
</div>
<div class="small-12 medium-6 large-6 columns">
<p class="text-left"><strong>Best Workflow Practices for ChIP-seq Analysis with Small Samples</strong></p>
<a href="https://www.diagenode.com/files/application_notes/Diagenode_AATI_Joint.pdf" class="details small button" target="_blank">DOWNLOAD</a></div>
</div>
</blockquote>
</div>
</div>
</div>
<div class="content" id="panel5">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<h2>TAG Kit for ChIPmentation</h2>
<ol>
<li><strong>What is the difference between tagmentation and ChIPmentation?</strong><br />Tagmentation is a reaction where an enzyme (a transposase) cleaves DNA and incorporates sequencing adaptors at the ends of the fragments in one step. In our ChIPmentation technology we combine chromatin immunoprecipitation and tagmentation in one streamlined workflow where the tagmentation step occurs directly on chromatin.<br /><br /></li>
<li><strong>What is the expected concentration of ChIPmentation libraries?</strong><br />The concentration of libraries that you need to reach will depend on the sensitivity of the machine and kits that you will use to perform the quality control and the sequencing of your libraries. Usually a concentration of 4-8 ng/&mu;l is enough for a quality control using the Qubit High Sensitivity assay (ThermoFischer Scientific) and the High Sensitivity chip for BioAnalyzer (Agilent) and for sequencing on Illumina HiSeq3000/4000.<br /><br /></li>
<li><strong>Does the ChIPmentation approach work on plants?</strong><br />Our ChIPmentation solution has been validated on human cells and we do not have any data on plants. It should be compatible. We would recommend using our Universal Plant ChIP Kit in combination with the TAG Kit for ChIPmentation and the 24 SI for ChIPmentation.<br /><br /></li>
<li><strong>What is the size of the fragments after the tagmentation?</strong><br />The size of the fragments at the end of the ChIPmentation protocol can vary depending on many parameters like the shearing efficiency, the antibody used or the tagmentation time. However, with our standard protocol we usually obtain a library peak which is around 200-300 bp (see example of results at the end of the manual). If many fragments larger than 500 bp are present , the best would be to contact your sequencing provider to ask what their requirements are, because it can vary depending on the sequencer. If you want to remove the large fragments you can use the size selection protocol described in the manual.<br /><br /></li>
<li><strong>What is the size of the adapters?</strong><br />The sum of the adapters is 128 bp.</li>
</ol>
</div>
<div class="extra-spaced">
<h2>MicroPlex Library Preparation Kit</h2>
<ol>
<li><strong>Can I use the available Illumina primers and validate them with the MicroPlex Kit v2?</strong><br /> Although the final flanking sequences of MicroPlex are the same as those used by Illumina, the PCR primers are not identical and part of them is supplied with the buffer. For this reason Illumina primers will not work as substitute.<br /><br /></li>
<li><strong>The BioAnalyzer profile of purified library shows the presence of low molecular weight peaks (primers/adaptors) in the samples. Should I re- purify the samples or they can be used directly to the sequencing? If the second purification is recommended, which ratio sample/AMPure beads should I use?</strong><br /> You can do a second round of purification using 1:1 ratio of AMPure beads to sample and this should get rid of the majority of the dimers.<br /><br /></li>
<li><strong>I am going to use the MicroPlex Library Preparation Kit v2 on ChIP samples . Our thermocycler has ramp rate 1.5&deg;/s max while the protocol recommends using a ramp rate 3 to 5&deg;/s. How would this affect the library prep?</strong><br /> We have not used a thermocycler with a ramp rate of 1.5 &deg;C, which seems faster than most of thermocyclers. Too fast of a ramp rate may affect the primer annealing and ligation steps.<br /><br /></li>
<li><strong>What is the function of the replication stop site in the adapter loops?</strong><br /> The replication stop site in the adaptor loops function to stop the polymerase from continuing to copy the rest of the stem loop.<br /><br /></li>
<li><strong>I want to do ChIP-seq. Which ChIP-seq kit can I use for sample preparation prior to Microplex Library Preparation Kit v2?</strong><br /> In our portfolio there are several ChIP-seq kits compatible with Microplex Library Preparation Kit v2. Depending on your sample type and target studied you can use the following kits: iDeal ChIP-seq Kit for Transcription Factors (Cat. No. C01010055), iDeal ChIP-seq Kit for Histones (Cat. No. C01010051), True MicroChIP kit (Cat. No. C01010130), Universal Plant ChIP-seq Kit (Cat. No. C01010152). All these kits exist in manual and automated versions.<br /><br /></li>
<li><strong>Is Microplex Library Preparation Kit v2 compatible with exome enrichment methods?</strong><br /> Microplex Library Preparation Kit v2 is compatible with major exome and target enrichment products, including Agilent SureSelect<sup>&reg;</sup>, Roche NimbleGen<sup>&reg;</sup> SeqCap<sup>&reg;</sup> EZ and custom panels.<br /><br /></li>
<li><strong>What is the nick that is mentioned in the kit method overview?</strong><br /> The nick is simply a gap between a stem adaptor and 3&rsquo; DNA end, as shown on the schema in the kit method overview.<br /><br /></li>
<li><strong>Are the indexes of the MicroPlex library preparation kit v2 located at i5 or i7?</strong><br /> The libraries generated with the MicroPlex kit v2 contain indices located at i7.<br /><br /></li>
<li><strong>Is there a need to use custom index read primers for the sequencing to read the 8nt iPCRtags?</strong><br /> There is no need for using custom Sequencing primer to sequence MicroPlex libraires. MicroPlex libraries can be sequenced using standard Illumina Sequencing kits and protocols.<br /><br /></li>
<li><strong>What is the advantage of using stem-loop adapter in the MicroPlex kit?</strong><br /> There are several advantages of using stem-loop adaptors. First of all, stem-loop adaptors prevent from self-ligation thus increases the ligation efficiency between the adapter and DNA fragment. Moreover, the background is reduced using ds adaptors with no single-stranded tails. Finally, adaptor-adaptor ligation is reduced using blocked 5&rsquo; ends.<br /><br /></li>
</ol>
</div>
<div class="extra-spaced">
<h2>IDeal Library Preparation Kit</h2>
<ol>
<li><strong>Are the index from the iDeal library Prep kit compatible with the MicroPlex library prep kit?</strong><br /> No, it is important to use only the indexes provided in the MicroPlex kit to ensure proper library preparation with this kit</li>
</ol>
</div>
</div>
</div>
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			'id' => '4997',
			'name' => 'ACE2 Enhances Sensitivity to PD-L1 Blockade by Inhibiting Macrophage-Induced Immunosuppression and Angiogenesis',
			'authors' => 'Peiyi Xie et al.',
			'description' => '<p><span>Anti-PD-L1-based combination immunotherapy has become the first-line treatment for unresectable hepatocellular carcinoma (HCC). However, the objective response rate is lower than 40%, highlighting the need to identify mechanisms of tolerance to immune checkpoint inhibitors and accurate biomarkers of response. Here, we employed next-generation sequencing to analyze HCC samples from 10 patients receiving anti-PD-L1 therapy. Activation of the renin-angiotensin system was elevated in nonresponders compared with responders, and ACE2 expression was significantly downregulated in nonresponders. ACE2 deficiency promoted HCC development and anti-PD-L1 resistance, whereas ACE2 overexpression inhibited HCC progression in immune competent mice. Mass cytometry by time of flight (CyTOF) revealed that ACE2 deficient murine orthotopic tumor tissues featured elevated M2-like tumor-associated macrophages (TAMs), displayed a CCR5+PD-L1+ immunosuppressive phenotype, and exhibited high VEGF&alpha; expression. ACE2 downregulated tumor intrinsic CCL5 expression by suppressing NF-&kappa;B signaling through the ACE2/angiotensin-(1&ndash;7)/Mas receptor axis. The lower CCL5 levels led to reduced activation of the JAK-STAT3 pathway and suppressed PD-L1 and VEGF&alpha; expression in macrophages, blocking macrophage infiltration and M2-like polarization. Pharmacological targeting of CCR5 using maraviroc enhanced the tumor suppressive effect of anti-PD-L1 therapy. Together, these findings suggest that activation of the ACE2 axis overcomes the immunosuppressive microenvironment of HCC and may serve as an immunotherapeutic target and predictive biomarker of response to PD-L1 blockade.</span></p>',
			'date' => '2024-11-04',
			'pmid' => 'https://aacrjournals.org/cancerres/article-abstract/doi/10.1158/0008-5472.CAN-24-0954/749696/ACE2-Enhances-Sensitivity-to-PD-L1-Blockade-by?redirectedFrom=fulltext',
			'doi' => 'https://doi.org/10.1158/0008-5472.CAN-24-0954',
			'modified' => '2024-11-07 11:22:24',
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		(int) 1 => array(
			'id' => '4976',
			'name' => 'Extracellular vesicle-mediated trafficking of molecular cues during human brain development',
			'authors' => 'Forero A. et al.',
			'description' => '<p><span>Cellular crosstalk is an essential process influenced by numerous factors, including secreted vesicles that transfer nucleic acids, lipids, and proteins between cells. Extracellular vesicles (EVs) have been the center of many studies focusing on neurodegenerative disorders, but whether EVs display cell-type-specific features for cellular crosstalk during neurodevelopment is unknown. Here, using human-induced pluripotent stem cell-derived cerebral organoids, neural progenitors, neurons, and astrocytes, we identify heterogeneity in EV protein content and dynamics in a cell-type-specific and time-dependent manner. Our results support the trafficking of key molecules via EVs in neurodevelopment, such as the transcription factor YAP1, and their localization to differing cell compartments depending on the EV recipient cell type. This study sheds new light on the biology of EVs during human brain development.</span></p>',
			'date' => '2024-10-22',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01106-9',
			'doi' => '10.1016/j.celrep.2024.114755',
			'modified' => '2024-09-23 10:19:53',
			'created' => '2024-09-23 10:19:53',
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		),
		(int) 2 => array(
			'id' => '4982',
			'name' => 'The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency',
			'authors' => 'Mathew Sheridan et al.',
			'description' => '<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Background</h3>
<p>The epigenetic factors KAT6A (MOZ/MYST3) and KMT2A (MLL/MLL1) interact in normal hematopoiesis to regulate progenitors&rsquo; self-renewal. Both proteins are recurrently translocated in AML, leading to impairment of critical differentiation pathways in these malignant cells. We evaluated the potential of different KAT6A therapeutic targeting strategies to alter the growth of KAT6A and KMT2A rearranged AMLs.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Methods</h3>
<p>We investigated the action and potential mechanisms of the first-in-class KAT6A inhibitor, WM-1119 in KAT6A and KMT2A rearranged&nbsp;(KAT6Ar and KMT2Ar) AML using cellular (flow cytometry, colony assays, cell growth) and molecular (shRNA knock-down, CRISPR knock-out, bulk and single-cell RNA-seq, ChIP-seq) assays. We also used two novel genetic murine KAT6A models combined with the most common KMT2Ar AML, KMT2A::MLLT3 AML. In these murine models, the catalytic activity of KAT6A, or the whole protein, can be conditionally abrogated or deleted. These models allowed us to compare the effects of specific KAT6A KAT activity inhibition with the complete deletion of the whole protein. Finally, we also tested these therapeutic approaches on human AML cell lines and primary patient AMLs.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Results</h3>
<p>We found that WM-1119 completely abrogated the proliferative and clonogenic potential of KAT6Ar cells<span>&nbsp;</span><i>in vitro.</i><span>&nbsp;</span>WM-1119 treatment was associated with a dramatic increase in myeloid differentiation program. The treatment also decreased stemness and leukemia pathways at the transcriptome level and led to loss of binding of the fusion protein at critical regulators of these pathways. In contrast, our pharmacologic and genetic results indicate that the catalytic activity of KAT6A plays a more limited role in KMT2Ar leukemogenicity, while targeting the whole KAT6A protein dramatically affects leukemic potential in murine KMT2A::MLLT3 AML.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Conclusion</h3>
<p>Our study indicates that inhibiting KAT6A KAT activity holds compelling promise for KAT6Ar AML patients. In contrast, targeted degradation of KAT6A, and not just its catalytic activity, may represent a more appropriate therapeutic approach for KMT2Ar AMLs.</p>',
			'date' => '2024-10-08',
			'pmid' => 'https://jhoonline.biomedcentral.com/articles/10.1186/s13045-024-01610-0',
			'doi' => 'https://doi.org/10.1186/s13045-024-01610-0',
			'modified' => '2024-10-11 10:00:42',
			'created' => '2024-10-11 10:00:42',
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		(int) 3 => array(
			'id' => '4983',
			'name' => 'Integrated multi-omics analysis of PBX1 in mouse adult neural stem- and progenitor cells identifies a transcriptional module that functionally links PBX1 to TCF3/4',
			'authors' => 'Vera Laub et al.',
			'description' => '<p><span>Developmental transcription factors act in networks, but how these networks achieve cell- and tissue specificity is still poorly understood. Here, we explored pre-B cell leukemia homeobox 1 (PBX1) in adult neurogenesis combining genomic, transcriptomic, and proteomic approaches. ChIP-seq analysis uncovered PBX1 binding to numerous genomic sites. Integration of PBX1 ChIP-seq with ATAC-seq data predicted interaction partners, which were subsequently validated by mass spectrometry. Whole transcriptome spatial RNA analysis revealed shared expression dynamics of&nbsp;</span><em>Pbx1</em><span><span>&nbsp;</span>and interacting factors. Among these were class I bHLH proteins TCF3 and TCF4. RNA-seq following<span>&nbsp;</span></span><em>Pbx1</em><span>,<span>&nbsp;</span></span><em>Tcf3</em><span><span>&nbsp;</span>or<span>&nbsp;</span></span><em>Tcf4</em><span><span>&nbsp;</span>knockdown identified proliferation- and differentiation associated genes as shared targets, while sphere formation assays following knockdown argued for functional cooperativity of PBX1 and TCF3 in progenitor cell proliferation. Notably, while physiological PBX1-TCF interaction has not yet been described, chromosomal translocation resulting in genomic<span>&nbsp;</span></span><em>TCF3::PBX1</em><span><span>&nbsp;</span>fusion characterizes a subtype of acute lymphoblastic leukemia. Introducing<span>&nbsp;</span></span><em>Pbx1</em><span><span>&nbsp;</span>into Nalm6 cells, a pre-B cell line expressing<span>&nbsp;</span></span><em>TCF3</em><span><span>&nbsp;</span>but lacking<span>&nbsp;</span></span><em>PBX1</em><span>, upregulated the leukemogenic genes<span>&nbsp;</span></span><em>BLK</em><span><span>&nbsp;</span>and<span>&nbsp;</span></span><em>NOTCH3</em><span>, arguing that functional PBX1-TCF cooperativity likely extends to hematopoiesis. Our study hence uncovers a transcriptional module orchestrating the balance between progenitor cell proliferation and differentiation in adult neurogenesis with potential implications for leukemia etiology.</span></p>',
			'date' => '2024-10-08',
			'pmid' => 'https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkae864/7815639',
			'doi' => 'https://doi.org/10.1093/nar/gkae864',
			'modified' => '2024-10-11 10:02:42',
			'created' => '2024-10-11 10:02:42',
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		),
		(int) 4 => array(
			'id' => '4985',
			'name' => 'HNF1β bookmarking involves Topoisomerase 1 activation and DNA topology relaxation in mitotic chromatin',
			'authors' => 'Alessia Bagattin et al.',
			'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HNF1&beta; mitotic site binding is preserved with a specific methanol/formaldehyde ChIP</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">BTBD2, an HNF1&beta; partner, mediates mitosis-specific interaction with TOP1</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">HNF1&beta; recruits TOP1 and induces DNA relaxation around bookmarked HNF1&beta; sites</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">An HNF1&beta; mutation, found in MODY patients, disrupts the interaction with TOP1</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">HNF1&beta; (<i>HNF1B</i>) is a transcription factor frequently mutated in patients with developmental renal disease. It binds to mitotic chromatin and reactivates gene expression after mitosis, a phenomenon referred to as bookmarking. Using a crosslinking method that circumvents the artifacts of formaldehyde, we demonstrate that&nbsp;HNF1&beta; remains associated with chromatin in a sequence-specific way in both interphase and mitosis. We identify an HNF1&beta;-interacting protein, BTBD2, that enables the interaction and activation of Topoisomerase 1 (TOP1) exclusively during mitosis. Our study identifies a shared microhomology domain between HNF1&beta; and TOP1, where a mutation, found in &ldquo;maturity onset diabetes of the young&rdquo; patients, disrupts their interaction. Importantly, HNF1&beta; recruits TOP1 and induces DNA relaxation around HNF1&beta; mitotic chromatin sites, elucidating its crucial role in chromatin remodeling and gene reactivation after mitotic exit. These findings shed light on how HNF1&beta; reactivates target gene expression after mitosis, providing insights into its crucial role in maintenance of cellular identity.</div>
</section>',
			'date' => '2024-10-08',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01156-2',
			'doi' => '10.1016/j.celrep.2024.114805',
			'modified' => '2024-10-14 09:04:44',
			'created' => '2024-10-14 09:04:44',
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		),
		(int) 5 => array(
			'id' => '4978',
			'name' => 'RNA polymerase II transcription initiation in holo-TFIID-depleted mouse embryonic stem cells',
			'authors' => 'Hisler V. et al.',
			'description' => '<p><span>The recognition of core promoter sequences by TFIID is the first step in RNA polymerase II (Pol II) transcription initiation. Metazoan holo-TFIID is a trilobular complex, composed of the TATA binding protein (TBP) and 13 TBP-associated factors (TAFs). Why and how TAFs are necessary for the formation of TFIID domains and how they contribute to transcription initiation remain unclear. Inducible TAF7 or TAF10 depletion, followed by comprehensive analysis of TFIID subcomplex formation, chromatin binding, and nascent transcription in mouse embryonic stem cells, result in the formation of a TAF7-lacking TFIID or a minimal core-TFIID complex, respectively. These partial complexes support TBP recruitment at promoters and nascent Pol II transcription at most genes early after depletion, but importantly, TAF10 is necessary for efficient Pol II pausing. We show that partially assembled TFIID complexes can sustain Pol II transcription initiation but cannot replace holo-TFIID over several cell divisions and/or development.</span></p>',
			'date' => '2024-09-30',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01142-2',
			'doi' => 'https://doi.org/10.1016/j.celrep.2024.114791',
			'modified' => '2024-10-04 10:18:22',
			'created' => '2024-10-04 10:18:22',
			'ProductsPublication' => array(
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		(int) 6 => array(
			'id' => '4963',
			'name' => 'An atlas of the human liver diurnal transcriptome and its perturbation by hepatitis C virus infection',
			'authors' => 'Mukherji A. et al.',
			'description' => '<p><span>Chronic liver disease and cancer are global health challenges. The role of the circadian clock as a regulator of liver physiology and disease is well established in rodents, however, the identity and epigenetic regulation of rhythmically expressed genes in human disease is less well studied. Here we unravel the rhythmic transcriptome and epigenome of human hepatocytes using male human liver chimeric mice. We identify a large number of rhythmically expressed protein coding genes in human hepatocytes of male chimeric mice, which includes key transcription factors, chromatin modifiers, and critical enzymes. We show that hepatitis C virus (HCV) infection, a major cause of liver disease and cancer, perturbs the transcriptome by altering the rhythmicity of the expression of more than 1000 genes, and affects the epigenome, leading to an activation of critical pathways mediating metabolic alterations, fibrosis, and cancer. HCV-perturbed rhythmic pathways remain dysregulated in patients with advanced liver disease. Collectively, these data support a role for virus-induced perturbation of the hepatic rhythmic transcriptome and pathways in cancer development and may provide opportunities for cancer prevention and biomarkers to predict HCC risk.</span></p>',
			'date' => '2024-08-29',
			'pmid' => 'https://www.nature.com/articles/s41467-024-51698-8',
			'doi' => 'https://doi.org/10.1038/s41467-024-51698-8',
			'modified' => '2024-09-02 10:17:48',
			'created' => '2024-09-02 10:17:48',
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			)
		),
		(int) 7 => array(
			'id' => '4968',
			'name' => 'Innate immune training restores pro-reparative myeloid functions to promote remyelination in the aged central nervous system',
			'authors' => 'Tiwari V. et al.',
			'description' => '<p><span>The reduced ability of the central nervous system to regenerate with increasing age limits functional recovery following demyelinating injury. Previous work has shown that myelin debris can overwhelm the metabolic capacity of microglia, thereby impeding tissue regeneration in aging, but the underlying mechanisms are unknown. In a model of demyelination, we found that a substantial number of genes that were not effectively activated in aged myeloid cells displayed epigenetic modifications associated with restricted chromatin accessibility. Ablation of two class I histone deacetylases in microglia was sufficient to restore the capacity of aged mice to remyelinate lesioned tissue. We used Bacillus Calmette-Guerin (BCG), a live-attenuated vaccine, to train the innate immune system and detected epigenetic reprogramming of brain-resident myeloid cells and functional restoration of myelin debris clearance and lesion recovery. Our results provide insight into aging-associated decline in myeloid function and how this decay can be prevented by innate immune reprogramming.</span></p>',
			'date' => '2024-07-24',
			'pmid' => 'https://www.cell.com/immunity/fulltext/S1074-7613(24)00348-0',
			'doi' => '',
			'modified' => '2024-09-02 17:05:54',
			'created' => '2024-09-02 17:05:54',
			'ProductsPublication' => array(
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			)
		),
		(int) 8 => array(
			'id' => '4954',
			'name' => 'A multiomic atlas of the aging hippocampus reveals molecular changes in response to environmental enrichment',
			'authors' => 'Perez R. F. at al. ',
			'description' => '<p><span>Aging involves the deterioration of organismal function, leading to the emergence of multiple pathologies. Environmental stimuli, including lifestyle, can influence the trajectory of this process and may be used as tools in the pursuit of healthy aging. To evaluate the role of epigenetic mechanisms in this context, we have generated bulk tissue and single cell multi-omic maps of the male mouse dorsal hippocampus in young and old animals exposed to environmental stimulation in the form of enriched environments. We present a molecular atlas of the aging process, highlighting two distinct axes, related to inflammation and to the dysregulation of mRNA metabolism, at the functional RNA and protein level. Additionally, we report the alteration of heterochromatin domains, including the loss of bivalent chromatin and the uncovering of a heterochromatin-switch phenomenon whereby constitutive heterochromatin loss is partially mitigated through gains in facultative heterochromatin. Notably, we observed the multi-omic reversal of a great number of aging-associated alterations in the context of environmental enrichment, which was particularly linked to glial and oligodendrocyte pathways. In conclusion, our work describes the epigenomic landscape of environmental stimulation in the context of aging and reveals how lifestyle intervention can lead to the multi-layered reversal of aging-associated decline.</span></p>',
			'date' => '2024-07-16',
			'pmid' => 'https://www.nature.com/articles/s41467-024-49608-z',
			'doi' => 'https://doi.org/10.1038/s41467-024-49608-z',
			'modified' => '2024-07-29 11:33:49',
			'created' => '2024-07-29 11:33:49',
			'ProductsPublication' => array(
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		),
		(int) 9 => array(
			'id' => '4952',
			'name' => 'Epigenetic alterations affecting hematopoietic regulatory networks as drivers of mixed myeloid/lymphoid leukemia',
			'authors' => 'Roger Mulet-Lazaro et al.',
			'description' => '<p><span>Leukemias with ambiguous lineage comprise several loosely defined entities, often without a clear mechanistic basis. Here, we extensively profile the epigenome and transcriptome of a subgroup of such leukemias with CpG Island Methylator Phenotype. These leukemias exhibit comparable hybrid myeloid/lymphoid epigenetic landscapes, yet heterogeneous genetic alterations, suggesting they are defined by their shared epigenetic profile rather than common genetic lesions. Gene expression enrichment reveals similarity with early T-cell precursor acute lymphoblastic leukemia and a lymphoid progenitor cell of origin. In line with this, integration of differential DNA methylation and gene expression shows widespread silencing of myeloid transcription factors. Moreover, binding sites for hematopoietic transcription factors, including CEBPA, SPI1 and LEF1, are uniquely inaccessible in these leukemias. Hypermethylation also results in loss of CTCF binding, accompanied by changes in chromatin interactions involving key transcription factors. In conclusion, epigenetic dysregulation, and not genetic lesions, explains the mixed phenotype of this group of leukemias with ambiguous lineage. The data collected here constitute a useful and comprehensive epigenomic reference for subsequent studies of acute myeloid leukemias, T-cell acute lymphoblastic leukemias and mixed-phenotype leukemias.</span></p>',
			'date' => '2024-07-07',
			'pmid' => 'https://www.nature.com/articles/s41467-024-49811-y',
			'doi' => 'https://doi.org/10.1038/s41467-024-49811-y',
			'modified' => '2024-07-10 12:21:42',
			'created' => '2024-07-10 12:21:42',
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		(int) 10 => array(
			'id' => '4911',
			'name' => 'Multiomics uncovers the epigenomic and transcriptomic response to viral and bacterial stimulation in turbot',
			'authors' => 'Aramburu O. et al.',
			'description' => '<p><span>Uncovering the epigenomic regulation of immune responses is essential for a comprehensive understanding of host defence mechanisms but remains poorly described in farmed fish. Here, we report the first annotation of the innate immune regulatory response in the genome of turbot (</span><em>Scophthalmus maximus</em><span>), a farmed flatfish. We integrated RNA-Seq with ATAC-Seq and ChIP-Seq (histone marks H3K4me3, H3K27ac and H3K27me3) using samples from head kidney. Sampling was performed 24 hours post-stimulation with viral (poly I:C) and bacterial (inactivate<span>&nbsp;</span></span><em>Vibrio anguillarum</em><span>) mimics<span>&nbsp;</span></span><em>in vivo</em><span><span>&nbsp;</span>and<span>&nbsp;</span></span><em>in vitro</em><span><span>&nbsp;</span>(primary leukocyte cultures). Among the 8,797 differentially expressed genes (DEGs), we observed enrichment of transcriptional activation pathways in response to<span>&nbsp;</span></span><em>Vibrio</em><span><span>&nbsp;</span>and immune response pathways - including interferon stimulated genes - for poly I:C. Meanwhile, metabolic and cell cycle were downregulated by both mimics. We identified notable differences in chromatin accessibility (20,617<span>&nbsp;</span></span><em>in vitro</em><span>, 59,892<span>&nbsp;</span></span><em>in vivo</em><span>) and H3K4me3 bound regions (11,454<span>&nbsp;</span></span><em>in vitro</em><span>, 10,275<span>&nbsp;</span></span><em>in viv</em><span>o) - i.e. marking active promoters - between stimulations and controls. Overlaps of DEGs with promoters showing differential accessibility or histone mark binding revealed a significant coupling of the transcriptome and chromatin state. DEGs with activation marks in their promoters were enriched for similar functions to the global DEG set, but not in all cases, suggesting key regulatory genes were in poised or bivalent states. Active promoters and putative enhancers were differentially enriched in transcription factor binding motifs, many of them common to viral and bacterial responses. Finally, an in-depth analysis of immune response changes in chromatin state surrounding key DEGs encoding transcription factors was performed. This comprehensive multi-omics investigation provides an improved understanding of the epigenomic basis for the turbot immune responses and provides novel functional genomic information that can be leveraged in selective breeding towards enhanced disease resistance.</span></p>',
			'date' => '2024-02-15',
			'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.02.15.580452v1',
			'doi' => 'https://doi.org/10.1101/2024.02.15.580452',
			'modified' => '2024-02-22 11:41:27',
			'created' => '2024-02-22 11:41:27',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '4884',
			'name' => 'SMARCB1 loss activates patient-specific distal oncogenic enhancers in malignant rhabdoid tumors',
			'authors' => 'Liu, N.Q. et al.',
			'description' => '<p><span>Malignant rhabdoid tumor (MRT) is a highly malignant and often lethal childhood cancer. MRTs are genetically defined by bi-allelic inactivating mutations in&nbsp;</span><i>SMARCB1</i><span>, a member of the BRG1/BRM-associated factors (BAF) chromatin remodeling complex. Mutations in BAF complex members are common in human cancer, yet their contribution to tumorigenesis remains in many cases poorly understood. Here, we study derailed regulatory landscapes as a consequence of<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>loss in the context of MRT. Our multi-omics approach on patient-derived MRT organoids reveals a dramatic reshaping of the regulatory landscape upon<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>reconstitution. Chromosome conformation capture experiments subsequently reveal patient-specific looping of distal enhancer regions with the promoter of the<span>&nbsp;</span></span><i>MYC</i><span><span>&nbsp;</span>oncogene. This intertumoral heterogeneity in<span>&nbsp;</span></span><i>MYC</i><span><span>&nbsp;</span>enhancer utilization is also present in patient MRT tissues as shown by combined single-cell RNA-seq and ATAC-seq. We show that loss of<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>activates patient-specific epigenetic reprogramming underlying MRT tumorigenesis.</span></p>',
			'date' => '2023-12-01',
			'pmid' => 'https://www.nature.com/articles/s41467-023-43498-3#Abs1',
			'doi' => '10.1038/s41467-023-43498-3',
			'modified' => '2023-12-05 08:45:53',
			'created' => '2023-12-05 08:45:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '4885',
			'name' => 'The genetic landscape of origins of replication in P. falciparum',
			'authors' => 'Casilda Muñoz Castellano et al.',
			'description' => '<p><span>Various origin mapping approaches have enabled genome-wide identification of origins of replication (ORI) in model organisms, but only a few studies have focused on divergent organisms. By employing three complementary approaches we provide a high-resolution map of ORIs in&nbsp;</span><em>Plasmodium falciparum</em><span>, the deadliest human malaria parasite. We profiled the distribution of origin of recognition complex (ORC) binding sites by ChIP-seq of two<span>&nbsp;</span></span><em>Pf</em><span>ORC subunits and mapped active ORIs using NFS and SNS-seq. We show that ORIs lack sequence specificity but are not randomly distributed, and group in clusters. Licensing is biased towards regions of higher GC content and associated with G-quadruplex forming sequences (G4FS). While strong transcription likely enhances firing, active origins are depleted from transcription start sites. Instead, most accumulate in transcriptionally active gene bodies. Single molecule analysis of nanopore reads containing multiple initiation events, which could have only come from individual nuclei, showed a relationship between the replication fork pace and the distance to the nearest origin. While some similarities were drawn with the canonic eukaryote model, the distribution of ORIs in<span>&nbsp;</span></span><em>P. falciparum</em><span><span>&nbsp;</span>is likely shaped by unique genomic features such as extreme AT-richness&mdash;a product of evolutionary pressure imposed by the parasitic lifestyle.</span></p>',
			'date' => '2023-12-01',
			'pmid' => 'https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkad1103/7457016#428428709',
			'doi' => 'doi.org/10.1093/nar/gkad1103',
			'modified' => '2023-12-05 08:47:24',
			'created' => '2023-12-05 08:47:24',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '4843',
			'name' => 'Differentiation block in acute myeloid leukemia regulated by intronicsequences of FTO',
			'authors' => 'Camera  F. et al.',
			'description' => '<p>Iroquois transcription factor gene IRX3 is highly expressed in 20&acirc;&euro;&ldquo;30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences &acirc;&circ;&frac14;220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with the IRX3 promoter, which correlate with IRX3 expression. Deletion of these intronic elements confirms a role in positively regulating IRX3. RNAseq revealed long non-coding (lnc) transcripts arising from this locus. FTO-lncAML knockdown (KD) induced differentiation of AML cells, loss of clonogenic activity, and reduced FTO intron 8:IRX3 promoter contacts. While both FTO-lncAML KD and IRX3 KD induced differentiation, FTO-lncAML but not IRX3 KD led to HOXA downregulation suggesting transcript activity in trans. FTO-lncAMLhigh AML samples expressed higher levels of HOXA and lower levels of differentiation genes. Thus, a regulatory module in FTO intron 8 consisting of clustered enhancer elements and a long non-coding RNA is active in human AML, impeding myeloid differentiation.</p>',
			'date' => '2023-08-01',
			'pmid' => 'https://www.sciencedirect.com/science/article/pii/S2589004223013962',
			'doi' => '10.1016/j.isci.2023.107319',
			'modified' => '2023-08-01 14:14:01',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '4851',
			'name' => 'Supraphysiological Androgens Promote the Tumor Suppressive Activity of the Androgen Receptor Through cMYC Repression and Recruitment of the DREAM Complex',
			'authors' => 'Nyquist  M. et al.',
			'description' => '<p>The androgen receptor (AR) pathway regulates key cell survival programs in prostate epithelium. The AR represents a near-universal driver and therapeutic vulnerability in metastatic prostate cancer, and targeting AR has a remarkable therapeutic index. Though most approaches directed toward AR focus on inhibiting AR signaling, laboratory and now clinical data have shown that high dose, supraphysiological androgen treatment (SPA) results in growth repression and improved outcomes in subsets of prostate cancer patients. A better understanding of the mechanisms contributing to SPA response and resistance could help guide patient selection and combination therapies to improve efficacy. To characterize SPA signaling, we integrated metrics of gene expression changes induced by SPA together with cistrome data and protein-interactomes. These analyses indicated that the Dimerization partner, RB-like, E2F and Multi-vulval class B (DREAM) complex mediates growth repression and downregulation of E2F targets in response to SPA. Notably, prostate cancers with complete genomic loss of RB1 responded to SPA treatment whereas loss of DREAM complex components such as RBL1/2 promoted resistance. Overexpression of MYC resulted in complete resistance to SPA and attenuated the SPA/AR-mediated repression of E2F target genes. These findings support a model of SPA-mediated growth repression that relies on the negative regulation of MYC by AR leading to repression of E2F1 signaling via the DREAM complex. The integrity of MYC signaling and DREAM complex assembly may consequently serve as determinants of SPA responses and as pathways mediating SPA resistance.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/37352376/',
			'doi' => '10.1158/0008-5472.CAN-22-2613',
			'modified' => '2023-08-01 18:09:31',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '4852',
			'name' => 'In skeletal muscle and neural crest cells, SMCHD1 regulates biologicalpathways relevant for Bosma syndrome and facioscapulohumeral dystrophyphenotype.',
			'authors' => 'Laberthonnière  C. et al.',
			'description' => '<p>Many genetic syndromes are linked to mutations in genes encoding factors that guide chromatin organization. Among them, several distinct rare genetic diseases are linked to mutations in SMCHD1 that encodes the structural maintenance of chromosomes flexible hinge domain containing 1 chromatin-associated factor. In humans, its function as well as the impact of its mutations remains poorly defined. To fill this gap, we determined the episignature associated with heterozygous SMCHD1 variants in primary cells and cell lineages derived from induced pluripotent stem cells for Bosma arhinia and microphthalmia syndrome (BAMS) and type 2 facioscapulohumeral dystrophy (FSHD2). In human tissues, SMCHD1 regulates the distribution of methylated CpGs, H3K27 trimethylation and CTCF at repressed chromatin but also at euchromatin. Based on the exploration of tissues affected either in FSHD or in BAMS, i.e. skeletal muscle fibers and neural crest stem cells, respectively, our results emphasize multiple functions for SMCHD1, in chromatin compaction, chromatin insulation and gene regulation with variable targets or phenotypical outcomes. We concluded that in rare genetic diseases, SMCHD1 variants impact gene expression in two ways: (i) by changing the chromatin context at a number of euchromatin loci or (ii) by directly regulating some loci encoding master transcription factors required for cell fate determination and tissue differentiation.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37334829',
			'doi' => '10.1093/nar/gkad523',
			'modified' => '2023-08-01 14:35:38',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '4861',
			'name' => 'Hypomethylation and overexpression of Th17-associated genes is ahallmark of intestinal CD4+ lymphocytes in Crohn's disease.',
			'authors' => 'Sun  Z. et al.',
			'description' => '<p>BACKGROUND: The development of Crohn's disease (CD) involves immune cell signaling pathways regulated by epigenetic modifications. Aberrant DNA methylation has been identified in peripheral blood and bulk intestinal tissue from CD patients. However, the DNA methylome of disease-associated intestinal CD4 + lymphocytes has not been evaluated. MATERIALS AND METHODS: Genome-wide DNA methylation sequencing was performed from terminal ileum CD4 + cells from 21 CD patients and 12 age and sex matched controls. Data was analyzed for differentially methylated CpGs (DMCs) and methylated regions (DMRs). Integration was performed with RNA-sequencing data to evaluate the functional impact of DNA methylation changes on gene expression. DMRs were overlapped with regions of differentially open chromatin (by ATAC-seq) and CCCTC-binding factor (CTCF) binding sites (by ChIP-seq) between peripherally-derived Th17 and Treg cells. RESULTS: CD4+ cells in CD patients had significantly increased DNA methylation compared to those from the controls. A total of 119,051 DMCs and 8,113 DMRs were detected. While hyper-methylated genes were mostly related to cell metabolism and homeostasis, hypomethylated genes were significantly enriched within the Th17 signaling pathway. The differentially enriched ATAC regions in Th17 cells (compared to Tregs) were hypomethylated in CD patients, suggesting heightened Th17 activity. There was significant overlap between hypomethylated DNA regions and CTCF-associated binding sites. CONCLUSIONS: The methylome of CD patients demonstrate an overall dominant hypermethylation yet hypomethylation is more concentrated in proinflammatory pathways, including Th17 differentiation. Hypomethylation of Th17-related genes associated with areas of open chromatin and CTCF binding sites constitutes a hallmark of CD-associated intestinal CD4 + cells.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37280154',
			'doi' => '10.1093/ecco-jcc/jjad093',
			'modified' => '2023-08-01 14:52:39',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 17 => array(
			'id' => '4862',
			'name' => 'Mutant FUS induces chromatin reorganization in the hippocampus andalters memory processes.',
			'authors' => 'Tzeplaeff  L. et al.',
			'description' => '<p>Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalization to hippocampal function and memory formation are still not characterized. Herein, we show that in these mice, the hippocampus paradoxically displays nuclear FUS accumulation. Multi-omic analyses showed that FUS binds to a set of genes characterized by the presence of an ETS/ELK-binding motifs, and involved in RNA metabolism, transcription, ribosome/mitochondria and chromatin organization. Importantly, hippocampal nuclei showed a decompaction of the neuronal chromatin at highly expressed genes and an inappropriate transcriptomic response was observed after spatial training of Fus mice. Furthermore, these mice lacked precision in a hippocampal-dependent spatial memory task and displayed decreased dendritic spine density. These studies shows that mutated FUS affects epigenetic regulation of the chromatin landscape in hippocampal neurons, which could participate in FTD/ALS pathogenic events. These data call for further investigation in the neurological phenotype of FUS-related diseases and open therapeutic strategies towards epigenetic drugs.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37327984',
			'doi' => '10.1016/j.pneurobio.2023.102483',
			'modified' => '2023-08-01 14:55:49',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 18 => array(
			'id' => '4782',
			'name' => 'Transient suppression of SUMOylation in embryonic stem cells generatesembryo-like structures.',
			'authors' => 'Cossec  J-C. et al.',
			'description' => '<p>Recent advances in synthetic embryology have opened new avenues for understanding the complex events controlling mammalian peri-implantation development. Here, we show that mouse embryonic stem cells (ESCs) solely exposed to chemical inhibition of SUMOylation generate embryo-like structures comprising anterior neural and trunk-associated regions. HypoSUMOylation-instructed ESCs give rise to spheroids that self-organize into gastrulating structures containing cell types spatially and functionally related to embryonic and extraembryonic compartments. Alternatively, spheroids cultured in a droplet microfluidic device form elongated structures that undergo axial organization reminiscent of natural embryo morphogenesis. Single-cell transcriptomics reveals various cellular lineages, including properly positioned anterior neuronal cell types and paraxial mesoderm segmented into somite-like structures. Transient SUMOylation suppression gradually increases DNA methylation genome wide and repressive mark deposition at Nanog. Interestingly, cell-to-cell variations in SUMOylation levels occur during early embryogenesis. Our approach provides a proof of principle for potentially powerful strategies to explore early embryogenesis by targeting chromatin roadblocks of cell fate change.</p>',
			'date' => '2023-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37061916',
			'doi' => '10.1016/j.celrep.2023.112380',
			'modified' => '2023-06-13 09:20:06',
			'created' => '2023-05-05 12:34:24',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 19 => array(
			'id' => '4693',
			'name' => 'ZEB1 controls a lineage-specific transcriptional program essential formelanoma cell state transitions',
			'authors' => 'Tang  Y. et al.',
			'description' => '<p>Cell plasticity sustains intra-tumor heterogeneity and treatment resistance in melanoma. Deciphering the transcriptional mechanisms governing reversible phenotypic transitions between proliferative/differentiated and invasive/stem-like states is required in order to design novel therapeutic strategies. EMT-inducing transcription factors, extensively known for their role in metastasis in carcinoma, display cell-type specific functions in melanoma, with a decreased ZEB2/ZEB1 expression ratio fostering adaptive resistance to targeted therapies. While ZEB1 direct target genes have been well characterized in carcinoma models, they remain unknown in melanoma. Here, we performed a genome-wide characterization of ZEB1 transcriptional targets, by combining ChIP-sequencing and RNA-sequencing, upon phenotype switching in melanoma models. We identified and validated ZEB1 binding peaks in the promoter of key lineage-specific genes related to melanoma cell identity. Comparative analyses with breast carcinoma cells demonstrated melanoma-specific ZEB1 binding, further supporting lineage specificity. Gain- or loss-of-function of ZEB1, combined with functional analyses, further demonstrated that ZEB1 negatively regulates proliferative/melanocytic programs and positively regulates both invasive and stem-like programs. We then developed single-cell spatial multiplexed analyses to characterize melanoma cell states with respect to ZEB1/ZEB2 expression in human melanoma samples. We characterized the intra-tumoral heterogeneity of ZEB1 and ZEB2 and further validated ZEB1 increased expression in invasive cells, but also in stem-like cells, highlighting its relevance in vivo in both populations. Overall, our results define ZEB1 as a major transcriptional regulator of cell states transitions and provide a better understanding of lineage-specific transcriptional programs sustaining intra-tumor heterogeneity in melanoma.</p>',
			'date' => '2023-02-01',
			'pmid' => 'https://doi.org/10.1101%2F2023.02.10.526467',
			'doi' => '10.1101/2023.02.10.526467',
			'modified' => '2023-04-14 09:11:23',
			'created' => '2023-02-28 12:19:11',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 20 => 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) 21 => array(
			'id' => '4651',
			'name' => 'TCDD induces multigenerational alterations in the expression ofmicroRNA in the thymus through epigenetic modifications',
			'authors' => 'Singh  Narendra P et al.',
			'description' => '<p>2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a potent AhR ligand, is an environmental contaminant that is known for mediating toxicity across generations. However, whether TCDD can induce multigenerational changes in the expression of miRNAs (miRs) has not been previously studied. In the current study, we investigated the effect of administration of TCDD in pregnant mice (F0) on gestational day 14, on the expression of miRs in the thymus of F0 and subsequent generations (F1 and F2). Of the 3200 miRs screened, 160 miRs were dysregulated similarly in F0, F1, and F2 generations while 46 miRs were differentially altered in F0-F2 generations. Pathway analysis revealed that the changes in miR signature profile mediated by TCDD affected the genes that regulate cell signaling, apoptosis, thymic atrophy, cancer, immunosuppression, and other physiological pathways. A significant number of miRs that showed altered expression exhibited dioxin response elements (DRE) on their promoters. Focusing on one such miR, namely miR-203 that expressed DREs and was induced across F0-F2 by TCDD, promoter analysis showed that one of the DREs expressed by miR-203 was functional to TCDD-mediated upregulation. Also, the histone methylation status of H3K4me3 in the miR-203 promoter was significantly increased near the transcriptional start site (TSS) in TCDD-treated thymocytes across F0-F2 generations. Genome-wide ChIP-seq study suggested that TCDD may cause alterations in histone methylation in certain genes across the three generations. Together, the current study demonstrates that gestational exposure to TCDD can alter the expression of miRs in F0 through direct activation of DREs as well as across F0, F1, and F2 generations through epigenetic pathways.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://academic.oup.com/pnasnexus/advance-article/doi/10.1093/pnasnexus/pgac290/6886578',
			'doi' => 'https://doi.org/10.1093/pnasnexus/pgac290',
			'modified' => '2023-03-13 10:55:36',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 22 => array(
			'id' => '4632',
			'name' => 'The histone acetyltransferase KAT6A is recruited to unmethylatedCpG islands via a DNA binding winged helix domain.',
			'authors' => 'Weber  L.M. et al.',
			'description' => '<p>The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrate that a winged helix (WH) domain at the very N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A with unmethylated CpG islands (CGIs) genome-wide. Mutation of the essential amino acids for DNA binding completely abrogates the enrichment of KAT6A at CGIs. In contrast, deletion of a second WH domain or the histone tail binding PHD fingers only subtly influences the binding of KAT6A to CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36537216',
			'doi' => '10.1093/nar/gkac1188',
			'modified' => '2023-03-28 09:01:38',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 23 => array(
			'id' => '4629',
			'name' => 'Polyglutamine-expanded ATXN7 alters a specific epigenetic signatureunderlying photoreceptor identity gene expression in SCA7 mouseretinopathy.',
			'authors' => 'Niewiadomska-Cimicka  A.et al.',
			'description' => '<p>BACKGROUND: Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disorder that primarily affects the cerebellum and retina. SCA7 is caused by a polyglutamine expansion in the ATXN7 protein, a subunit of the transcriptional coactivator SAGA that acetylates histone H3 to deposit narrow H3K9ac mark at DNA regulatory elements of active genes. Defective histone acetylation has been presented as a possible cause for gene deregulation in SCA7 mouse models. However, the topography of acetylation defects at the whole genome level and its relationship to changes in gene expression remain to be determined. METHODS: We performed deep RNA-sequencing and chromatin immunoprecipitation coupled to high-throughput sequencing to examine the genome-wide correlation between gene deregulation and alteration of the active transcription marks, e.g. SAGA-related H3K9ac, CBP-related H3K27ac and RNA polymerase II (RNAPII), in a SCA7 mouse retinopathy model. RESULTS: Our analyses revealed that active transcription marks are reduced at most gene promoters in SCA7 retina, while a limited number of genes show changes in expression. We found that SCA7 retinopathy is caused by preferential downregulation of hundreds of highly expressed genes that define morphological and physiological identities of mature photoreceptors. We further uncovered that these photoreceptor genes harbor unusually broad H3K9ac profiles spanning the entire gene bodies and have a low RNAPII pausing. This broad H3K9ac signature co-occurs with other features that delineate superenhancers, including broad H3K27ac, binding sites for photoreceptor specific transcription factors and expression of enhancer-related non-coding RNAs (eRNAs). In SCA7 retina, downregulated photoreceptor genes show decreased H3K9 and H3K27 acetylation and eRNA expression as well as increased RNAPII pausing, suggesting that superenhancer-related features are altered. CONCLUSIONS: Our study thus provides evidence that distinctive epigenetic configurations underlying high expression of cell-type specific genes are preferentially impaired in SCA7, resulting in a defect in the maintenance of identity features of mature photoreceptors. Our results also suggest that continuous SAGA-driven acetylation plays a role in preserving post-mitotic neuronal identity.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36539812',
			'doi' => '10.1186/s12929-022-00892-1',
			'modified' => '2023-03-28 09:07:19',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 24 => 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) 25 => array(
			'id' => '4494',
			'name' => 'Cryptococcal Hsf3 controls intramitochondrial ROS homeostasis byregulating the respiratory process.',
			'authors' => 'Gao  X.et al.',
			'description' => '<p>Mitochondrial quality control prevents accumulation of intramitochondrial-derived reactive oxygen species (mtROS), thereby protecting cells against DNA damage, genome instability, and programmed cell death. However, underlying mechanisms are incompletely understood, particularly in fungal species. Here, we show that Cryptococcus neoformans heat shock factor 3 (CnHsf3) exhibits an atypical function in regulating mtROS independent of the unfolded protein response. CnHsf3 acts in nuclei and mitochondria, and nuclear- and mitochondrial-targeting signals are required for its organelle-specific functions. It represses the expression of genes involved in the tricarboxylic acid cycle while promoting expression of genes involved in electron transfer chain. In addition, CnHsf3 responds to multiple intramitochondrial stresses; this response is mediated by oxidation of the cysteine residue on its DNA binding domain, which enhances DNA binding. Our results reveal a function of HSF proteins in regulating mtROS homeostasis that is independent of the unfolded protein response.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36109512',
			'doi' => '10.1038/s41467-022-33168-1',
			'modified' => '2022-11-18 12:43:17',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 26 => array(
			'id' => '4496',
			'name' => 'Dominant role of DNA methylation over H3K9me3 for IAP silencingin endoderm.',
			'authors' => 'Wang  Z. et al.',
			'description' => '<p>Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications H3K9me3 and DNA methylation. On ERVs, these modifications are mainly deposited by the histone methyltransferase Setdb1 and by the maintenance DNA methyltransferase Dnmt1. Knock-out of either Setdb1 or Dnmt1 leads to ERV de-repression in various cell types. However, it is currently not known if H3K9me3 and DNA methylation depend on each other for ERV silencing. Here we show that conditional knock-out of Setdb1 in mouse embryonic endoderm results in ERV de-repression in visceral endoderm (VE) descendants and does not occur in definitive endoderm (DE). Deletion of Setdb1 in VE progenitors results in loss of H3K9me3 and reduced DNA methylation of Intracisternal A-particle (IAP) elements, consistent with up-regulation of this ERV family. In DE, loss of Setdb1 does not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 knock-out results in IAP de-repression in both visceral and definitive endoderm cells, while H3K9me3 is unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm cells. Our findings suggest that Setdb1-meditated H3K9me3 is not sufficient for IAP silencing, but rather critical for maintaining high DNA methylation.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36123357',
			'doi' => '10.1038/s41467-022-32978-7',
			'modified' => '2022-11-21 10:26:30',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 27 => array(
			'id' => '4415',
			'name' => 'HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependentgene repression in murine erythroleukaemia.',
			'authors' => 'Gregoricchio  S. et al.',
			'description' => '<p>Although originally described as transcriptional activator, SPI1/PU.1, a major player in haematopoiesis whose alterations are associated with haematological malignancies, has the ability to repress transcription. Here, we investigated the mechanisms underlying gene repression in the erythroid lineage, in which SPI1 exerts an oncogenic function by blocking differentiation. We show that SPI1 represses genes by binding active enhancers that are located in intergenic or gene body regions. HDAC1 acts as a cooperative mediator of SPI1-induced transcriptional repression by deacetylating SPI1-bound enhancers in a subset of genes, including those involved in erythroid differentiation. Enhancer deacetylation impacts on promoter acetylation, chromatin accessibility and RNA pol II occupancy. In addition to the activities of HDAC1, polycomb repressive complex 2 (PRC2) reinforces gene repression by depositing H3K27me3 at promoter sequences when SPI1 is located at enhancer sequences. Moreover, our study identified a synergistic relationship between PRC2 and HDAC1 complexes in mediating the transcriptional repression activity of SPI1, ultimately inducing synergistic adverse effects on leukaemic cell survival. Our results highlight the importance of the mechanism underlying transcriptional repression in leukemic cells, involving complex functional connections between SPI1 and the epigenetic regulators PRC2 and HDAC1.</p>',
			'date' => '2022-08-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35871293',
			'doi' => '10.1093/nar/gkac613',
			'modified' => '2022-09-15 08:59:26',
			'created' => '2022-09-08 16:32:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 28 => array(
			'id' => '4516',
			'name' => 'Dual role of histone variant H3.3B in spermatogenesis: positiveregulation of piRNA transcription and implication in X-chromosomeinactivation.',
			'authors' => 'Fontaine  E. et al.',
			'description' => '<p>The histone variant H3.3 is encoded by two distinct genes, H3f3a and H3f3b, exhibiting identical amino-acid sequence. H3.3 is required for spermatogenesis, but the molecular mechanism of its spermatogenic function remains obscure. Here, we have studied the role of each one of H3.3A and H3.3B proteins in spermatogenesis. We have generated transgenic conditional knock-out/knock-in (cKO/KI) epitope-tagged FLAG-FLAG-HA-H3.3B (H3.3BHA) and FLAG-FLAG-HA-H3.3A (H3.3AHA) mouse lines. We show that H3.3B, but not H3.3A, is required for spermatogenesis and male fertility. Analysis of the molecular mechanism unveils that the absence of H3.3B led to alterations in the meiotic/post-meiotic transition. Genome-wide RNA-seq reveals that the depletion of H3.3B in meiotic cells is associated with increased expression of the whole sex X and Y chromosomes as well as of both RLTR10B and RLTR10B2 retrotransposons. In contrast, the absence of H3.3B resulted in down-regulation of the expression of piRNA clusters. ChIP-seq experiments uncover that RLTR10B and RLTR10B2 retrotransposons, the whole sex chromosomes and the piRNA clusters are markedly enriched of H3.3. Taken together, our data dissect the molecular mechanism of H3.3B functions during spermatogenesis and demonstrate that H3.3B, depending on its chromatin localization, is involved in either up-regulation or down-regulation of expression of defined large chromatin regions.</p>',
			'date' => '2022-07-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35766398',
			'doi' => '10.1093/nar/gkac541',
			'modified' => '2022-11-24 08:51:34',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 29 => array(
			'id' => '4393',
			'name' => 'TBX2 acts as a potent transcriptional silencer of tumour suppressor genesthrough interaction with the CoREST complex to sustain theproliferation of breast cancers.',
			'authors' => 'McIntyre  A.J. et al.',
			'description' => '<p>Chromosome 17q23 amplification occurs in 20\% of primary breast tumours and is associated with poor outcome. The TBX2 gene is located on 17q23 and is often over-expressed in this breast tumour subset. TBX2 is an anti-senescence gene, promoting cell growth and survival through repression of Tumour Suppressor Genes (TSGs), such as NDRG1 and CST6. Previously we found that TBX2 cooperates with the PRC2 complex to repress several TSGs, and that PRC2 inhibition restored NDRG1 expression to impede cellular proliferation. Here, we now identify CoREST proteins, LSD1 and ZNF217, as novel interactors of TBX2. Genetic or pharmacological targeting of CoREST emulated TBX2 loss, inducing NDRG1 expression and abolishing breast cancer growth in vitro and in vivo. Furthermore, we uncover that TBX2/CoREST targeting of NDRG1 is achieved by recruitment of TBX2 to the NDRG1 promoter by Sp1, the abolishment of which resulted in NDRG1 upregulation and diminished cancer cell proliferation. Through ChIP-seq we reveal that 30\% of TBX2-bound promoters are shared with ZNF217 and identify novel targets repressed by TBX2/CoREST; of these targets a lncRNA, LINC00111, behaves as a negative regulator of cell proliferation. Overall, these data indicate that inhibition of CoREST proteins represents a promising therapeutic intervention for TBX2-addicted breast tumours.</p>',
			'date' => '2022-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35687133',
			'doi' => '10.1093/nar/gkac494',
			'modified' => '2022-08-11 14:23:06',
			'created' => '2022-08-11 12:14:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 30 => array(
			'id' => '4836',
			'name' => 'Caffeine intake exerts dual genome-wide effects on hippocampal metabolismand learning-dependent transcription.',
			'authors' => 'Paiva  I. et al.',
			'description' => '<p>Caffeine is the most widely consumed psychoactive substance in the world. Strikingly, the molecular pathways engaged by its regular consumption remain unclear. We herein addressed the mechanisms associated with habitual (chronic) caffeine consumption in the mouse hippocampus using untargeted orthogonal omics techniques. Our results revealed that chronic caffeine exerts concerted pleiotropic effects in the hippocampus at the epigenomic, proteomic, and metabolomic levels. Caffeine lowered metabolism-related processes (e.g., at the level of metabolomics and gene expression) in bulk tissue, while it induced neuron-specific epigenetic changes at synaptic transmission/plasticity-related genes and increased experience-driven transcriptional activity. Altogether, these findings suggest that regular caffeine intake improves the signal-to-noise ratio during information encoding, in part through fine-tuning of metabolic genes, while boosting the salience of information processing during learning in neuronal circuits.</p>',
			'date' => '2022-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35536645',
			'doi' => '10.1172/JCI149371',
			'modified' => '2023-08-01 13:52:29',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 31 => array(
			'id' => '4221',
			'name' => 'Epigenetic Mechanisms Mediating Cell State Transitions in Chondrocytes',
			'authors' => 'Wuelling M. et al.',
			'description' => '<p><span>Epigenetic modifications play critical roles in regulating cell lineage differentiation, but the epigenetic mechanisms guiding specific differentiation steps within a cell lineage have rarely been investigated. To decipher such mechanisms, we used the defined transition from proliferating (PC) into hypertrophic chondrocytes (HC) during endochondral ossification as a model. We established a map of activating and repressive histone modifications for each cell type. ChromHMM state transition analysis and Pareto-based integration of differential levels of mRNA and epigenetic marks revealed that differentiation-associated gene repression is initiated by the addition of H3K27me3 to promoters still carrying substantial levels of activating marks. Moreover, the integrative analysis identified genes specifically expressed in cells undergoing the transition into hypertrophy. Investigation of enhancer profiles detected surprising differences in enhancer number, location, and transcription factor binding sites between the two closely related cell types. Furthermore, cell type-specific upregulation of gene expression was associated with increased numbers of H3K27ac peaks. Pathway analysis identified PC-specific enhancers associated with chondrogenic genes, whereas HC-specific enhancers mainly control metabolic pathways linking epigenetic signature to biological functions. Since HC-specific enhancers show a higher conservation in postnatal tissues, the switch to metabolic pathways seems to be a hallmark of differentiated tissues. Surprisingly, the analysis of H3K27ac levels at super-enhancers revealed a rapid adaption of H3K27ac occupancy to changes in gene expression, supporting the importance of enhancer modulation for acute alterations in gene expression. &copy; 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).</span></p>',
			'date' => '2022-05-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33534175/',
			'doi' => '10.1002/jbmr.4263',
			'modified' => '2022-04-25 11:46:32',
			'created' => '2022-04-21 12:00:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 32 => array(
			'id' => '4402',
			'name' => 'The CpG Island-Binding Protein SAMD1 Contributes to anUnfavorable Gene Signature in HepG2 Hepatocellular CarcinomaCells.',
			'authors' => 'Simon  C. et al.',
			'description' => '<p>The unmethylated CpG island-binding protein SAMD1 is upregulated in many human cancer types, but its cancer-related role has not yet been investigated. Here, we used the hepatocellular carcinoma cell line HepG2 as a cancer model and investigated the cellular and transcriptional roles of SAMD1 using ChIP-Seq and RNA-Seq. SAMD1 targets several thousand gene promoters, where it acts predominantly as a transcriptional repressor. HepG2 cells with SAMD1 deletion showed slightly reduced proliferation, but strongly impaired clonogenicity. This phenotype was accompanied by the decreased expression of pro-proliferative genes, including MYC target genes. Consistently, we observed a decrease in the active H3K4me2 histone mark at most promoters, irrespective of SAMD1 binding. Conversely, we noticed an increase in interferon response pathways and a gain of H3K4me2 at a subset of enhancers that were enriched for IFN-stimulated response elements (ISREs). We identified key transcription factor genes, such as , , and , that were directly repressed by SAMD1. Moreover, SAMD1 deletion also led to the derepression of the PI3K-inhibitor , contributing to diminished mTOR signaling and ribosome biogenesis pathways. Our work suggests that SAMD1 is involved in establishing a pro-proliferative setting in hepatocellular carcinoma cells. Inhibiting SAMD1's function in liver cancer cells may therefore lead to a more favorable gene signature.</p>',
			'date' => '2022-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35453756',
			'doi' => '10.3390/biology11040557',
			'modified' => '2022-08-11 14:45:43',
			'created' => '2022-08-11 12:14:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 33 => array(
			'id' => '4524',
			'name' => 'Local euchromatin enrichment in lamina-associated domains anticipatestheir repositioning in the adipogenic lineage.',
			'authors' => 'Madsen-Østerbye  J. et al.',
			'description' => '<p>BACKGROUND: Interactions of chromatin with the nuclear lamina via lamina-associated domains (LADs) confer structural stability to the genome. The dynamics of positioning of LADs during differentiation, and how LADs impinge on developmental gene expression, remains, however, elusive. RESULTS: We examined changes in the association of lamin B1 with the genome in the first 72 h of differentiation of adipose stem cells into adipocytes. We demonstrate a repositioning of entire stand-alone LADs and of LAD edges as a prominent nuclear structural feature of early adipogenesis. Whereas adipogenic genes are released from LADs, LADs sequester downregulated or repressed genes irrelevant for the adipose lineage. However, LAD repositioning only partly concurs with gene expression changes. Differentially expressed genes in LADs, including LADs conserved throughout differentiation, reside in local euchromatic and lamin-depleted sub-domains. In these sub-domains, pre-differentiation histone modification profiles correlate with the LAD versus inter-LAD outcome of these genes during adipogenic commitment. Lastly, we link differentially expressed genes in LADs to short-range enhancers which overall co-partition with these genes in LADs versus inter-LADs during differentiation. CONCLUSIONS: We conclude that LADs are predictable structural features of adipose nuclear architecture that restrain non-adipogenic genes in a repressive environment.</p>',
			'date' => '2022-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35410387',
			'doi' => '10.1186/s13059-022-02662-6',
			'modified' => '2022-11-24 09:08:01',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 34 => array(
			'id' => '4235',
			'name' => 'NuA4 and H2A.Z control environmental responses and autotrophicgrowth in Arabidopsis',
			'authors' => 'Bieluszewski T. et al.',
			'description' => '<p>Nucleosomal acetyltransferase of H4 (NuA4) is an essential transcriptional coactivator in eukaryotes, but remains poorly characterized in plants. Here, we describe Arabidopsis homologs of the NuA4 scaffold proteins Enhancer of Polycomb-Like 1 (AtEPL1) and Esa1-Associated Factor 1 (AtEAF1). Loss of AtEAF1 results in inhibition of growth and chloroplast development. These effects are stronger in the Atepl1 mutant and are further enhanced by loss of Golden2-Like (GLK) transcription factors, suggesting that NuA4 activates nuclear plastid genes alongside GLK. We demonstrate that AtEPL1 is necessary for nucleosomal acetylation of histones H4 and H2A.Z by NuA4 in vitro. These chromatin marks are diminished genome-wide in Atepl1, while another active chromatin mark, H3K9 acetylation (H3K9ac), is locally enhanced. Expression of many chloroplast-related genes depends on NuA4, as they are downregulated with loss of H4ac and H2A.Zac. Finally, we demonstrate that NuA4 promotes H2A.Z deposition and by doing so prevents spurious activation of stress response genes.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35022409',
			'doi' => '10.1038/s41467-021-27882-5',
			'modified' => '2022-05-19 17:02:00',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 35 => array(
			'id' => '4772',
			'name' => 'Three classes of epigenomic regulators converge to hyperactivate theessential maternal gene deadhead within a heterochromatin mini-domain.',
			'authors' => 'Torres-Campana  D. et al.',
			'description' => '<p>The formation of a diploid zygote is a highly complex cellular process that is entirely controlled by maternal gene products stored in the egg cytoplasm. This highly specialized transcriptional program is tightly controlled at the chromatin level in the female germline. As an extreme case in point, the massive and specific ovarian expression of the essential thioredoxin Deadhead (DHD) is critically regulated in Drosophila by the histone demethylase Lid and its partner, the histone deacetylase complex Sin3A/Rpd3, via yet unknown mechanisms. Here, we identified Snr1 and Mod(mdg4) as essential for dhd expression and investigated how these epigenomic effectors act with Lid and Sin3A to hyperactivate dhd. Using Cut\&amp;Run chromatin profiling with a dedicated data analysis procedure, we found that dhd is intriguingly embedded in an H3K27me3/H3K9me3-enriched mini-domain flanked by DNA regulatory elements, including a dhd promoter-proximal element essential for its expression. Surprisingly, Lid, Sin3a, Snr1 and Mod(mdg4) impact H3K27me3 and this regulatory element in distinct manners. However, we show that these effectors activate dhd independently of H3K27me3/H3K9me3, and that dhd remains silent in the absence of these marks. Together, our study demonstrates an atypical and critical role for chromatin regulators Lid, Sin3A, Snr1 and Mod(mdg4) to trigger tissue-specific hyperactivation within a unique heterochromatin mini-domain.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8759638/',
			'doi' => '10.1371/journal.pgen.1009615',
			'modified' => '2023-04-17 09:46:00',
			'created' => '2023-04-14 13:41:22',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 36 => 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) 37 => array(
			'id' => '4245',
			'name' => 'Decreased PRC2 activity supports the survival of basal-like breastcancer cells to cytotoxic treatments',
			'authors' => 'Mieczkowska IK et al.',
			'description' => '<p>Breast cancer (BC) is the most common cancer occurring in women but also rarely develops in men. Recent advances in early diagnosis and development of targeted therapies have greatly improved the survival rate of BC patients. However, the basal-like BC subtype (BLBC), largely overlapping with the triple-negative BC subtype (TNBC), lacks such drug targets and conventional cytotoxic chemotherapies often remain the only treatment option. Thus, the development of resistance to cytotoxic therapies has fatal consequences. To assess the involvement of epigenetic mechanisms and their therapeutic potential increasing cytotoxic drug efficiency, we combined high-throughput RNA- and ChIP-sequencing analyses in BLBC cells. Tumor cells surviving chemotherapy upregulated transcriptional programs of epithelial-to-mesenchymal transition (EMT) and stemness. To our surprise, the same cells showed a pronounced reduction of polycomb repressive complex 2 (PRC2) activity via downregulation of its subunits Ezh2, Suz12, Rbbp7 and Mtf2. Mechanistically, loss of PRC2 activity leads to the de-repression of a set of genes through an epigenetic switch from repressive H3K27me3 to activating H3K27ac mark at regulatory regions. We identified Nfatc1 as an upregulated gene upon loss of PRC2 activity and directly implicated in the transcriptional changes happening upon survival to chemotherapy. Blocking NFATc1 activation reduced epithelial-to-mesenchymal transition, aggressiveness, and therapy resistance of BLBC cells. Our data demonstrate a previously unknown function of PRC2 maintaining low Nfatc1 expression levels and thereby repressing aggressiveness and therapy resistance in BLBC.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34845197',
			'doi' => '10.1038/s41419-021-04407-y',
			'modified' => '2022-05-20 09:21:56',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 38 => array(
			'id' => '4276',
			'name' => 'Ago1 controls myogenic differentiation by regulating eRNA-mediatedCBP-guided epigenome reprogramming.',
			'authors' => 'Fallatah Bodor et al.',
			'description' => '<p>The role of chromatin-associated RNAi components in the nucleus of mammalian cells and in particular in the context of developmental programs remains to be elucidated. Here, we investigate the function of nuclear Argonaute 1 (Ago1) in gene expression regulation during skeletal muscle differentiation. We show that Ago1 is required for activation of the myogenic program by supporting chromatin modification mediated by developmental enhancer activation. Mechanistically, we demonstrate that Ago1 directly controls global H3K27 acetylation (H3K27ac) by regulating enhancer RNA (eRNA)-CREB-binding protein (CBP) acetyltransferase interaction, a key step in enhancer-driven gene activation. In particular, we show that Ago1 is specifically required for myogenic differentiation 1 (MyoD) and downstream myogenic gene activation, whereas its depletion leads to failure of CBP acetyltransferase activation and blocking of the myogenic program. Our work establishes a role of the mammalian enhancer-associated RNAi component Ago1 in epigenome regulation and activation of developmental programs.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.celrep.2021.110066',
			'doi' => '10.1016/j.celrep.2021.110066',
			'modified' => '2022-05-23 09:53:14',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 39 => array(
			'id' => '4833',
			'name' => 'Extensive NEUROG3 occupancy in the human pancreatic endocrine generegulatory network.',
			'authors' => 'Schreiber  V. et al.',
			'description' => '<p>OBJECTIVE: Mice lacking the bHLH transcription factor (TF) Neurog3 do not form pancreatic islet cells, including insulin-secreting beta cells, the absence of which leads to diabetes. In humans, homozygous mutations of NEUROG3 manifest with neonatal or childhood diabetes. Despite this critical role in islet cell development, the precise function of and downstream genetic programs regulated directly by NEUROG3 remain elusive. Therefore, we mapped genome-wide NEUROG3 occupancy in human induced pluripotent stem cell (hiPSC)-derived endocrine progenitors and determined NEUROG3 dependency of associated genes to uncover direct targets. METHODS: We generated a novel hiPSC line (NEUROG3-HA-P2A-Venus) where NEUROG3 is HA-tagged and fused to a self-cleaving fluorescent VENUS reporter. We used the CUT\&amp;RUN technique to map NEUROG3 occupancy and epigenetic marks in pancreatic endocrine progenitors (PEP) that were differentiated from this hiPSC line. We integrated NEUROG3 occupancy data with chromatin status and gene expression in PEPs as well as their NEUROG3-dependence. In addition, we investigated whether NEUROG3 binds type 2 diabetes mellitus (T2DM)-associated variants at the PEP stage. RESULTS: CUT\&amp;RUN revealed a total of 863 NEUROG3 binding sites assigned to 1263 unique genes. NEUROG3 occupancy was found at promoters as well as at distant cis-regulatory elements that frequently overlapped within PEP active enhancers. De novo motif analyses defined a NEUROG3 consensus binding motif and suggested potential co-regulation of NEUROG3 target genes by FOXA or RFX transcription factors. We found that 22\% of the genes downregulated in NEUROG3 PEPs, and 10\% of genes enriched in NEUROG3-Venus positive endocrine cells were bound by NEUROG3 and thus likely to be directly regulated. NEUROG3 binds to 138 transcription factor genes, some with important roles in islet cell development or function, such as NEUROD1, PAX4, NKX2-2, SOX4, MLXIPL, LMX1B, RFX3, and NEUROG3 itself, and many others with unknown islet function. Unexpectedly, we uncovered that NEUROG3 targets genes critical for insulin secretion in beta cells (e.g., GCK, ABCC8/KCNJ11, CACNA1A, CHGA, SCG2, SLC30A8, and PCSK1). Thus, analysis of NEUROG3 occupancy suggests that the transient expression of NEUROG3 not only promotes islet destiny in uncommitted pancreatic progenitors, but could also initiate endocrine programs essential for beta cell function. Lastly, we identified eight T2DM risk SNPs within NEUROG3-bound regions. CONCLUSION: Mapping NEUROG3 genome occupancy in PEPs uncovered unexpectedly broad, direct control of the endocrine genes, raising novel hypotheses on how this master regulator controls islet and beta cell differentiation.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://doi.org/10.1101%2F2021.04.14.439685',
			'doi' => '10.1016/j.molmet.2021.101313',
			'modified' => '2023-08-01 13:46:35',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 40 => array(
			'id' => '4285',
			'name' => 'Alveolar macrophages from persons living with HIV show impairedepigenetic response to Mycobacterium tuberculosis.',
			'authors' => 'Correa-Macedo Wilian et al.',
			'description' => '<p>Persons living with HIV (PLWH) are at increased risk of tuberculosis (TB). HIV-associated TB is often the result of recent infection with Mycobacterium tuberculosis (Mtb) followed by rapid progression to disease. Alveolar macrophages (AM) are the first cells of the innate immune system that engage Mtb, but how HIV and antiretroviral therapy (ART) impact on the anti-mycobacterial response of AM is not known. To investigate the impact of HIV and ART on the transcriptomic and epigenetic response of AM to Mtb, we obtained AM by bronchoalveolar lavage from 20 PLWH receiving ART, 16 control subjects who were HIV-free (HC), and 14 subjects who received ART as pre-exposure prophylaxis (PrEP) to prevent HIV infection. Following in-vitro challenge with Mtb, AM from each group displayed overlapping but distinct profiles of significantly up- and down-regulated genes in response to Mtb. Comparatively, AM isolated from both PLWH and PrEP subjects presented a substantially weaker transcriptional response. In addition, AM from HC subjects challenged with Mtb responded with pronounced chromatin accessibility changes while AM obtained from PLWH and PrEP subjects displayed no significant changes in their chromatin state. Collectively, these results revealed a stronger adverse effect of ART than HIV on the epigenetic landscape and transcriptional responsiveness of AM.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473646/',
			'doi' => '10.1172/JCI148013',
			'modified' => '2022-05-24 09:08:39',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 41 => array(
			'id' => '4297',
			'name' => 'INTS11 regulates hematopoiesis by promoting PRC2 function.',
			'authors' => 'Zhang Peng et al.',
			'description' => '<p>INTS11, the catalytic subunit of the Integrator (INT) complex, is crucial for the biogenesis of small nuclear RNAs and enhancer RNAs. However, the role of INTS11 in hematopoietic stem and progenitor cell (HSPC) biology is unknown. Here, we report that INTS11 is required for normal hematopoiesis and hematopoietic-specific genetic deletion of leads to cell cycle arrest and impairment of fetal and adult HSPCs. We identified a novel INTS11-interacting protein complex, Polycomb repressive complex 2 (PRC2), that maintains HSPC functions. Loss of INTS11 destabilizes the PRC2 complex, decreases the level of histone H3 lysine 27 trimethylation (H3K27me3), and derepresses PRC2 target genes. Reexpression of INTS11 or PRC2 proteins in -deficient HSPCs restores the levels of PRC2 and H3K27me3 as well as HSPC functions. Collectively, our data demonstrate that INTS11 is an essential regulator of HSPC homeostasis through the INTS11-PRC2 axis.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34516911',
			'doi' => '10.1126/sciadv.abh1684',
			'modified' => '2022-05-30 09:31:00',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 42 => array(
			'id' => '4304',
			'name' => 'The related coactivator complexes SAGA and ATAC control embryonicstem cell self-renewal through acetyltransferase-independent mechanisms',
			'authors' => 'Fischer Veronique et al.',
			'description' => '<p>SUMMARY SAGA (Spt-Ada-Gcn5 acetyltransferase) and ATAC (Ada-two-A-containing) are two related coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development, but the role of these complexes in RNA polymerase II transcription is less understood. To determine whether SAGA and ATAC have redundant or specific functions, we compare the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC are required for complex assembly and mouse ESC growth and self-renewal. Surprisingly, depletion of HAT module subunits causes a global decrease in histone H3K9 acetylation, but does not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for self-renewal of mouse ESCs by regulating transcription through different pathways in a HAT-independent manner.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34433046',
			'doi' => '10.1016/j.celrep.2021.109598',
			'modified' => '2022-05-30 09:57:39',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 43 => array(
			'id' => '4345',
			'name' => 'Altered Chromatin States Drive Cryptic Transcription in AgingMammalian Stem Cells.',
			'authors' => 'McCauley Brenna S et al.',
			'description' => '<p>A repressive chromatin state featuring trimethylated lysine 36 on histone H3 (H3K36me3) and DNA methylation suppresses cryptic transcription in embryonic stem cells. Cryptic transcription is elevated with age in yeast and nematodes, and reducing it extends yeast lifespan, though whether this occurs in mammals is unknown. We show that cryptic transcription is elevated in aged mammalian stem cells, including murine hematopoietic stem cells (mHSCs) and neural stem cells (NSCs) and human mesenchymal stem cells (hMSCs). Precise mapping allowed quantification of age-associated cryptic transcription in hMSCs aged . Regions with significant age-associated cryptic transcription have a unique chromatin signature: decreased H3K36me3 and increased H3K4me1, H3K4me3, and H3K27ac with age. Genomic regions undergoing such changes resemble known promoter sequences and are bound by TBP even in young cells. Hence, the more permissive chromatin state at intragenic cryptic promoters likely underlies increased cryptic transcription in aged mammalian stem cells.</p>',
			'date' => '2021-08-01',
			'pmid' => 'https://doi.org/10.1038%2Fs43587-021-00091-x',
			'doi' => '10.1038/s43587-021-00091-x',
			'modified' => '2022-06-22 12:30:19',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 44 => array(
			'id' => '4333',
			'name' => 'Metabolically controlled histone H4K5 acylation/acetylation ratiodrives BRD4 genomic distribution.',
			'authors' => 'Gao M. et al.',
			'description' => '<p>In addition to acetylation, histones are modified by a series of competing longer-chain acylations. Most of these acylation marks are enriched and co-exist with acetylation on active gene regulatory elements. Their seemingly redundant functions hinder our understanding of histone acylations' specific roles. Here, by using an acute lymphoblastic leukemia (ALL) cell model and blasts from individuals with B-precusor ALL (B-ALL), we demonstrate a role of mitochondrial activity in controlling the histone acylation/acetylation ratio, especially at histone H4 lysine 5 (H4K5). An increase in the ratio of non-acetyl acylations (crotonylation or butyrylation) over acetylation on H4K5 weakens bromodomain containing protein 4 (BRD4) bromodomain-dependent chromatin interaction and enhances BRD4 nuclear mobility and availability for binding transcription start site regions of active genes. Our data suggest that the metabolism-driven control of the histone acetylation/longer-chain acylation(s) ratio could be a common mechanism regulating the bromodomain factors' functional genomic distribution.</p>',
			'date' => '2021-07-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.celrep.2021.109460',
			'doi' => '10.1016/j.celrep.2021.109460',
			'modified' => '2022-08-03 16:14:09',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 45 => array(
			'id' => '4343',
			'name' => 'The SAM domain-containing protein 1 (SAMD1) acts as a repressivechromatin regulator at unmethylated CpG islands',
			'authors' => 'Stielow B. et al. ',
			'description' => '<p>CpG islands (CGIs) are key regulatory DNA elements at most promoters, but how they influence the chromatin status and transcription remains elusive. Here, we identify and characterize SAMD1 (SAM domain-containing protein 1) as an unmethylated CGI-binding protein. SAMD1 has an atypical winged-helix domain that directly recognizes unmethylated CpG-containing DNA via simultaneous interactions with both the major and the minor groove. The SAM domain interacts with L3MBTL3, but it can also homopolymerize into a closed pentameric ring. At a genome-wide level, SAMD1 localizes to H3K4me3-decorated CGIs, where it acts as a repressor. SAMD1 tethers L3MBTL3 to chromatin and interacts with the KDM1A histone demethylase complex to modulate H3K4me2 and H3K4me3 levels at CGIs, thereby providing a mechanism for SAMD1-mediated transcriptional repression. The absence of SAMD1 impairs ES cell differentiation processes, leading to misregulation of key biological pathways. Together, our work establishes SAMD1 as a newly identified chromatin regulator acting at unmethylated CGIs.</p>',
			'date' => '2021-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33980486',
			'doi' => '10.1126/sciadv.abf2229',
			'modified' => '2022-08-03 16:34:24',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 46 => array(
			'id' => '4192',
			'name' => 'Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-inducedprogrammed cell death in Arabidopsis.',
			'authors' => 'Dvořák Tomaštíková E. et al.',
			'description' => '<p>The Polycomb Repressive Complex 2 (PRC2) is well-known for its role in controlling developmental transitions by suppressing the premature expression of key developmental regulators. Previous work revealed that PRC2 also controls the onset of senescence, a form of developmental programmed cell death (PCD) in plants. Whether the induction of PCD in response to stress is similarly suppressed by the PRC2 remained largely unknown. In this study, we explored whether PCD triggered in response to immunity- and disease-promoting pathogen effectors is associated with changes in the distribution of the PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) modification in Arabidopsis thaliana. We furthermore tested the distribution of the heterochromatic histone mark H3K9me2, which is established, to a large extent, by the H3K9 methyltransferase KRYPTONITE, and occupies chromatin regions generally not targeted by PRC2. We report that effector-induced PCD caused major changes in the distribution of both repressive epigenetic modifications and that both modifications have a regulatory role and impact on the onset of PCD during pathogen infection. Our work highlights that the transition to pathogen-induced PCD is epigenetically controlled, revealing striking similarities to developmental PCD.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33566101',
			'doi' => '10.1093/plphys/kiab035',
			'modified' => '2022-01-06 14:12:23',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 47 => array(
			'id' => '4273',
			'name' => 'An integrated multi-omics analysis identifies prognostic molecularsubtypes of non-muscle-invasive bladder cancer',
			'authors' => 'Lindskrog Sia Viborg et al.',
			'description' => '<p>The molecular landscape in non-muscle-invasive bladder cancer (NMIBC) is characterized by large biological heterogeneity with variable clinical outcomes. Here, we perform an integrative multi-omics analysis of patients diagnosed with NMIBC (n&thinsp;=&thinsp;834). Transcriptomic analysis identifies four classes (1, 2a, 2b and 3) reflecting tumor biology and disease aggressiveness. Both transcriptome-based subtyping and the level of chromosomal instability provide independent prognostic value beyond established prognostic clinicopathological parameters. High chromosomal instability, p53-pathway disruption and APOBEC-related mutations are significantly associated with transcriptomic class 2a and poor outcome. RNA-derived immune cell infiltration is associated with chromosomally unstable tumors and enriched in class 2b. Spatial proteomics analysis confirms the higher infiltration of class 2b tumors and demonstrates an association between higher immune cell infiltration and lower recurrence rates. Finally, the independent prognostic value of the transcriptomic classes is documented in 1228 validation samples using a single sample classification tool. The classifier provides a framework for biomarker discovery and for optimizing treatment and surveillance in next-generation clinical trials.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863885',
			'doi' => '10.1038/s41467-021-22465-w',
			'modified' => '2022-05-23 09:49:43',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 48 => array(
			'id' => '4109',
			'name' => 'VPRBP functions downstream of the androgen receptor and OGT to restrict p53 activation in prostate cancer ',
			'authors' => 'Poulose N. et al. ',
			'description' => '<p>Androgen receptor (AR) is a major driver of prostate cancer (PCa) initiation and progression. O-GlcNAc transferase (OGT), the enzyme that catalyses the covalent addition of UDP-N-acetylglucosamine (UDP-GlcNAc) to serine and threonine residues of proteins, is often up-regulated in PCa with its expression correlated with high Gleason score. In this study we have identified an AR and OGT co-regulated factor, VPRBP/DCAF1. We show that VPRBP is regulated by the AR at the transcript level, and by OGT at the protein level. In human tissue samples, VPRBP protein expression correlated with AR amplification, OGT overexpression and poor prognosis. VPRBP knockdown in prostate cancer cells led to a significant decrease in cell proliferation, p53 stabilization, nucleolar fragmentation and increased p53 recruitment to the chromatin. In conclusion, we have shown that VPRBP/DCAF1 promotes prostate cancer cell proliferation by restraining p53 activation under the influence of the AR and OGT.</p>',
			'date' => '2021-02-21',
			'pmid' => 'https://www.biorxiv.org/content/10.1101/2021.02.28.433236v1',
			'doi' => '',
			'modified' => '2021-07-07 11:59:15',
			'created' => '2021-07-07 11:59:15',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 49 => array(
			'id' => '4124',
			'name' => 'JAZF1, A Novel p400/TIP60/NuA4 Complex Member, Regulates H2A.ZAcetylation at Regulatory Regions.',
			'authors' => 'Procida, Tara and Friedrich, Tobias and Jack, Antonia P M and Peritore,Martina and Bönisch, Clemens and Eberl, H Christian and Daus, Nadine andKletenkov, Konstantin and Nist, Andrea and Stiewe, Thorsten and Borggrefe,Tilman and Mann, Matthias and Bartk',
			'description' => '<p>Histone variants differ in amino acid sequence, expression timing and genomic localization sites from canonical histones and convey unique functions to eukaryotic cells. Their tightly controlled spatial and temporal deposition into specific chromatin regions is accomplished by dedicated chaperone and/or remodeling complexes. While quantitatively identifying the chaperone complexes of many human H2A variants by using mass spectrometry, we also found additional members of the known H2A.Z chaperone complexes p400/TIP60/NuA4 and SRCAP. We discovered JAZF1, a nuclear/nucleolar protein, as a member of a p400 sub-complex containing MBTD1 but excluding ANP32E. Depletion of JAZF1 results in transcriptome changes that affect, among other pathways, ribosome biogenesis. To identify the underlying molecular mechanism contributing to JAZF1's function in gene regulation, we performed genome-wide ChIP-seq analyses. Interestingly, depletion of JAZF1 leads to reduced H2A.Z acetylation levels at &gt; 1000 regulatory sites without affecting H2A.Z nucleosome positioning. Since JAZF1 associates with the histone acetyltransferase TIP60, whose depletion causes a correlated H2A.Z deacetylation of several JAZF1-targeted enhancer regions, we speculate that JAZF1 acts as chromatin modulator by recruiting TIP60's enzymatic activity. Altogether, this study uncovers JAZF1 as a member of a TIP60-containing p400 chaperone complex orchestrating H2A.Z acetylation at regulatory regions controlling the expression of genes, many of which are involved in ribosome biogenesis.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33445503',
			'doi' => '10.3390/ijms22020678',
			'modified' => '2021-12-07 10:00:44',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 50 => array(
			'id' => '4179',
			'name' => 'Histone demethylase JMJD2B/KDM4B regulates transcriptional program viadistinctive epigenetic targets and protein interactors for the maintenanceof trophoblast stem cells.',
			'authors' => 'Mak, Kylie Hin-Man et al.',
			'description' => '<p>Trophoblast stem cell (TSC) is crucial to the formation of placenta in mammals. Histone demethylase JMJD2 (also known as KDM4) family proteins have been previously shown to support self-renewal and differentiation of stem cells. However, their roles in the context of the trophoblast lineage remain unclear. Here, we find that knockdown of Jmjd2b resulted in differentiation of TSCs, suggesting an indispensable role of JMJD2B/KDM4B in maintaining the stemness. Through the integration of transcriptome and ChIP-seq profiling data, we show that JMJD2B is associated with a loss of H3K36me3 in a subset of embryonic lineage genes which are marked by H3K9me3 for stable repression. By characterizing the JMJD2B binding motifs and other transcription factor binding datasets, we discover that JMJD2B forms a protein complex with AP-2 family transcription factor TFAP2C and histone demethylase LSD1. The JMJD2B-TFAP2C-LSD1 complex predominantly occupies active gene promoters, whereas the TFAP2C-LSD1 complex is located at putative enhancers, suggesting that these proteins mediate enhancer-promoter interaction for gene regulation. We conclude that JMJD2B is vital to the TSC transcriptional program and safeguards the trophoblast cell fate via distinctive protein interactors and epigenetic targets.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33441614',
			'doi' => '10.1038/s41598-020-79601-7',
			'modified' => '2021-12-21 16:43:16',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 51 => array(
			'id' => '4210',
			'name' => 'Trans- and cis-acting effects of Firre on epigenetic features of theinactive X chromosome.',
			'authors' => 'Fang, He and Bonora, Giancarlo and Lewandowski, Jordan P and Thakur,Jitendra and Filippova, Galina N and Henikoff, Steven and Shendure, Jay andDuan, Zhijun and Rinn, John L and Deng, Xinxian and Noble, William S andDisteche, Christine M',
			'description' => '<p>Firre encodes a lncRNA involved in nuclear organization. Here, we show that Firre RNA expressed from the active X chromosome maintains histone H3K27me3 enrichment on the inactive X chromosome (Xi) in somatic cells. This trans-acting effect involves SUZ12, reflecting interactions between Firre RNA and components of the Polycomb repressive complexes. Without Firre RNA, H3K27me3 decreases on the Xi and the&nbsp;Xi-perinucleolar location is disrupted, possibly due to decreased CTCF binding on the Xi. We also observe widespread gene dysregulation, but not on the Xi. These effects are measurably rescued by ectopic expression of mouse or human Firre/FIRRE transgenes, supporting conserved trans-acting roles. We also find that the compact 3D structure of the Xi partly depends on the Firre locus and its RNA. In common lymphoid progenitors and T-cells Firre exerts a cis-acting effect on maintenance of H3K27me3 in a 26&thinsp;Mb region around the locus, demonstrating cell type-specific trans- and cis-acting roles of this lncRNA.</p>',
			'date' => '2020-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33247132',
			'doi' => '10.1038/s41467-020-19879-3',
			'modified' => '2022-01-13 15:03:45',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 52 => array(
			'id' => '4206',
			'name' => 'H2A.Z is dispensable for both basal and activated transcription inpost-mitotic mouse muscles.',
			'authors' => 'Belotti E. et al.',
			'description' => '<p>While the histone variant H2A.Z is known to be required for mitosis, it is also enriched in nucleosomes surrounding the transcription start site of active promoters, implicating H2A.Z in transcription. However, evidence obtained so far mainly rely on correlational data generated in actively dividing cells. We have exploited a paradigm in which transcription is uncoupled from the cell cycle by developing an in vivo system to inactivate H2A.Z in terminally differentiated post-mitotic muscle cells. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is a marker but not an active driver of transcription.</p>',
			'date' => '2020-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32266374',
			'doi' => '10.1093/nar/gkaa157',
			'modified' => '2022-01-13 13:46:38',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		)
	),
	'Testimonial' => array(),
	'Area' => array(),
	'SafetySheet' => array(
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			'id' => '702',
			'name' => 'MicroPlex Library Preparation Kit v3 SDS GB en',
			'language' => 'en',
			'url' => 'files/SDS/MicroPlex/SDS-C05010001_C05010002-MicroPlex_Library_Preparation_Kit_v3-GB-en-1_0.pdf',
			'countries' => 'GB',
			'modified' => '2020-07-02 10:30:25',
			'created' => '2020-07-02 10:30:25',
			'ProductsSafetySheet' => array(
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		),
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			'id' => '704',
			'name' => 'MicroPlex Library Preparation Kit v3 SDS US en',
			'language' => 'en',
			'url' => 'files/SDS/MicroPlex/SDS-C05010001_C05010002-MicroPlex_Library_Preparation_Kit_v3-US-en-1_0.pdf',
			'countries' => 'US',
			'modified' => '2020-07-02 10:31:26',
			'created' => '2020-07-02 10:31:26',
			'ProductsSafetySheet' => array(
				[maximum depth reached]
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			'id' => '699',
			'name' => 'MicroPlex Library Preparation Kit v3 SDS DE de',
			'language' => 'de',
			'url' => 'files/SDS/MicroPlex/SDS-C05010001_C05010002-MicroPlex_Library_Preparation_Kit_v3-DE-de-1_0.pdf',
			'countries' => 'DE',
			'modified' => '2020-07-02 10:29:06',
			'created' => '2020-07-02 10:29:06',
			'ProductsSafetySheet' => array(
				[maximum depth reached]
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			'id' => '703',
			'name' => 'MicroPlex Library Preparation Kit v3 SDS JP ja',
			'language' => 'ja',
			'url' => 'files/SDS/MicroPlex/SDS-C05010001_C05010002-MicroPlex_Library_Preparation_Kit_v3-JP-ja-1_0.pdf',
			'countries' => 'JP',
			'modified' => '2020-07-02 10:30:53',
			'created' => '2020-07-02 10:30:53',
			'ProductsSafetySheet' => array(
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			'name' => 'MicroPlex Library Preparation Kit v3 SDS BE nl',
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<li><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns">C05010003 - 24 Dual indexes for MicroPlex Kit v3 /48 rxns</a></li>
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<p style="padding-left: 30px;">NEW! Unique dual indexes :</p>
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<li><strong>1 tube</strong>, <strong>2 hours</strong>, <strong>3 steps</strong> protocol</li>
<li><strong>Input</strong>: 50 pg &ndash; 50 ng</li>
<li><strong>Reduce potential bias</strong> - few PCR amplification cycles needed</li>
<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
<li><strong>Great multiplexing flexibility</strong> with 24 dual indexes (8 nt)</li>
<li><strong>Validated with the IP-<a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit">Star<sup>&reg;</sup></a></strong><a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit"> Automated Platform</a></li>
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<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
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<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
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<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
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<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
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<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
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<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
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<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
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</li>
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<p>Diagenode&rsquo;s <strong>MicroPlex Library Preparation Kits v3</strong> have been extensively validated for ChIP-seq samples and are optimized to generate DNA libraries with high molecular complexity from the lowest input amounts &ndash; down to 50 pg. The kit MicroPlex v3 includes all buffers and enzymes necessary for the library preparation. For flexibility of the choice different formats of compatible primer indexes are available separately:</p>
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<li><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns">C05010003 - 24 Dual indexes for MicroPlex Kit v3 /48 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1">C05010004 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set I /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2">C05010005 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set II /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3">C05010006 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set III /96 rxns</a></li>
<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4">C05010007 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV /96 rxns</a></li>
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<p style="padding-left: 30px;">NEW! Unique dual indexes :</p>
<ul>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1">C05010008 - 24 UDI for MicroPlex Kit v3 - Set I</a></li>
<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2">C05010009 - 24 UDI for MicroPlex Kit v3 - Set II</a></li>
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<p>Read more about <a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">library preparation for ChIP-seq</a></p>
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<li><strong>1 tube</strong>, <strong>2 hours</strong>, <strong>3 steps</strong> protocol</li>
<li><strong>Input</strong>: 50 pg &ndash; 50 ng</li>
<li><strong>Reduce potential bias</strong> - few PCR amplification cycles needed</li>
<li><strong>High sensitivity ChIP-seq</strong> - low PCR duplication rate</li>
<li><strong>Great multiplexing flexibility</strong> with 24 dual indexes (8 nt)</li>
<li><strong>Validated with the IP-<a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit">Star<sup>&reg;</sup></a></strong><a href="https://www.diagenode.com/en/p/sx-8g-ip-star-compact-automated-system-1-unit"> Automated Platform</a></li>
</ul>
<h3>How it works</h3>
<center><img alt="MicroPlex Library Preparation Kit v3 /48 rxns" src="https://www.diagenode.com/img/product/kits/microplex-3-method-overview.png" /></center>
<p style="margin-bottom: 0;"><small><strong>Microplex workflow - protocol with dual indexes</strong><br />An input of 50 pg to 50 ng of fragmented dsDNA is converted into sequencing-ready libraries for Illumina&reg; NGS platforms using a fast and simple 3-step protocol</small></p>
<ul class="accordion" data-accordion="" id="readmore" style="margin-left: 0;">
<li class="accordion-navigation"><a href="#first" style="background: #ffffff; padding: 0rem; margin: 0rem; color: #13b2a2;"><small>Read more about MicroPlex workflow</small></a>
<div id="first" class="content">
<p><small><strong>Step 1. Template Preparation</strong> provides efficient repair of the fragmented double-stranded DNA input.</small></p>
<p><small>In this step, the DNA is repaired and yields molecules with blunt ends.</small></p>
<p><small><strong>Step 2. Library Synthesis.</strong> enables ligation of MicroPlex patented stem- loop adapters.</small></p>
<p><small>In the next step, stem-loop adaptors with blocked 5&rsquo; ends are ligated with high efficiency to the 5&rsquo; end of the genomic DNA, leaving a nick at the 3&rsquo; end. The adaptors cannot ligate to each other and do not have single- strand tails, both of which contribute to non-specific background found with many other NGS preparations.</small></p>
<p><small><strong>Step 3. Library Amplification</strong> enables extension of the template, cleavage of the stem-loop adaptors, and amplification of the library. Illumina- compatible indexes are also introduced using a high-fidelity, highly- processive, low-bias DNA polymerase.</small></p>
<p><small>In the final step, the 3&rsquo; ends of the genomic DNA are extended to complete library synthesis and Illumina-compatible indexes are added through a high-fidelity amplification. Any remaining free adaptors are destroyed. Hands-on time and the risk of contamination are minimized by using a single tube and eliminating intermediate purifications.</small></p>
<p><small>Obtained libraries are purified, quantified and sized. The libraries pooling can be performed as well before sequencing.</small></p>
</div>
</li>
</ul>
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<p><span style="font-weight: 400;">Most of the major next-generation sequencing platforms require ligation of specific adaptor oligos to </span><a href="../applications/dna-rna-shearing"><span style="font-weight: 400;">fragmented DNA or RNA</span></a><span style="font-weight: 400;"> prior to sequencing</span></p>
<p><span style="font-weight: 400;">After input DNA has been fragmented, it is end-repaired and blunt-ended</span><span style="font-weight: 400;">. The next step is a A-tailing in which dAMP is added to the 3&acute; end of the blunt phosphorylated DNA fragments to prevent concatemerization and to allow the ligation of adaptors with complementary dT overhangs. In addition, barcoded adapters can be incorporated to facilitate multiplexing prior to or during amplification.</span></p>
<center><img src="https://www.diagenode.com/img/categories/library-prep/flux.png" /></center>
<p><span style="font-weight: 400;">Diagenode offers a comprehensive product portfolio for library preparation:<br /></span></p>
<strong><a href="https://www.diagenode.com/en/categories/Library-preparation-for-RNA-seq">D-Plex&nbsp;RNA-seq Library Preparation Kits</a></strong><br />
<p><span style="font-weight: 400;">Diagenode&rsquo;s new RNA-sequencing solutions utilize the innovative c</span><span style="font-weight: 400;">apture and a</span><span style="font-weight: 400;">mplification by t</span><span style="font-weight: 400;">ailing and s</span><span style="font-weight: 400;">witching&rdquo;</span><span style="font-weight: 400;">, a ligation-free method to produce DNA libraries for next generation sequencing from low input amounts of RNA. </span><span style="font-weight: 400;"></span><a href="../categories/Library-preparation-for-RNA-seq">Learn more</a></p>
<strong><a href="../categories/library-preparation-for-ChIP-seq">ChIP-seq and DNA sequencing library preparation solutions</a></strong><br />
<p><span style="font-weight: 400;">Our kits have been optimized for DNA library preparation used for next generation sequencing for a wide range of inputs. Using a simple three-step protocols, our</span><a href="http://www.diagenode.com/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns"><span style="font-weight: 400;"> </span></a><span style="font-weight: 400;">kits are an optimal choice for library preparation from DNA inputs down to 50 pg.&nbsp;</span><a href="../categories/library-preparation-for-ChIP-seq">Learn more</a></p>
<a href="../p/bioruptor-pico-sonication-device"><span style="font-weight: 400;"></span><strong>Bioruptor Pico - short fragments</strong></a><a href="../categories/library-preparation-for-ChIP-seq-and-DNA-sequencing"><span style="font-weight: 400;"></span></a><br />
<p><span style="font-weight: 400;"></span><span style="font-weight: 400;">Our well-cited Bioruptor Pico is the shearing device of choice for chromatin and DNA fragmentation. Obtain uniform and tight fragment distributions &nbsp;between 150bp -2kb. </span><a href="../p/bioruptor-pico-sonication-device">Learn more</a></p>
<strong><a href="../p/megaruptor2-1-unit"><span href="../p/bioruptor-pico-sonication-device">Megaruptor</span>&reg; - long fragments</a></strong><a href="../p/bioruptor-pico-sonication-device"><span style="font-weight: 400;"></span></a><a href="../categories/library-preparation-for-ChIP-seq-and-DNA-sequencing"><span style="font-weight: 400;"></span></a><br />
<p><span style="font-weight: 400;"></span><span style="font-weight: 400;">The Megaruptor is designed to shear DNA from 3kb-75kb for long-read sequencing.&nbsp; <a href="../p/megaruptor2-1-unit">Learn more</a></span></p>
<span href="../p/bioruptor-pico-sonication-device"></span><span style="font-weight: 400;"></span></div>
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<div class="large-12 columns text-justify">
<p>Library preparation following ChIP can be challenging due to the limited amount of DNA recovered after ChIP. Diagenode has developed the optimal solutions for ChIP-seq using two different approaches: the ligation-based library preparation on purified DNA or the tagmentation-based ChIPmentation.</p>
</div>
</div>
<div class="row extra-spaced">
<div class="large-12 columns"><center><a href="https://www.diagenode.com/en/pages/form-microplex-promo" target="_blank"></a></center></div>
</div>
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div id="portal" class="main-portal">
<div class="portal-inner"><nav class="portal-nav">
<ul data-tab="" class="tips-menu">
<li><a href="#panel1" class="tips portal button">Ligation-based library prep</a></li>
<li><a href="#panel2" class="tips portal button">ChIPmentation</a></li>
<li><a href="#panel3" class="tips portal button">Kit choice guide</a></li>
<li><a href="#panel4" class="tips portal button">Resources</a></li>
<li><a href="#panel5" class="tips portal button">FAQs</a></li>
</ul>
</nav></div>
</div>
<div class="tabs-content">
<div class="content active" id="panel1">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v5" style="color: #13b29c;"><i class="fa fa-caret-right"></i> Standard input library prep</a>
<div id="v5" class="content">
<div class="small-12 medium-12 large-12 columns">
<p>The <strong>iDeal Library Preparation Kit</strong> reliably converts DNA into indexed libraries for next-generation sequencing, with input amounts down to <strong>5 ng</strong>. Our kit offers a simple and fast workflow, high yields, and ready-to-sequence DNA on the Illumina platform.</p>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> <strong>Sample</strong>: Fragmented dsDNA</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Input</strong>: 5 ng &ndash; 1 &micro;g</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Fast protocol</strong>: 3 hours</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Easy processing</strong>: 3 steps</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Indexing</strong>: single indexes for multiplexing up to 24 samples</li>
<li><i class="fa fa-arrow-circle-right"></i> Manual and automated protocols available</li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<ul class="square">
<li>MeDIP-seq library prep</li>
<li>Genomic DNA sequencing</li>
<li>High input ChIP-seq</li>
</ul>
</div>
<div class="extra-spaced">
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010020</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" style="color: #b21329;" target="_blank">iDeal Library Preparation Kit x24 (incl. Index Primer Set 1)</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010021</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" style="color: #b21329;" target="_blank">Index Primer Set 2 (iDeal Lib. Prep Kit x24)</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
</li>
</ul>
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v4" style="color: #13b29c;"><i class="fa fa-caret-right"></i> Low input library prep</a>
<div id="v4" class="content active"><center><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" target="_blank"><img src="https://www.diagenode.com/img/banners/banner-microplex-v3-580.jpg" class="extra-spaced" /></a></center>
<div align="center"><a href="https://www.diagenode.com/pages/form-microplex3" class="center alert radius button extra-spaced"><i class="fa fa-info"></i> Contact us</a></div>
<div class="extra-spaced">
<p>Diagenode&rsquo;s <strong>MicroPlex Library Preparation kits</strong> have been extensively validated for ChIP-seq samples. Generated libraries are compatible with single-end or paired-end sequencing. MicroPlex chemistry (using stem-loop adapters ) is specifically developed and optimized to generate DNA libraries with high molecular complexity from the lowest input amounts. Only <strong>50 pg to 50 ng</strong> of fragmented double-stranded DNA is required for library preparation. The entire <strong>three-step workflow</strong> takes place in a <strong>single tube</strong> or well in about <strong>2 hours</strong>. No intermediate purification steps and no sample transfers are necessary to prevent handling errors and loss of valuable samples.</p>
</div>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> <strong>Sample</strong>: Fragmented dsDNA</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Low input</strong>: 50 pg &ndash; 50 ng</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Fast protocol</strong>: 2 hours</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>Easy processing</strong>: 3 steps in 1 tube</li>
<li><i class="fa fa-arrow-circle-right"></i> <strong>No intermediate purification</strong></li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
<li><i class="fa fa-arrow-circle-right"></i> Manual and automated protocols available</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<ul class="square">
<li>ChIP-seq library prep from ChIP-derived DNA</li>
<li>Low input DNA sequencing</li>
</ul>
</div>
<h2>Two versions are available:</h2>
<ul class="accordion" data-accordion="">
<li class="accordion-navigation"><a href="#v2" style="color: #13b29c;"><i class="fa fa-caret-right"></i> MicroPlex Library Preparation Kit v2 with single indexes</a>
<div id="v2" class="content">
<p>The MicroPlex Library Preparation Kit v2 contains all necessary reagents including single indexes for multiplexing up to 48 samples using single barcoding.</p>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010012</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v2 (12 indexes)</a></td>
<td class="format">12 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</li>
<li class="accordion-navigation"><a href="#v3" style="color: #13b29c;"><i class="fa fa-caret-right"></i> MicroPlex Library Preparation Kit v3 with dual indexes &nbsp;&nbsp;<strong><span class="diacol">NEW!</span></strong></a>
<div id="v3" class="content active">
<p>In this version the library preparation reagents and the dual indexes are available separately allowing for the flexibility choosing the number of indexes. MicroPlex v3 has multiplexing capacities up to 384 samples.</p>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010001</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v3 /48 rxns</a></td>
<td class="format">48 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010002</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" style="color: #b21329;" target="_blank">MicroPlex Library Preparation Kit v3 /96 rxns</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
<h4>DUAL INDEXES</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C05010003</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" style="color: #b21329;" target="_blank">24 Dual indexes for MicroPlex Kit v3</a></td>
<td class="format">48 rxns</td>
<td><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010004</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set I</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010005</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set II</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010006</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set III</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C05010007</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" style="color: #b21329;" target="_blank">96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV</a></td>
<td class="format">96 rxns</td>
<td><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</li>
</ul>
</div>
</li>
</ul>
</div>
</div>
</div>
<div class="content active" id="panel2">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<p>The TAG Kit for ChIPmentation offers an optimized ChIP-seq library preparation solution based on tagmentation. This kit includes reagents for tagmentation-based library preparation integrated in the IP and is compatible with any ChIP protocol based on magnetic beads. The primer indexes for multiplexing&nbsp;must be purchased separately and are available as a reference: <a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" target="_blank">24 SI for ChIPmentation</a>, Cat. No. C01011031. Alternatively, for histone marks, Diagenode proposes the complete solution (including all buffers for ChIP, tagmentation and multiplexing): <a href="https://www.diagenode.com/en/p/manual-chipmentation-kit-for-histones-24-rxns" target="_blank">ChIPmentation for Histones</a>.</p>
</div>
<div class="extra-spaced">
<h2>Features</h2>
<ul class="nobullet">
<li><i class="fa fa-arrow-circle-right"></i> Sample: chromatin-antibody-magnetic beads complexes</li>
<li><i class="fa fa-arrow-circle-right"></i> Input: chromatin from 5 K &ndash; 4 M cells</li>
<li><i class="fa fa-arrow-circle-right"></i> Easy and fast protocol</li>
<li><i class="fa fa-arrow-circle-right"></i> Compatible with any ChIP protocol based on magnetic beads</li>
<li><i class="fa fa-arrow-circle-right"></i> No adapter dimers</li>
<li><i class="fa fa-arrow-circle-right"></i> Sequencing technology: Illumina</li>
</ul>
</div>
<div class="extra-spaced">
<h2>Applications</h2>
<p class="lead"><em><strong>TAG kit for ChIPmentation</strong></em></p>
<ul class="square">
<li>ChIPmentation library preparation</li>
</ul>
<p class="lead"><em><strong>24 SI for for ChIPmentation</strong></em></p>
<ul class="square">
<li>ChIPmentation library preparation</li>
<li>Tagmentation-based library preparation methods like ATAC-seq, CUT&amp;Tag</li>
</ul>
</div>
<h4>KITS</h4>
<table>
<thead>
<tr>
<th>Cat. No.</th>
<th>Product</th>
<th>Format</th>
<th width="120"></th>
</tr>
</thead>
<tbody class="list">
<tr>
<td class="catalog_number"><span class="success label">C01011030</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" style="color: #b21329;" target="_blank">TAG Kit for ChIPmentation</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
<tr>
<td class="catalog_number"><span class="success label">C01011031</span></td>
<td class="name"><a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" style="color: #b21329;" target="_blank">24 SI for ChIPmentation</a></td>
<td class="format">24 rxns</td>
<td><a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" class="tiny details button radius" target="_blank"><i class="fa fa-eye"></i></a></td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
<div class="content" id="panel3">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<h3 class="text-center diacol"><em>How to choose your library preparation kit?</em></h3>
</div>
<table class="noborder">
<tbody>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Sample</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Chromatin-antibody-beads complex</p>
</td>
<td colspan="2">
<p class="text-center" style="font-size: 15px;">Purified DNA</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Purified DNA</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td colspan="2"><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Application</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">ChIPmentation</p>
</td>
<td colspan="2">
<p class="text-center" style="font-size: 15px;">ChIP-seq library prep<br /> Low input DNA sequencing</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">MeDIP-seq library prep<br /> Genomic DNA sequencing<br /> High input ChIP-seq</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td colspan="2"><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Input</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Chromatin: 5 K to 4 M cells</p>
</td>
<td colspan="2&quot;">
<p class="text-center" style="font-size: 15px;">DNA: 50 pg &ndash; 50 ng</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">DNA: 5 ng &ndash; 1 &micro;g</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow-45-left.png" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow-45-right.png" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Multiplexing</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 24 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 384 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 48 samples</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Up to 24 samples</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Indexes</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Dual indexes (DI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
<td>
<p class="text-center" style="font-size: 15px;">Single indexes (SI)</p>
</td>
</tr>
<tr style="background-color: #fff;">
<td></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
<td><center><img src="https://www.diagenode.com/img/long-arrow.gif" /></center></td>
</tr>
<tr valign="top">
<td class="text-right">
<p style="font-size: 15px;"><strong>Kit</strong></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>TAG Kit for ChIPmentation</strong><br /> (indexes not included in the kit)</p>
<p class="text-center"><strong>Kit</strong><br /> <a href="https://www.diagenode.com/en/p/tag-kit-for-chipmentation-24" target="_blank">C01011030 &ndash; 24 rxns</a></p>
<p class="text-center"><strong>Single indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-si-for-chipmentation" target="_blank">C01011031 &ndash; 24 SI/24 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>MicroPlex Library Preparation Kit v3</strong><br />(dual indexes not included in the kit)</p>
<p class="text-center"><strong>Kit</strong><br /> <a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-48-rxns" target="_blank">C05010001 - 48 rxns</a><br /> <a href="https://www.diagenode.com/en/p/microplex-lib-prep-kit-v3-96-rxns" target="_blank">C05010002 - 96 rxns</a></p>
<br />
<p class="text-center"><strong>Unique dual indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1" target="_blank">C05010008 - Set I 24 UDI / 24 rxns</a><br /> <a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set2" target="_blank">C05010009 - Set II 24 UDI/ 24 rxns</a></p>
<p class="text-center"><strong>Dual indexes</strong><br /> <a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns" target="_blank">C05010003 - 24 DI/ 48 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-1" target="_blank">C05010004 - Set I 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-2" target="_blank">C05010005 - Set II 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-3" target="_blank">C05010006 - Set III 96 DI/ 96 rxns</a><br /> <a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4" target="_blank">C05010007 - Set IV 96 DI/ 96 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>MicroPlex Library Preparation Kit v2</strong><br />(single indexes included in the kit)</p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x12-12-indices-12-rxns" target="_blank">C05010012 - 12 SI/ 12 rxns</a><br /> <a href="https://www.diagenode.com/en/p/microplex-library-preparation-kit-v2-x48-12-indices-48-rxns" target="_blank">C05010013 - 12 SI/ 48 rxns</a></p>
</td>
<td>
<p class="text-center" style="font-size: 15px;"><strong>iDeal Library Preparation Kit</strong><br />(Set 1 of indexes included in the kit)</p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/ideal-library-preparation-kit-x24-incl-index-primer-set-1-24-rxns" target="_blank">C05010020 - 12 SI/ 24 rxns</a></p>
<p class="text-center" style="font-size: 15px;"><strong>Index Primer Set 2</strong></p>
<p class="text-center"><a href="https://www.diagenode.com/en/p/ideal-library-index-primer-set-2-24-rxns" target="_blank">C05010021 - 12 SI/ 24 rxns</a></p>
</td>
</tr>
</tbody>
</table>
</div>
</div>
</div>
<div class="content" id="panel4">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<p>Combined chromatin immunoprecipitation and next-generation sequencing (ChIP-seq) has become the gold standard to investigate genome-wide epigenetic profiles. However, ChIP from a limited amount of cells has been a challenge. Here we provide a complete and robust workflow solution for successful ChIP-seq from small numbers of cells using the True MicroChIP kit and MicroPlex Library Preparation kit.</p>
<blockquote><span class="label-green" style="margin-bottom: 16px; margin-left: -22px;">APPLICATION NOTE</span>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><center><img src="https://www.diagenode.com/img/categories/microplex/chip-efficiency-on-10000-cells.jpg" /></center>
<p><small><em>ChIP efficiency on 10,000 cells</em></small></p>
</div>
<div class="small-12 medium-6 large-6 columns">
<p><strong>From minuscule amounts to magnificent results:</strong><br /> reliable ChIP-seq data from 10,000 cells with the True MicroChIP&trade; and the MicroPlex Library Preparation&trade; kits.</p>
<a href="https://www.diagenode.com/files/application_notes/True_MicroChIP_and_MicroPlex_kits_Application_Note.pdf" class="details small button" target="_blank">DOWNLOAD</a></div>
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</blockquote>
<blockquote><span class="label-green" style="margin-bottom: 16px; margin-left: -22px;">APPLICATION NOTE</span>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><center><img src="https://www.diagenode.com/img/categories/microplex/quality-control-check.jpg" /></center>
<p class="text-left"><small><em>Quality control check of a ChIP-seq library on the Fragment Analyzer. High Efficiency ChIP performed on 10,000 cells</em></small></p>
</div>
<div class="small-12 medium-6 large-6 columns">
<p class="text-left"><strong>Best Workflow Practices for ChIP-seq Analysis with Small Samples</strong></p>
<a href="https://www.diagenode.com/files/application_notes/Diagenode_AATI_Joint.pdf" class="details small button" target="_blank">DOWNLOAD</a></div>
</div>
</blockquote>
</div>
</div>
</div>
<div class="content" id="panel5">
<div class="row">
<div class="small-12 medium-12 large-12 columns">
<div class="extra-spaced">
<h2>TAG Kit for ChIPmentation</h2>
<ol>
<li><strong>What is the difference between tagmentation and ChIPmentation?</strong><br />Tagmentation is a reaction where an enzyme (a transposase) cleaves DNA and incorporates sequencing adaptors at the ends of the fragments in one step. In our ChIPmentation technology we combine chromatin immunoprecipitation and tagmentation in one streamlined workflow where the tagmentation step occurs directly on chromatin.<br /><br /></li>
<li><strong>What is the expected concentration of ChIPmentation libraries?</strong><br />The concentration of libraries that you need to reach will depend on the sensitivity of the machine and kits that you will use to perform the quality control and the sequencing of your libraries. Usually a concentration of 4-8 ng/&mu;l is enough for a quality control using the Qubit High Sensitivity assay (ThermoFischer Scientific) and the High Sensitivity chip for BioAnalyzer (Agilent) and for sequencing on Illumina HiSeq3000/4000.<br /><br /></li>
<li><strong>Does the ChIPmentation approach work on plants?</strong><br />Our ChIPmentation solution has been validated on human cells and we do not have any data on plants. It should be compatible. We would recommend using our Universal Plant ChIP Kit in combination with the TAG Kit for ChIPmentation and the 24 SI for ChIPmentation.<br /><br /></li>
<li><strong>What is the size of the fragments after the tagmentation?</strong><br />The size of the fragments at the end of the ChIPmentation protocol can vary depending on many parameters like the shearing efficiency, the antibody used or the tagmentation time. However, with our standard protocol we usually obtain a library peak which is around 200-300 bp (see example of results at the end of the manual). If many fragments larger than 500 bp are present , the best would be to contact your sequencing provider to ask what their requirements are, because it can vary depending on the sequencer. If you want to remove the large fragments you can use the size selection protocol described in the manual.<br /><br /></li>
<li><strong>What is the size of the adapters?</strong><br />The sum of the adapters is 128 bp.</li>
</ol>
</div>
<div class="extra-spaced">
<h2>MicroPlex Library Preparation Kit</h2>
<ol>
<li><strong>Can I use the available Illumina primers and validate them with the MicroPlex Kit v2?</strong><br /> Although the final flanking sequences of MicroPlex are the same as those used by Illumina, the PCR primers are not identical and part of them is supplied with the buffer. For this reason Illumina primers will not work as substitute.<br /><br /></li>
<li><strong>The BioAnalyzer profile of purified library shows the presence of low molecular weight peaks (primers/adaptors) in the samples. Should I re- purify the samples or they can be used directly to the sequencing? If the second purification is recommended, which ratio sample/AMPure beads should I use?</strong><br /> You can do a second round of purification using 1:1 ratio of AMPure beads to sample and this should get rid of the majority of the dimers.<br /><br /></li>
<li><strong>I am going to use the MicroPlex Library Preparation Kit v2 on ChIP samples . Our thermocycler has ramp rate 1.5&deg;/s max while the protocol recommends using a ramp rate 3 to 5&deg;/s. How would this affect the library prep?</strong><br /> We have not used a thermocycler with a ramp rate of 1.5 &deg;C, which seems faster than most of thermocyclers. Too fast of a ramp rate may affect the primer annealing and ligation steps.<br /><br /></li>
<li><strong>What is the function of the replication stop site in the adapter loops?</strong><br /> The replication stop site in the adaptor loops function to stop the polymerase from continuing to copy the rest of the stem loop.<br /><br /></li>
<li><strong>I want to do ChIP-seq. Which ChIP-seq kit can I use for sample preparation prior to Microplex Library Preparation Kit v2?</strong><br /> In our portfolio there are several ChIP-seq kits compatible with Microplex Library Preparation Kit v2. Depending on your sample type and target studied you can use the following kits: iDeal ChIP-seq Kit for Transcription Factors (Cat. No. C01010055), iDeal ChIP-seq Kit for Histones (Cat. No. C01010051), True MicroChIP kit (Cat. No. C01010130), Universal Plant ChIP-seq Kit (Cat. No. C01010152). All these kits exist in manual and automated versions.<br /><br /></li>
<li><strong>Is Microplex Library Preparation Kit v2 compatible with exome enrichment methods?</strong><br /> Microplex Library Preparation Kit v2 is compatible with major exome and target enrichment products, including Agilent SureSelect<sup>&reg;</sup>, Roche NimbleGen<sup>&reg;</sup> SeqCap<sup>&reg;</sup> EZ and custom panels.<br /><br /></li>
<li><strong>What is the nick that is mentioned in the kit method overview?</strong><br /> The nick is simply a gap between a stem adaptor and 3&rsquo; DNA end, as shown on the schema in the kit method overview.<br /><br /></li>
<li><strong>Are the indexes of the MicroPlex library preparation kit v2 located at i5 or i7?</strong><br /> The libraries generated with the MicroPlex kit v2 contain indices located at i7.<br /><br /></li>
<li><strong>Is there a need to use custom index read primers for the sequencing to read the 8nt iPCRtags?</strong><br /> There is no need for using custom Sequencing primer to sequence MicroPlex libraires. MicroPlex libraries can be sequenced using standard Illumina Sequencing kits and protocols.<br /><br /></li>
<li><strong>What is the advantage of using stem-loop adapter in the MicroPlex kit?</strong><br /> There are several advantages of using stem-loop adaptors. First of all, stem-loop adaptors prevent from self-ligation thus increases the ligation efficiency between the adapter and DNA fragment. Moreover, the background is reduced using ds adaptors with no single-stranded tails. Finally, adaptor-adaptor ligation is reduced using blocked 5&rsquo; ends.<br /><br /></li>
</ol>
</div>
<div class="extra-spaced">
<h2>IDeal Library Preparation Kit</h2>
<ol>
<li><strong>Are the index from the iDeal library Prep kit compatible with the MicroPlex library prep kit?</strong><br /> No, it is important to use only the indexes provided in the MicroPlex kit to ensure proper library preparation with this kit</li>
</ol>
</div>
</div>
</div>
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			'description' => '<p>Diagenode offers innovative DNA library preparation solutions such as a hyperactive tagmentase and the &ldquo;capture and amplification by tailing and switching&rdquo; (CATS), a ligation-free method to produce DNA libraries for next generation sequencing from low input amounts of DNA. Our powerfull ChIP-seq library preparation kits are also&nbsp;a great solution for low input DNA library preparation (discover our <a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">Diagenode MicroPlex family</a>).&nbsp;</p>
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			'id' => '4997',
			'name' => 'ACE2 Enhances Sensitivity to PD-L1 Blockade by Inhibiting Macrophage-Induced Immunosuppression and Angiogenesis',
			'authors' => 'Peiyi Xie et al.',
			'description' => '<p><span>Anti-PD-L1-based combination immunotherapy has become the first-line treatment for unresectable hepatocellular carcinoma (HCC). However, the objective response rate is lower than 40%, highlighting the need to identify mechanisms of tolerance to immune checkpoint inhibitors and accurate biomarkers of response. Here, we employed next-generation sequencing to analyze HCC samples from 10 patients receiving anti-PD-L1 therapy. Activation of the renin-angiotensin system was elevated in nonresponders compared with responders, and ACE2 expression was significantly downregulated in nonresponders. ACE2 deficiency promoted HCC development and anti-PD-L1 resistance, whereas ACE2 overexpression inhibited HCC progression in immune competent mice. Mass cytometry by time of flight (CyTOF) revealed that ACE2 deficient murine orthotopic tumor tissues featured elevated M2-like tumor-associated macrophages (TAMs), displayed a CCR5+PD-L1+ immunosuppressive phenotype, and exhibited high VEGF&alpha; expression. ACE2 downregulated tumor intrinsic CCL5 expression by suppressing NF-&kappa;B signaling through the ACE2/angiotensin-(1&ndash;7)/Mas receptor axis. The lower CCL5 levels led to reduced activation of the JAK-STAT3 pathway and suppressed PD-L1 and VEGF&alpha; expression in macrophages, blocking macrophage infiltration and M2-like polarization. Pharmacological targeting of CCR5 using maraviroc enhanced the tumor suppressive effect of anti-PD-L1 therapy. Together, these findings suggest that activation of the ACE2 axis overcomes the immunosuppressive microenvironment of HCC and may serve as an immunotherapeutic target and predictive biomarker of response to PD-L1 blockade.</span></p>',
			'date' => '2024-11-04',
			'pmid' => 'https://aacrjournals.org/cancerres/article-abstract/doi/10.1158/0008-5472.CAN-24-0954/749696/ACE2-Enhances-Sensitivity-to-PD-L1-Blockade-by?redirectedFrom=fulltext',
			'doi' => 'https://doi.org/10.1158/0008-5472.CAN-24-0954',
			'modified' => '2024-11-07 11:22:24',
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		(int) 1 => array(
			'id' => '4976',
			'name' => 'Extracellular vesicle-mediated trafficking of molecular cues during human brain development',
			'authors' => 'Forero A. et al.',
			'description' => '<p><span>Cellular crosstalk is an essential process influenced by numerous factors, including secreted vesicles that transfer nucleic acids, lipids, and proteins between cells. Extracellular vesicles (EVs) have been the center of many studies focusing on neurodegenerative disorders, but whether EVs display cell-type-specific features for cellular crosstalk during neurodevelopment is unknown. Here, using human-induced pluripotent stem cell-derived cerebral organoids, neural progenitors, neurons, and astrocytes, we identify heterogeneity in EV protein content and dynamics in a cell-type-specific and time-dependent manner. Our results support the trafficking of key molecules via EVs in neurodevelopment, such as the transcription factor YAP1, and their localization to differing cell compartments depending on the EV recipient cell type. This study sheds new light on the biology of EVs during human brain development.</span></p>',
			'date' => '2024-10-22',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01106-9',
			'doi' => '10.1016/j.celrep.2024.114755',
			'modified' => '2024-09-23 10:19:53',
			'created' => '2024-09-23 10:19:53',
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		(int) 2 => array(
			'id' => '4982',
			'name' => 'The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency',
			'authors' => 'Mathew Sheridan et al.',
			'description' => '<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Background</h3>
<p>The epigenetic factors KAT6A (MOZ/MYST3) and KMT2A (MLL/MLL1) interact in normal hematopoiesis to regulate progenitors&rsquo; self-renewal. Both proteins are recurrently translocated in AML, leading to impairment of critical differentiation pathways in these malignant cells. We evaluated the potential of different KAT6A therapeutic targeting strategies to alter the growth of KAT6A and KMT2A rearranged AMLs.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Methods</h3>
<p>We investigated the action and potential mechanisms of the first-in-class KAT6A inhibitor, WM-1119 in KAT6A and KMT2A rearranged&nbsp;(KAT6Ar and KMT2Ar) AML using cellular (flow cytometry, colony assays, cell growth) and molecular (shRNA knock-down, CRISPR knock-out, bulk and single-cell RNA-seq, ChIP-seq) assays. We also used two novel genetic murine KAT6A models combined with the most common KMT2Ar AML, KMT2A::MLLT3 AML. In these murine models, the catalytic activity of KAT6A, or the whole protein, can be conditionally abrogated or deleted. These models allowed us to compare the effects of specific KAT6A KAT activity inhibition with the complete deletion of the whole protein. Finally, we also tested these therapeutic approaches on human AML cell lines and primary patient AMLs.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Results</h3>
<p>We found that WM-1119 completely abrogated the proliferative and clonogenic potential of KAT6Ar cells<span>&nbsp;</span><i>in vitro.</i><span>&nbsp;</span>WM-1119 treatment was associated with a dramatic increase in myeloid differentiation program. The treatment also decreased stemness and leukemia pathways at the transcriptome level and led to loss of binding of the fusion protein at critical regulators of these pathways. In contrast, our pharmacologic and genetic results indicate that the catalytic activity of KAT6A plays a more limited role in KMT2Ar leukemogenicity, while targeting the whole KAT6A protein dramatically affects leukemic potential in murine KMT2A::MLLT3 AML.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Conclusion</h3>
<p>Our study indicates that inhibiting KAT6A KAT activity holds compelling promise for KAT6Ar AML patients. In contrast, targeted degradation of KAT6A, and not just its catalytic activity, may represent a more appropriate therapeutic approach for KMT2Ar AMLs.</p>',
			'date' => '2024-10-08',
			'pmid' => 'https://jhoonline.biomedcentral.com/articles/10.1186/s13045-024-01610-0',
			'doi' => 'https://doi.org/10.1186/s13045-024-01610-0',
			'modified' => '2024-10-11 10:00:42',
			'created' => '2024-10-11 10:00:42',
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			'id' => '4983',
			'name' => 'Integrated multi-omics analysis of PBX1 in mouse adult neural stem- and progenitor cells identifies a transcriptional module that functionally links PBX1 to TCF3/4',
			'authors' => 'Vera Laub et al.',
			'description' => '<p><span>Developmental transcription factors act in networks, but how these networks achieve cell- and tissue specificity is still poorly understood. Here, we explored pre-B cell leukemia homeobox 1 (PBX1) in adult neurogenesis combining genomic, transcriptomic, and proteomic approaches. ChIP-seq analysis uncovered PBX1 binding to numerous genomic sites. Integration of PBX1 ChIP-seq with ATAC-seq data predicted interaction partners, which were subsequently validated by mass spectrometry. Whole transcriptome spatial RNA analysis revealed shared expression dynamics of&nbsp;</span><em>Pbx1</em><span><span>&nbsp;</span>and interacting factors. Among these were class I bHLH proteins TCF3 and TCF4. RNA-seq following<span>&nbsp;</span></span><em>Pbx1</em><span>,<span>&nbsp;</span></span><em>Tcf3</em><span><span>&nbsp;</span>or<span>&nbsp;</span></span><em>Tcf4</em><span><span>&nbsp;</span>knockdown identified proliferation- and differentiation associated genes as shared targets, while sphere formation assays following knockdown argued for functional cooperativity of PBX1 and TCF3 in progenitor cell proliferation. Notably, while physiological PBX1-TCF interaction has not yet been described, chromosomal translocation resulting in genomic<span>&nbsp;</span></span><em>TCF3::PBX1</em><span><span>&nbsp;</span>fusion characterizes a subtype of acute lymphoblastic leukemia. Introducing<span>&nbsp;</span></span><em>Pbx1</em><span><span>&nbsp;</span>into Nalm6 cells, a pre-B cell line expressing<span>&nbsp;</span></span><em>TCF3</em><span><span>&nbsp;</span>but lacking<span>&nbsp;</span></span><em>PBX1</em><span>, upregulated the leukemogenic genes<span>&nbsp;</span></span><em>BLK</em><span><span>&nbsp;</span>and<span>&nbsp;</span></span><em>NOTCH3</em><span>, arguing that functional PBX1-TCF cooperativity likely extends to hematopoiesis. Our study hence uncovers a transcriptional module orchestrating the balance between progenitor cell proliferation and differentiation in adult neurogenesis with potential implications for leukemia etiology.</span></p>',
			'date' => '2024-10-08',
			'pmid' => 'https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkae864/7815639',
			'doi' => 'https://doi.org/10.1093/nar/gkae864',
			'modified' => '2024-10-11 10:02:42',
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		(int) 4 => array(
			'id' => '4985',
			'name' => 'HNF1β bookmarking involves Topoisomerase 1 activation and DNA topology relaxation in mitotic chromatin',
			'authors' => 'Alessia Bagattin et al.',
			'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HNF1&beta; mitotic site binding is preserved with a specific methanol/formaldehyde ChIP</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">BTBD2, an HNF1&beta; partner, mediates mitosis-specific interaction with TOP1</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">HNF1&beta; recruits TOP1 and induces DNA relaxation around bookmarked HNF1&beta; sites</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">An HNF1&beta; mutation, found in MODY patients, disrupts the interaction with TOP1</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">HNF1&beta; (<i>HNF1B</i>) is a transcription factor frequently mutated in patients with developmental renal disease. It binds to mitotic chromatin and reactivates gene expression after mitosis, a phenomenon referred to as bookmarking. Using a crosslinking method that circumvents the artifacts of formaldehyde, we demonstrate that&nbsp;HNF1&beta; remains associated with chromatin in a sequence-specific way in both interphase and mitosis. We identify an HNF1&beta;-interacting protein, BTBD2, that enables the interaction and activation of Topoisomerase 1 (TOP1) exclusively during mitosis. Our study identifies a shared microhomology domain between HNF1&beta; and TOP1, where a mutation, found in &ldquo;maturity onset diabetes of the young&rdquo; patients, disrupts their interaction. Importantly, HNF1&beta; recruits TOP1 and induces DNA relaxation around HNF1&beta; mitotic chromatin sites, elucidating its crucial role in chromatin remodeling and gene reactivation after mitotic exit. These findings shed light on how HNF1&beta; reactivates target gene expression after mitosis, providing insights into its crucial role in maintenance of cellular identity.</div>
</section>',
			'date' => '2024-10-08',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01156-2',
			'doi' => '10.1016/j.celrep.2024.114805',
			'modified' => '2024-10-14 09:04:44',
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		(int) 5 => array(
			'id' => '4978',
			'name' => 'RNA polymerase II transcription initiation in holo-TFIID-depleted mouse embryonic stem cells',
			'authors' => 'Hisler V. et al.',
			'description' => '<p><span>The recognition of core promoter sequences by TFIID is the first step in RNA polymerase II (Pol II) transcription initiation. Metazoan holo-TFIID is a trilobular complex, composed of the TATA binding protein (TBP) and 13 TBP-associated factors (TAFs). Why and how TAFs are necessary for the formation of TFIID domains and how they contribute to transcription initiation remain unclear. Inducible TAF7 or TAF10 depletion, followed by comprehensive analysis of TFIID subcomplex formation, chromatin binding, and nascent transcription in mouse embryonic stem cells, result in the formation of a TAF7-lacking TFIID or a minimal core-TFIID complex, respectively. These partial complexes support TBP recruitment at promoters and nascent Pol II transcription at most genes early after depletion, but importantly, TAF10 is necessary for efficient Pol II pausing. We show that partially assembled TFIID complexes can sustain Pol II transcription initiation but cannot replace holo-TFIID over several cell divisions and/or development.</span></p>',
			'date' => '2024-09-30',
			'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01142-2',
			'doi' => 'https://doi.org/10.1016/j.celrep.2024.114791',
			'modified' => '2024-10-04 10:18:22',
			'created' => '2024-10-04 10:18:22',
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		(int) 6 => array(
			'id' => '4963',
			'name' => 'An atlas of the human liver diurnal transcriptome and its perturbation by hepatitis C virus infection',
			'authors' => 'Mukherji A. et al.',
			'description' => '<p><span>Chronic liver disease and cancer are global health challenges. The role of the circadian clock as a regulator of liver physiology and disease is well established in rodents, however, the identity and epigenetic regulation of rhythmically expressed genes in human disease is less well studied. Here we unravel the rhythmic transcriptome and epigenome of human hepatocytes using male human liver chimeric mice. We identify a large number of rhythmically expressed protein coding genes in human hepatocytes of male chimeric mice, which includes key transcription factors, chromatin modifiers, and critical enzymes. We show that hepatitis C virus (HCV) infection, a major cause of liver disease and cancer, perturbs the transcriptome by altering the rhythmicity of the expression of more than 1000 genes, and affects the epigenome, leading to an activation of critical pathways mediating metabolic alterations, fibrosis, and cancer. HCV-perturbed rhythmic pathways remain dysregulated in patients with advanced liver disease. Collectively, these data support a role for virus-induced perturbation of the hepatic rhythmic transcriptome and pathways in cancer development and may provide opportunities for cancer prevention and biomarkers to predict HCC risk.</span></p>',
			'date' => '2024-08-29',
			'pmid' => 'https://www.nature.com/articles/s41467-024-51698-8',
			'doi' => 'https://doi.org/10.1038/s41467-024-51698-8',
			'modified' => '2024-09-02 10:17:48',
			'created' => '2024-09-02 10:17:48',
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		(int) 7 => array(
			'id' => '4968',
			'name' => 'Innate immune training restores pro-reparative myeloid functions to promote remyelination in the aged central nervous system',
			'authors' => 'Tiwari V. et al.',
			'description' => '<p><span>The reduced ability of the central nervous system to regenerate with increasing age limits functional recovery following demyelinating injury. Previous work has shown that myelin debris can overwhelm the metabolic capacity of microglia, thereby impeding tissue regeneration in aging, but the underlying mechanisms are unknown. In a model of demyelination, we found that a substantial number of genes that were not effectively activated in aged myeloid cells displayed epigenetic modifications associated with restricted chromatin accessibility. Ablation of two class I histone deacetylases in microglia was sufficient to restore the capacity of aged mice to remyelinate lesioned tissue. We used Bacillus Calmette-Guerin (BCG), a live-attenuated vaccine, to train the innate immune system and detected epigenetic reprogramming of brain-resident myeloid cells and functional restoration of myelin debris clearance and lesion recovery. Our results provide insight into aging-associated decline in myeloid function and how this decay can be prevented by innate immune reprogramming.</span></p>',
			'date' => '2024-07-24',
			'pmid' => 'https://www.cell.com/immunity/fulltext/S1074-7613(24)00348-0',
			'doi' => '',
			'modified' => '2024-09-02 17:05:54',
			'created' => '2024-09-02 17:05:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '4954',
			'name' => 'A multiomic atlas of the aging hippocampus reveals molecular changes in response to environmental enrichment',
			'authors' => 'Perez R. F. at al. ',
			'description' => '<p><span>Aging involves the deterioration of organismal function, leading to the emergence of multiple pathologies. Environmental stimuli, including lifestyle, can influence the trajectory of this process and may be used as tools in the pursuit of healthy aging. To evaluate the role of epigenetic mechanisms in this context, we have generated bulk tissue and single cell multi-omic maps of the male mouse dorsal hippocampus in young and old animals exposed to environmental stimulation in the form of enriched environments. We present a molecular atlas of the aging process, highlighting two distinct axes, related to inflammation and to the dysregulation of mRNA metabolism, at the functional RNA and protein level. Additionally, we report the alteration of heterochromatin domains, including the loss of bivalent chromatin and the uncovering of a heterochromatin-switch phenomenon whereby constitutive heterochromatin loss is partially mitigated through gains in facultative heterochromatin. Notably, we observed the multi-omic reversal of a great number of aging-associated alterations in the context of environmental enrichment, which was particularly linked to glial and oligodendrocyte pathways. In conclusion, our work describes the epigenomic landscape of environmental stimulation in the context of aging and reveals how lifestyle intervention can lead to the multi-layered reversal of aging-associated decline.</span></p>',
			'date' => '2024-07-16',
			'pmid' => 'https://www.nature.com/articles/s41467-024-49608-z',
			'doi' => 'https://doi.org/10.1038/s41467-024-49608-z',
			'modified' => '2024-07-29 11:33:49',
			'created' => '2024-07-29 11:33:49',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '4952',
			'name' => 'Epigenetic alterations affecting hematopoietic regulatory networks as drivers of mixed myeloid/lymphoid leukemia',
			'authors' => 'Roger Mulet-Lazaro et al.',
			'description' => '<p><span>Leukemias with ambiguous lineage comprise several loosely defined entities, often without a clear mechanistic basis. Here, we extensively profile the epigenome and transcriptome of a subgroup of such leukemias with CpG Island Methylator Phenotype. These leukemias exhibit comparable hybrid myeloid/lymphoid epigenetic landscapes, yet heterogeneous genetic alterations, suggesting they are defined by their shared epigenetic profile rather than common genetic lesions. Gene expression enrichment reveals similarity with early T-cell precursor acute lymphoblastic leukemia and a lymphoid progenitor cell of origin. In line with this, integration of differential DNA methylation and gene expression shows widespread silencing of myeloid transcription factors. Moreover, binding sites for hematopoietic transcription factors, including CEBPA, SPI1 and LEF1, are uniquely inaccessible in these leukemias. Hypermethylation also results in loss of CTCF binding, accompanied by changes in chromatin interactions involving key transcription factors. In conclusion, epigenetic dysregulation, and not genetic lesions, explains the mixed phenotype of this group of leukemias with ambiguous lineage. The data collected here constitute a useful and comprehensive epigenomic reference for subsequent studies of acute myeloid leukemias, T-cell acute lymphoblastic leukemias and mixed-phenotype leukemias.</span></p>',
			'date' => '2024-07-07',
			'pmid' => 'https://www.nature.com/articles/s41467-024-49811-y',
			'doi' => 'https://doi.org/10.1038/s41467-024-49811-y',
			'modified' => '2024-07-10 12:21:42',
			'created' => '2024-07-10 12:21:42',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '4911',
			'name' => 'Multiomics uncovers the epigenomic and transcriptomic response to viral and bacterial stimulation in turbot',
			'authors' => 'Aramburu O. et al.',
			'description' => '<p><span>Uncovering the epigenomic regulation of immune responses is essential for a comprehensive understanding of host defence mechanisms but remains poorly described in farmed fish. Here, we report the first annotation of the innate immune regulatory response in the genome of turbot (</span><em>Scophthalmus maximus</em><span>), a farmed flatfish. We integrated RNA-Seq with ATAC-Seq and ChIP-Seq (histone marks H3K4me3, H3K27ac and H3K27me3) using samples from head kidney. Sampling was performed 24 hours post-stimulation with viral (poly I:C) and bacterial (inactivate<span>&nbsp;</span></span><em>Vibrio anguillarum</em><span>) mimics<span>&nbsp;</span></span><em>in vivo</em><span><span>&nbsp;</span>and<span>&nbsp;</span></span><em>in vitro</em><span><span>&nbsp;</span>(primary leukocyte cultures). Among the 8,797 differentially expressed genes (DEGs), we observed enrichment of transcriptional activation pathways in response to<span>&nbsp;</span></span><em>Vibrio</em><span><span>&nbsp;</span>and immune response pathways - including interferon stimulated genes - for poly I:C. Meanwhile, metabolic and cell cycle were downregulated by both mimics. We identified notable differences in chromatin accessibility (20,617<span>&nbsp;</span></span><em>in vitro</em><span>, 59,892<span>&nbsp;</span></span><em>in vivo</em><span>) and H3K4me3 bound regions (11,454<span>&nbsp;</span></span><em>in vitro</em><span>, 10,275<span>&nbsp;</span></span><em>in viv</em><span>o) - i.e. marking active promoters - between stimulations and controls. Overlaps of DEGs with promoters showing differential accessibility or histone mark binding revealed a significant coupling of the transcriptome and chromatin state. DEGs with activation marks in their promoters were enriched for similar functions to the global DEG set, but not in all cases, suggesting key regulatory genes were in poised or bivalent states. Active promoters and putative enhancers were differentially enriched in transcription factor binding motifs, many of them common to viral and bacterial responses. Finally, an in-depth analysis of immune response changes in chromatin state surrounding key DEGs encoding transcription factors was performed. This comprehensive multi-omics investigation provides an improved understanding of the epigenomic basis for the turbot immune responses and provides novel functional genomic information that can be leveraged in selective breeding towards enhanced disease resistance.</span></p>',
			'date' => '2024-02-15',
			'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.02.15.580452v1',
			'doi' => 'https://doi.org/10.1101/2024.02.15.580452',
			'modified' => '2024-02-22 11:41:27',
			'created' => '2024-02-22 11:41:27',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '4884',
			'name' => 'SMARCB1 loss activates patient-specific distal oncogenic enhancers in malignant rhabdoid tumors',
			'authors' => 'Liu, N.Q. et al.',
			'description' => '<p><span>Malignant rhabdoid tumor (MRT) is a highly malignant and often lethal childhood cancer. MRTs are genetically defined by bi-allelic inactivating mutations in&nbsp;</span><i>SMARCB1</i><span>, a member of the BRG1/BRM-associated factors (BAF) chromatin remodeling complex. Mutations in BAF complex members are common in human cancer, yet their contribution to tumorigenesis remains in many cases poorly understood. Here, we study derailed regulatory landscapes as a consequence of<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>loss in the context of MRT. Our multi-omics approach on patient-derived MRT organoids reveals a dramatic reshaping of the regulatory landscape upon<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>reconstitution. Chromosome conformation capture experiments subsequently reveal patient-specific looping of distal enhancer regions with the promoter of the<span>&nbsp;</span></span><i>MYC</i><span><span>&nbsp;</span>oncogene. This intertumoral heterogeneity in<span>&nbsp;</span></span><i>MYC</i><span><span>&nbsp;</span>enhancer utilization is also present in patient MRT tissues as shown by combined single-cell RNA-seq and ATAC-seq. We show that loss of<span>&nbsp;</span></span><i>SMARCB1</i><span><span>&nbsp;</span>activates patient-specific epigenetic reprogramming underlying MRT tumorigenesis.</span></p>',
			'date' => '2023-12-01',
			'pmid' => 'https://www.nature.com/articles/s41467-023-43498-3#Abs1',
			'doi' => '10.1038/s41467-023-43498-3',
			'modified' => '2023-12-05 08:45:53',
			'created' => '2023-12-05 08:45:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '4885',
			'name' => 'The genetic landscape of origins of replication in P. falciparum',
			'authors' => 'Casilda Muñoz Castellano et al.',
			'description' => '<p><span>Various origin mapping approaches have enabled genome-wide identification of origins of replication (ORI) in model organisms, but only a few studies have focused on divergent organisms. By employing three complementary approaches we provide a high-resolution map of ORIs in&nbsp;</span><em>Plasmodium falciparum</em><span>, the deadliest human malaria parasite. We profiled the distribution of origin of recognition complex (ORC) binding sites by ChIP-seq of two<span>&nbsp;</span></span><em>Pf</em><span>ORC subunits and mapped active ORIs using NFS and SNS-seq. We show that ORIs lack sequence specificity but are not randomly distributed, and group in clusters. Licensing is biased towards regions of higher GC content and associated with G-quadruplex forming sequences (G4FS). While strong transcription likely enhances firing, active origins are depleted from transcription start sites. Instead, most accumulate in transcriptionally active gene bodies. Single molecule analysis of nanopore reads containing multiple initiation events, which could have only come from individual nuclei, showed a relationship between the replication fork pace and the distance to the nearest origin. While some similarities were drawn with the canonic eukaryote model, the distribution of ORIs in<span>&nbsp;</span></span><em>P. falciparum</em><span><span>&nbsp;</span>is likely shaped by unique genomic features such as extreme AT-richness&mdash;a product of evolutionary pressure imposed by the parasitic lifestyle.</span></p>',
			'date' => '2023-12-01',
			'pmid' => 'https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkad1103/7457016#428428709',
			'doi' => 'doi.org/10.1093/nar/gkad1103',
			'modified' => '2023-12-05 08:47:24',
			'created' => '2023-12-05 08:47:24',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '4843',
			'name' => 'Differentiation block in acute myeloid leukemia regulated by intronicsequences of FTO',
			'authors' => 'Camera  F. et al.',
			'description' => '<p>Iroquois transcription factor gene IRX3 is highly expressed in 20&acirc;&euro;&ldquo;30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences &acirc;&circ;&frac14;220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with the IRX3 promoter, which correlate with IRX3 expression. Deletion of these intronic elements confirms a role in positively regulating IRX3. RNAseq revealed long non-coding (lnc) transcripts arising from this locus. FTO-lncAML knockdown (KD) induced differentiation of AML cells, loss of clonogenic activity, and reduced FTO intron 8:IRX3 promoter contacts. While both FTO-lncAML KD and IRX3 KD induced differentiation, FTO-lncAML but not IRX3 KD led to HOXA downregulation suggesting transcript activity in trans. FTO-lncAMLhigh AML samples expressed higher levels of HOXA and lower levels of differentiation genes. Thus, a regulatory module in FTO intron 8 consisting of clustered enhancer elements and a long non-coding RNA is active in human AML, impeding myeloid differentiation.</p>',
			'date' => '2023-08-01',
			'pmid' => 'https://www.sciencedirect.com/science/article/pii/S2589004223013962',
			'doi' => '10.1016/j.isci.2023.107319',
			'modified' => '2023-08-01 14:14:01',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '4851',
			'name' => 'Supraphysiological Androgens Promote the Tumor Suppressive Activity of the Androgen Receptor Through cMYC Repression and Recruitment of the DREAM Complex',
			'authors' => 'Nyquist  M. et al.',
			'description' => '<p>The androgen receptor (AR) pathway regulates key cell survival programs in prostate epithelium. The AR represents a near-universal driver and therapeutic vulnerability in metastatic prostate cancer, and targeting AR has a remarkable therapeutic index. Though most approaches directed toward AR focus on inhibiting AR signaling, laboratory and now clinical data have shown that high dose, supraphysiological androgen treatment (SPA) results in growth repression and improved outcomes in subsets of prostate cancer patients. A better understanding of the mechanisms contributing to SPA response and resistance could help guide patient selection and combination therapies to improve efficacy. To characterize SPA signaling, we integrated metrics of gene expression changes induced by SPA together with cistrome data and protein-interactomes. These analyses indicated that the Dimerization partner, RB-like, E2F and Multi-vulval class B (DREAM) complex mediates growth repression and downregulation of E2F targets in response to SPA. Notably, prostate cancers with complete genomic loss of RB1 responded to SPA treatment whereas loss of DREAM complex components such as RBL1/2 promoted resistance. Overexpression of MYC resulted in complete resistance to SPA and attenuated the SPA/AR-mediated repression of E2F target genes. These findings support a model of SPA-mediated growth repression that relies on the negative regulation of MYC by AR leading to repression of E2F1 signaling via the DREAM complex. The integrity of MYC signaling and DREAM complex assembly may consequently serve as determinants of SPA responses and as pathways mediating SPA resistance.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/37352376/',
			'doi' => '10.1158/0008-5472.CAN-22-2613',
			'modified' => '2023-08-01 18:09:31',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '4852',
			'name' => 'In skeletal muscle and neural crest cells, SMCHD1 regulates biologicalpathways relevant for Bosma syndrome and facioscapulohumeral dystrophyphenotype.',
			'authors' => 'Laberthonnière  C. et al.',
			'description' => '<p>Many genetic syndromes are linked to mutations in genes encoding factors that guide chromatin organization. Among them, several distinct rare genetic diseases are linked to mutations in SMCHD1 that encodes the structural maintenance of chromosomes flexible hinge domain containing 1 chromatin-associated factor. In humans, its function as well as the impact of its mutations remains poorly defined. To fill this gap, we determined the episignature associated with heterozygous SMCHD1 variants in primary cells and cell lineages derived from induced pluripotent stem cells for Bosma arhinia and microphthalmia syndrome (BAMS) and type 2 facioscapulohumeral dystrophy (FSHD2). In human tissues, SMCHD1 regulates the distribution of methylated CpGs, H3K27 trimethylation and CTCF at repressed chromatin but also at euchromatin. Based on the exploration of tissues affected either in FSHD or in BAMS, i.e. skeletal muscle fibers and neural crest stem cells, respectively, our results emphasize multiple functions for SMCHD1, in chromatin compaction, chromatin insulation and gene regulation with variable targets or phenotypical outcomes. We concluded that in rare genetic diseases, SMCHD1 variants impact gene expression in two ways: (i) by changing the chromatin context at a number of euchromatin loci or (ii) by directly regulating some loci encoding master transcription factors required for cell fate determination and tissue differentiation.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37334829',
			'doi' => '10.1093/nar/gkad523',
			'modified' => '2023-08-01 14:35:38',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '4861',
			'name' => 'Hypomethylation and overexpression of Th17-associated genes is ahallmark of intestinal CD4+ lymphocytes in Crohn's disease.',
			'authors' => 'Sun  Z. et al.',
			'description' => '<p>BACKGROUND: The development of Crohn's disease (CD) involves immune cell signaling pathways regulated by epigenetic modifications. Aberrant DNA methylation has been identified in peripheral blood and bulk intestinal tissue from CD patients. However, the DNA methylome of disease-associated intestinal CD4 + lymphocytes has not been evaluated. MATERIALS AND METHODS: Genome-wide DNA methylation sequencing was performed from terminal ileum CD4 + cells from 21 CD patients and 12 age and sex matched controls. Data was analyzed for differentially methylated CpGs (DMCs) and methylated regions (DMRs). Integration was performed with RNA-sequencing data to evaluate the functional impact of DNA methylation changes on gene expression. DMRs were overlapped with regions of differentially open chromatin (by ATAC-seq) and CCCTC-binding factor (CTCF) binding sites (by ChIP-seq) between peripherally-derived Th17 and Treg cells. RESULTS: CD4+ cells in CD patients had significantly increased DNA methylation compared to those from the controls. A total of 119,051 DMCs and 8,113 DMRs were detected. While hyper-methylated genes were mostly related to cell metabolism and homeostasis, hypomethylated genes were significantly enriched within the Th17 signaling pathway. The differentially enriched ATAC regions in Th17 cells (compared to Tregs) were hypomethylated in CD patients, suggesting heightened Th17 activity. There was significant overlap between hypomethylated DNA regions and CTCF-associated binding sites. CONCLUSIONS: The methylome of CD patients demonstrate an overall dominant hypermethylation yet hypomethylation is more concentrated in proinflammatory pathways, including Th17 differentiation. Hypomethylation of Th17-related genes associated with areas of open chromatin and CTCF binding sites constitutes a hallmark of CD-associated intestinal CD4 + cells.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37280154',
			'doi' => '10.1093/ecco-jcc/jjad093',
			'modified' => '2023-08-01 14:52:39',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 17 => array(
			'id' => '4862',
			'name' => 'Mutant FUS induces chromatin reorganization in the hippocampus andalters memory processes.',
			'authors' => 'Tzeplaeff  L. et al.',
			'description' => '<p>Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalization to hippocampal function and memory formation are still not characterized. Herein, we show that in these mice, the hippocampus paradoxically displays nuclear FUS accumulation. Multi-omic analyses showed that FUS binds to a set of genes characterized by the presence of an ETS/ELK-binding motifs, and involved in RNA metabolism, transcription, ribosome/mitochondria and chromatin organization. Importantly, hippocampal nuclei showed a decompaction of the neuronal chromatin at highly expressed genes and an inappropriate transcriptomic response was observed after spatial training of Fus mice. Furthermore, these mice lacked precision in a hippocampal-dependent spatial memory task and displayed decreased dendritic spine density. These studies shows that mutated FUS affects epigenetic regulation of the chromatin landscape in hippocampal neurons, which could participate in FTD/ALS pathogenic events. These data call for further investigation in the neurological phenotype of FUS-related diseases and open therapeutic strategies towards epigenetic drugs.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37327984',
			'doi' => '10.1016/j.pneurobio.2023.102483',
			'modified' => '2023-08-01 14:55:49',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 18 => array(
			'id' => '4782',
			'name' => 'Transient suppression of SUMOylation in embryonic stem cells generatesembryo-like structures.',
			'authors' => 'Cossec  J-C. et al.',
			'description' => '<p>Recent advances in synthetic embryology have opened new avenues for understanding the complex events controlling mammalian peri-implantation development. Here, we show that mouse embryonic stem cells (ESCs) solely exposed to chemical inhibition of SUMOylation generate embryo-like structures comprising anterior neural and trunk-associated regions. HypoSUMOylation-instructed ESCs give rise to spheroids that self-organize into gastrulating structures containing cell types spatially and functionally related to embryonic and extraembryonic compartments. Alternatively, spheroids cultured in a droplet microfluidic device form elongated structures that undergo axial organization reminiscent of natural embryo morphogenesis. Single-cell transcriptomics reveals various cellular lineages, including properly positioned anterior neuronal cell types and paraxial mesoderm segmented into somite-like structures. Transient SUMOylation suppression gradually increases DNA methylation genome wide and repressive mark deposition at Nanog. Interestingly, cell-to-cell variations in SUMOylation levels occur during early embryogenesis. Our approach provides a proof of principle for potentially powerful strategies to explore early embryogenesis by targeting chromatin roadblocks of cell fate change.</p>',
			'date' => '2023-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37061916',
			'doi' => '10.1016/j.celrep.2023.112380',
			'modified' => '2023-06-13 09:20:06',
			'created' => '2023-05-05 12:34:24',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 19 => array(
			'id' => '4693',
			'name' => 'ZEB1 controls a lineage-specific transcriptional program essential formelanoma cell state transitions',
			'authors' => 'Tang  Y. et al.',
			'description' => '<p>Cell plasticity sustains intra-tumor heterogeneity and treatment resistance in melanoma. Deciphering the transcriptional mechanisms governing reversible phenotypic transitions between proliferative/differentiated and invasive/stem-like states is required in order to design novel therapeutic strategies. EMT-inducing transcription factors, extensively known for their role in metastasis in carcinoma, display cell-type specific functions in melanoma, with a decreased ZEB2/ZEB1 expression ratio fostering adaptive resistance to targeted therapies. While ZEB1 direct target genes have been well characterized in carcinoma models, they remain unknown in melanoma. Here, we performed a genome-wide characterization of ZEB1 transcriptional targets, by combining ChIP-sequencing and RNA-sequencing, upon phenotype switching in melanoma models. We identified and validated ZEB1 binding peaks in the promoter of key lineage-specific genes related to melanoma cell identity. Comparative analyses with breast carcinoma cells demonstrated melanoma-specific ZEB1 binding, further supporting lineage specificity. Gain- or loss-of-function of ZEB1, combined with functional analyses, further demonstrated that ZEB1 negatively regulates proliferative/melanocytic programs and positively regulates both invasive and stem-like programs. We then developed single-cell spatial multiplexed analyses to characterize melanoma cell states with respect to ZEB1/ZEB2 expression in human melanoma samples. We characterized the intra-tumoral heterogeneity of ZEB1 and ZEB2 and further validated ZEB1 increased expression in invasive cells, but also in stem-like cells, highlighting its relevance in vivo in both populations. Overall, our results define ZEB1 as a major transcriptional regulator of cell states transitions and provide a better understanding of lineage-specific transcriptional programs sustaining intra-tumor heterogeneity in melanoma.</p>',
			'date' => '2023-02-01',
			'pmid' => 'https://doi.org/10.1101%2F2023.02.10.526467',
			'doi' => '10.1101/2023.02.10.526467',
			'modified' => '2023-04-14 09:11:23',
			'created' => '2023-02-28 12:19:11',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 20 => 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) 21 => array(
			'id' => '4651',
			'name' => 'TCDD induces multigenerational alterations in the expression ofmicroRNA in the thymus through epigenetic modifications',
			'authors' => 'Singh  Narendra P et al.',
			'description' => '<p>2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a potent AhR ligand, is an environmental contaminant that is known for mediating toxicity across generations. However, whether TCDD can induce multigenerational changes in the expression of miRNAs (miRs) has not been previously studied. In the current study, we investigated the effect of administration of TCDD in pregnant mice (F0) on gestational day 14, on the expression of miRs in the thymus of F0 and subsequent generations (F1 and F2). Of the 3200 miRs screened, 160 miRs were dysregulated similarly in F0, F1, and F2 generations while 46 miRs were differentially altered in F0-F2 generations. Pathway analysis revealed that the changes in miR signature profile mediated by TCDD affected the genes that regulate cell signaling, apoptosis, thymic atrophy, cancer, immunosuppression, and other physiological pathways. A significant number of miRs that showed altered expression exhibited dioxin response elements (DRE) on their promoters. Focusing on one such miR, namely miR-203 that expressed DREs and was induced across F0-F2 by TCDD, promoter analysis showed that one of the DREs expressed by miR-203 was functional to TCDD-mediated upregulation. Also, the histone methylation status of H3K4me3 in the miR-203 promoter was significantly increased near the transcriptional start site (TSS) in TCDD-treated thymocytes across F0-F2 generations. Genome-wide ChIP-seq study suggested that TCDD may cause alterations in histone methylation in certain genes across the three generations. Together, the current study demonstrates that gestational exposure to TCDD can alter the expression of miRs in F0 through direct activation of DREs as well as across F0, F1, and F2 generations through epigenetic pathways.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://academic.oup.com/pnasnexus/advance-article/doi/10.1093/pnasnexus/pgac290/6886578',
			'doi' => 'https://doi.org/10.1093/pnasnexus/pgac290',
			'modified' => '2023-03-13 10:55:36',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 22 => array(
			'id' => '4632',
			'name' => 'The histone acetyltransferase KAT6A is recruited to unmethylatedCpG islands via a DNA binding winged helix domain.',
			'authors' => 'Weber  L.M. et al.',
			'description' => '<p>The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrate that a winged helix (WH) domain at the very N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A with unmethylated CpG islands (CGIs) genome-wide. Mutation of the essential amino acids for DNA binding completely abrogates the enrichment of KAT6A at CGIs. In contrast, deletion of a second WH domain or the histone tail binding PHD fingers only subtly influences the binding of KAT6A to CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36537216',
			'doi' => '10.1093/nar/gkac1188',
			'modified' => '2023-03-28 09:01:38',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 23 => array(
			'id' => '4629',
			'name' => 'Polyglutamine-expanded ATXN7 alters a specific epigenetic signatureunderlying photoreceptor identity gene expression in SCA7 mouseretinopathy.',
			'authors' => 'Niewiadomska-Cimicka  A.et al.',
			'description' => '<p>BACKGROUND: Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disorder that primarily affects the cerebellum and retina. SCA7 is caused by a polyglutamine expansion in the ATXN7 protein, a subunit of the transcriptional coactivator SAGA that acetylates histone H3 to deposit narrow H3K9ac mark at DNA regulatory elements of active genes. Defective histone acetylation has been presented as a possible cause for gene deregulation in SCA7 mouse models. However, the topography of acetylation defects at the whole genome level and its relationship to changes in gene expression remain to be determined. METHODS: We performed deep RNA-sequencing and chromatin immunoprecipitation coupled to high-throughput sequencing to examine the genome-wide correlation between gene deregulation and alteration of the active transcription marks, e.g. SAGA-related H3K9ac, CBP-related H3K27ac and RNA polymerase II (RNAPII), in a SCA7 mouse retinopathy model. RESULTS: Our analyses revealed that active transcription marks are reduced at most gene promoters in SCA7 retina, while a limited number of genes show changes in expression. We found that SCA7 retinopathy is caused by preferential downregulation of hundreds of highly expressed genes that define morphological and physiological identities of mature photoreceptors. We further uncovered that these photoreceptor genes harbor unusually broad H3K9ac profiles spanning the entire gene bodies and have a low RNAPII pausing. This broad H3K9ac signature co-occurs with other features that delineate superenhancers, including broad H3K27ac, binding sites for photoreceptor specific transcription factors and expression of enhancer-related non-coding RNAs (eRNAs). In SCA7 retina, downregulated photoreceptor genes show decreased H3K9 and H3K27 acetylation and eRNA expression as well as increased RNAPII pausing, suggesting that superenhancer-related features are altered. CONCLUSIONS: Our study thus provides evidence that distinctive epigenetic configurations underlying high expression of cell-type specific genes are preferentially impaired in SCA7, resulting in a defect in the maintenance of identity features of mature photoreceptors. Our results also suggest that continuous SAGA-driven acetylation plays a role in preserving post-mitotic neuronal identity.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36539812',
			'doi' => '10.1186/s12929-022-00892-1',
			'modified' => '2023-03-28 09:07:19',
			'created' => '2023-02-21 09:59:46',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 24 => 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) 25 => array(
			'id' => '4494',
			'name' => 'Cryptococcal Hsf3 controls intramitochondrial ROS homeostasis byregulating the respiratory process.',
			'authors' => 'Gao  X.et al.',
			'description' => '<p>Mitochondrial quality control prevents accumulation of intramitochondrial-derived reactive oxygen species (mtROS), thereby protecting cells against DNA damage, genome instability, and programmed cell death. However, underlying mechanisms are incompletely understood, particularly in fungal species. Here, we show that Cryptococcus neoformans heat shock factor 3 (CnHsf3) exhibits an atypical function in regulating mtROS independent of the unfolded protein response. CnHsf3 acts in nuclei and mitochondria, and nuclear- and mitochondrial-targeting signals are required for its organelle-specific functions. It represses the expression of genes involved in the tricarboxylic acid cycle while promoting expression of genes involved in electron transfer chain. In addition, CnHsf3 responds to multiple intramitochondrial stresses; this response is mediated by oxidation of the cysteine residue on its DNA binding domain, which enhances DNA binding. Our results reveal a function of HSF proteins in regulating mtROS homeostasis that is independent of the unfolded protein response.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36109512',
			'doi' => '10.1038/s41467-022-33168-1',
			'modified' => '2022-11-18 12:43:17',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 26 => array(
			'id' => '4496',
			'name' => 'Dominant role of DNA methylation over H3K9me3 for IAP silencingin endoderm.',
			'authors' => 'Wang  Z. et al.',
			'description' => '<p>Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications H3K9me3 and DNA methylation. On ERVs, these modifications are mainly deposited by the histone methyltransferase Setdb1 and by the maintenance DNA methyltransferase Dnmt1. Knock-out of either Setdb1 or Dnmt1 leads to ERV de-repression in various cell types. However, it is currently not known if H3K9me3 and DNA methylation depend on each other for ERV silencing. Here we show that conditional knock-out of Setdb1 in mouse embryonic endoderm results in ERV de-repression in visceral endoderm (VE) descendants and does not occur in definitive endoderm (DE). Deletion of Setdb1 in VE progenitors results in loss of H3K9me3 and reduced DNA methylation of Intracisternal A-particle (IAP) elements, consistent with up-regulation of this ERV family. In DE, loss of Setdb1 does not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 knock-out results in IAP de-repression in both visceral and definitive endoderm cells, while H3K9me3 is unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm cells. Our findings suggest that Setdb1-meditated H3K9me3 is not sufficient for IAP silencing, but rather critical for maintaining high DNA methylation.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36123357',
			'doi' => '10.1038/s41467-022-32978-7',
			'modified' => '2022-11-21 10:26:30',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 27 => array(
			'id' => '4415',
			'name' => 'HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependentgene repression in murine erythroleukaemia.',
			'authors' => 'Gregoricchio  S. et al.',
			'description' => '<p>Although originally described as transcriptional activator, SPI1/PU.1, a major player in haematopoiesis whose alterations are associated with haematological malignancies, has the ability to repress transcription. Here, we investigated the mechanisms underlying gene repression in the erythroid lineage, in which SPI1 exerts an oncogenic function by blocking differentiation. We show that SPI1 represses genes by binding active enhancers that are located in intergenic or gene body regions. HDAC1 acts as a cooperative mediator of SPI1-induced transcriptional repression by deacetylating SPI1-bound enhancers in a subset of genes, including those involved in erythroid differentiation. Enhancer deacetylation impacts on promoter acetylation, chromatin accessibility and RNA pol II occupancy. In addition to the activities of HDAC1, polycomb repressive complex 2 (PRC2) reinforces gene repression by depositing H3K27me3 at promoter sequences when SPI1 is located at enhancer sequences. Moreover, our study identified a synergistic relationship between PRC2 and HDAC1 complexes in mediating the transcriptional repression activity of SPI1, ultimately inducing synergistic adverse effects on leukaemic cell survival. Our results highlight the importance of the mechanism underlying transcriptional repression in leukemic cells, involving complex functional connections between SPI1 and the epigenetic regulators PRC2 and HDAC1.</p>',
			'date' => '2022-08-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35871293',
			'doi' => '10.1093/nar/gkac613',
			'modified' => '2022-09-15 08:59:26',
			'created' => '2022-09-08 16:32:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 28 => array(
			'id' => '4516',
			'name' => 'Dual role of histone variant H3.3B in spermatogenesis: positiveregulation of piRNA transcription and implication in X-chromosomeinactivation.',
			'authors' => 'Fontaine  E. et al.',
			'description' => '<p>The histone variant H3.3 is encoded by two distinct genes, H3f3a and H3f3b, exhibiting identical amino-acid sequence. H3.3 is required for spermatogenesis, but the molecular mechanism of its spermatogenic function remains obscure. Here, we have studied the role of each one of H3.3A and H3.3B proteins in spermatogenesis. We have generated transgenic conditional knock-out/knock-in (cKO/KI) epitope-tagged FLAG-FLAG-HA-H3.3B (H3.3BHA) and FLAG-FLAG-HA-H3.3A (H3.3AHA) mouse lines. We show that H3.3B, but not H3.3A, is required for spermatogenesis and male fertility. Analysis of the molecular mechanism unveils that the absence of H3.3B led to alterations in the meiotic/post-meiotic transition. Genome-wide RNA-seq reveals that the depletion of H3.3B in meiotic cells is associated with increased expression of the whole sex X and Y chromosomes as well as of both RLTR10B and RLTR10B2 retrotransposons. In contrast, the absence of H3.3B resulted in down-regulation of the expression of piRNA clusters. ChIP-seq experiments uncover that RLTR10B and RLTR10B2 retrotransposons, the whole sex chromosomes and the piRNA clusters are markedly enriched of H3.3. Taken together, our data dissect the molecular mechanism of H3.3B functions during spermatogenesis and demonstrate that H3.3B, depending on its chromatin localization, is involved in either up-regulation or down-regulation of expression of defined large chromatin regions.</p>',
			'date' => '2022-07-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35766398',
			'doi' => '10.1093/nar/gkac541',
			'modified' => '2022-11-24 08:51:34',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 29 => array(
			'id' => '4393',
			'name' => 'TBX2 acts as a potent transcriptional silencer of tumour suppressor genesthrough interaction with the CoREST complex to sustain theproliferation of breast cancers.',
			'authors' => 'McIntyre  A.J. et al.',
			'description' => '<p>Chromosome 17q23 amplification occurs in 20\% of primary breast tumours and is associated with poor outcome. The TBX2 gene is located on 17q23 and is often over-expressed in this breast tumour subset. TBX2 is an anti-senescence gene, promoting cell growth and survival through repression of Tumour Suppressor Genes (TSGs), such as NDRG1 and CST6. Previously we found that TBX2 cooperates with the PRC2 complex to repress several TSGs, and that PRC2 inhibition restored NDRG1 expression to impede cellular proliferation. Here, we now identify CoREST proteins, LSD1 and ZNF217, as novel interactors of TBX2. Genetic or pharmacological targeting of CoREST emulated TBX2 loss, inducing NDRG1 expression and abolishing breast cancer growth in vitro and in vivo. Furthermore, we uncover that TBX2/CoREST targeting of NDRG1 is achieved by recruitment of TBX2 to the NDRG1 promoter by Sp1, the abolishment of which resulted in NDRG1 upregulation and diminished cancer cell proliferation. Through ChIP-seq we reveal that 30\% of TBX2-bound promoters are shared with ZNF217 and identify novel targets repressed by TBX2/CoREST; of these targets a lncRNA, LINC00111, behaves as a negative regulator of cell proliferation. Overall, these data indicate that inhibition of CoREST proteins represents a promising therapeutic intervention for TBX2-addicted breast tumours.</p>',
			'date' => '2022-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35687133',
			'doi' => '10.1093/nar/gkac494',
			'modified' => '2022-08-11 14:23:06',
			'created' => '2022-08-11 12:14:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 30 => array(
			'id' => '4836',
			'name' => 'Caffeine intake exerts dual genome-wide effects on hippocampal metabolismand learning-dependent transcription.',
			'authors' => 'Paiva  I. et al.',
			'description' => '<p>Caffeine is the most widely consumed psychoactive substance in the world. Strikingly, the molecular pathways engaged by its regular consumption remain unclear. We herein addressed the mechanisms associated with habitual (chronic) caffeine consumption in the mouse hippocampus using untargeted orthogonal omics techniques. Our results revealed that chronic caffeine exerts concerted pleiotropic effects in the hippocampus at the epigenomic, proteomic, and metabolomic levels. Caffeine lowered metabolism-related processes (e.g., at the level of metabolomics and gene expression) in bulk tissue, while it induced neuron-specific epigenetic changes at synaptic transmission/plasticity-related genes and increased experience-driven transcriptional activity. Altogether, these findings suggest that regular caffeine intake improves the signal-to-noise ratio during information encoding, in part through fine-tuning of metabolic genes, while boosting the salience of information processing during learning in neuronal circuits.</p>',
			'date' => '2022-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35536645',
			'doi' => '10.1172/JCI149371',
			'modified' => '2023-08-01 13:52:29',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 31 => array(
			'id' => '4221',
			'name' => 'Epigenetic Mechanisms Mediating Cell State Transitions in Chondrocytes',
			'authors' => 'Wuelling M. et al.',
			'description' => '<p><span>Epigenetic modifications play critical roles in regulating cell lineage differentiation, but the epigenetic mechanisms guiding specific differentiation steps within a cell lineage have rarely been investigated. To decipher such mechanisms, we used the defined transition from proliferating (PC) into hypertrophic chondrocytes (HC) during endochondral ossification as a model. We established a map of activating and repressive histone modifications for each cell type. ChromHMM state transition analysis and Pareto-based integration of differential levels of mRNA and epigenetic marks revealed that differentiation-associated gene repression is initiated by the addition of H3K27me3 to promoters still carrying substantial levels of activating marks. Moreover, the integrative analysis identified genes specifically expressed in cells undergoing the transition into hypertrophy. Investigation of enhancer profiles detected surprising differences in enhancer number, location, and transcription factor binding sites between the two closely related cell types. Furthermore, cell type-specific upregulation of gene expression was associated with increased numbers of H3K27ac peaks. Pathway analysis identified PC-specific enhancers associated with chondrogenic genes, whereas HC-specific enhancers mainly control metabolic pathways linking epigenetic signature to biological functions. Since HC-specific enhancers show a higher conservation in postnatal tissues, the switch to metabolic pathways seems to be a hallmark of differentiated tissues. Surprisingly, the analysis of H3K27ac levels at super-enhancers revealed a rapid adaption of H3K27ac occupancy to changes in gene expression, supporting the importance of enhancer modulation for acute alterations in gene expression. &copy; 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).</span></p>',
			'date' => '2022-05-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/33534175/',
			'doi' => '10.1002/jbmr.4263',
			'modified' => '2022-04-25 11:46:32',
			'created' => '2022-04-21 12:00:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 32 => array(
			'id' => '4402',
			'name' => 'The CpG Island-Binding Protein SAMD1 Contributes to anUnfavorable Gene Signature in HepG2 Hepatocellular CarcinomaCells.',
			'authors' => 'Simon  C. et al.',
			'description' => '<p>The unmethylated CpG island-binding protein SAMD1 is upregulated in many human cancer types, but its cancer-related role has not yet been investigated. Here, we used the hepatocellular carcinoma cell line HepG2 as a cancer model and investigated the cellular and transcriptional roles of SAMD1 using ChIP-Seq and RNA-Seq. SAMD1 targets several thousand gene promoters, where it acts predominantly as a transcriptional repressor. HepG2 cells with SAMD1 deletion showed slightly reduced proliferation, but strongly impaired clonogenicity. This phenotype was accompanied by the decreased expression of pro-proliferative genes, including MYC target genes. Consistently, we observed a decrease in the active H3K4me2 histone mark at most promoters, irrespective of SAMD1 binding. Conversely, we noticed an increase in interferon response pathways and a gain of H3K4me2 at a subset of enhancers that were enriched for IFN-stimulated response elements (ISREs). We identified key transcription factor genes, such as , , and , that were directly repressed by SAMD1. Moreover, SAMD1 deletion also led to the derepression of the PI3K-inhibitor , contributing to diminished mTOR signaling and ribosome biogenesis pathways. Our work suggests that SAMD1 is involved in establishing a pro-proliferative setting in hepatocellular carcinoma cells. Inhibiting SAMD1's function in liver cancer cells may therefore lead to a more favorable gene signature.</p>',
			'date' => '2022-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35453756',
			'doi' => '10.3390/biology11040557',
			'modified' => '2022-08-11 14:45:43',
			'created' => '2022-08-11 12:14:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 33 => array(
			'id' => '4524',
			'name' => 'Local euchromatin enrichment in lamina-associated domains anticipatestheir repositioning in the adipogenic lineage.',
			'authors' => 'Madsen-Østerbye  J. et al.',
			'description' => '<p>BACKGROUND: Interactions of chromatin with the nuclear lamina via lamina-associated domains (LADs) confer structural stability to the genome. The dynamics of positioning of LADs during differentiation, and how LADs impinge on developmental gene expression, remains, however, elusive. RESULTS: We examined changes in the association of lamin B1 with the genome in the first 72 h of differentiation of adipose stem cells into adipocytes. We demonstrate a repositioning of entire stand-alone LADs and of LAD edges as a prominent nuclear structural feature of early adipogenesis. Whereas adipogenic genes are released from LADs, LADs sequester downregulated or repressed genes irrelevant for the adipose lineage. However, LAD repositioning only partly concurs with gene expression changes. Differentially expressed genes in LADs, including LADs conserved throughout differentiation, reside in local euchromatic and lamin-depleted sub-domains. In these sub-domains, pre-differentiation histone modification profiles correlate with the LAD versus inter-LAD outcome of these genes during adipogenic commitment. Lastly, we link differentially expressed genes in LADs to short-range enhancers which overall co-partition with these genes in LADs versus inter-LADs during differentiation. CONCLUSIONS: We conclude that LADs are predictable structural features of adipose nuclear architecture that restrain non-adipogenic genes in a repressive environment.</p>',
			'date' => '2022-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35410387',
			'doi' => '10.1186/s13059-022-02662-6',
			'modified' => '2022-11-24 09:08:01',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 34 => array(
			'id' => '4235',
			'name' => 'NuA4 and H2A.Z control environmental responses and autotrophicgrowth in Arabidopsis',
			'authors' => 'Bieluszewski T. et al.',
			'description' => '<p>Nucleosomal acetyltransferase of H4 (NuA4) is an essential transcriptional coactivator in eukaryotes, but remains poorly characterized in plants. Here, we describe Arabidopsis homologs of the NuA4 scaffold proteins Enhancer of Polycomb-Like 1 (AtEPL1) and Esa1-Associated Factor 1 (AtEAF1). Loss of AtEAF1 results in inhibition of growth and chloroplast development. These effects are stronger in the Atepl1 mutant and are further enhanced by loss of Golden2-Like (GLK) transcription factors, suggesting that NuA4 activates nuclear plastid genes alongside GLK. We demonstrate that AtEPL1 is necessary for nucleosomal acetylation of histones H4 and H2A.Z by NuA4 in vitro. These chromatin marks are diminished genome-wide in Atepl1, while another active chromatin mark, H3K9 acetylation (H3K9ac), is locally enhanced. Expression of many chloroplast-related genes depends on NuA4, as they are downregulated with loss of H4ac and H2A.Zac. Finally, we demonstrate that NuA4 promotes H2A.Z deposition and by doing so prevents spurious activation of stress response genes.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35022409',
			'doi' => '10.1038/s41467-021-27882-5',
			'modified' => '2022-05-19 17:02:00',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 35 => array(
			'id' => '4772',
			'name' => 'Three classes of epigenomic regulators converge to hyperactivate theessential maternal gene deadhead within a heterochromatin mini-domain.',
			'authors' => 'Torres-Campana  D. et al.',
			'description' => '<p>The formation of a diploid zygote is a highly complex cellular process that is entirely controlled by maternal gene products stored in the egg cytoplasm. This highly specialized transcriptional program is tightly controlled at the chromatin level in the female germline. As an extreme case in point, the massive and specific ovarian expression of the essential thioredoxin Deadhead (DHD) is critically regulated in Drosophila by the histone demethylase Lid and its partner, the histone deacetylase complex Sin3A/Rpd3, via yet unknown mechanisms. Here, we identified Snr1 and Mod(mdg4) as essential for dhd expression and investigated how these epigenomic effectors act with Lid and Sin3A to hyperactivate dhd. Using Cut\&amp;Run chromatin profiling with a dedicated data analysis procedure, we found that dhd is intriguingly embedded in an H3K27me3/H3K9me3-enriched mini-domain flanked by DNA regulatory elements, including a dhd promoter-proximal element essential for its expression. Surprisingly, Lid, Sin3a, Snr1 and Mod(mdg4) impact H3K27me3 and this regulatory element in distinct manners. However, we show that these effectors activate dhd independently of H3K27me3/H3K9me3, and that dhd remains silent in the absence of these marks. Together, our study demonstrates an atypical and critical role for chromatin regulators Lid, Sin3A, Snr1 and Mod(mdg4) to trigger tissue-specific hyperactivation within a unique heterochromatin mini-domain.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8759638/',
			'doi' => '10.1371/journal.pgen.1009615',
			'modified' => '2023-04-17 09:46:00',
			'created' => '2023-04-14 13:41:22',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 36 => 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) 37 => array(
			'id' => '4245',
			'name' => 'Decreased PRC2 activity supports the survival of basal-like breastcancer cells to cytotoxic treatments',
			'authors' => 'Mieczkowska IK et al.',
			'description' => '<p>Breast cancer (BC) is the most common cancer occurring in women but also rarely develops in men. Recent advances in early diagnosis and development of targeted therapies have greatly improved the survival rate of BC patients. However, the basal-like BC subtype (BLBC), largely overlapping with the triple-negative BC subtype (TNBC), lacks such drug targets and conventional cytotoxic chemotherapies often remain the only treatment option. Thus, the development of resistance to cytotoxic therapies has fatal consequences. To assess the involvement of epigenetic mechanisms and their therapeutic potential increasing cytotoxic drug efficiency, we combined high-throughput RNA- and ChIP-sequencing analyses in BLBC cells. Tumor cells surviving chemotherapy upregulated transcriptional programs of epithelial-to-mesenchymal transition (EMT) and stemness. To our surprise, the same cells showed a pronounced reduction of polycomb repressive complex 2 (PRC2) activity via downregulation of its subunits Ezh2, Suz12, Rbbp7 and Mtf2. Mechanistically, loss of PRC2 activity leads to the de-repression of a set of genes through an epigenetic switch from repressive H3K27me3 to activating H3K27ac mark at regulatory regions. We identified Nfatc1 as an upregulated gene upon loss of PRC2 activity and directly implicated in the transcriptional changes happening upon survival to chemotherapy. Blocking NFATc1 activation reduced epithelial-to-mesenchymal transition, aggressiveness, and therapy resistance of BLBC cells. Our data demonstrate a previously unknown function of PRC2 maintaining low Nfatc1 expression levels and thereby repressing aggressiveness and therapy resistance in BLBC.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34845197',
			'doi' => '10.1038/s41419-021-04407-y',
			'modified' => '2022-05-20 09:21:56',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 38 => array(
			'id' => '4276',
			'name' => 'Ago1 controls myogenic differentiation by regulating eRNA-mediatedCBP-guided epigenome reprogramming.',
			'authors' => 'Fallatah Bodor et al.',
			'description' => '<p>The role of chromatin-associated RNAi components in the nucleus of mammalian cells and in particular in the context of developmental programs remains to be elucidated. Here, we investigate the function of nuclear Argonaute 1 (Ago1) in gene expression regulation during skeletal muscle differentiation. We show that Ago1 is required for activation of the myogenic program by supporting chromatin modification mediated by developmental enhancer activation. Mechanistically, we demonstrate that Ago1 directly controls global H3K27 acetylation (H3K27ac) by regulating enhancer RNA (eRNA)-CREB-binding protein (CBP) acetyltransferase interaction, a key step in enhancer-driven gene activation. In particular, we show that Ago1 is specifically required for myogenic differentiation 1 (MyoD) and downstream myogenic gene activation, whereas its depletion leads to failure of CBP acetyltransferase activation and blocking of the myogenic program. Our work establishes a role of the mammalian enhancer-associated RNAi component Ago1 in epigenome regulation and activation of developmental programs.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.celrep.2021.110066',
			'doi' => '10.1016/j.celrep.2021.110066',
			'modified' => '2022-05-23 09:53:14',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 39 => array(
			'id' => '4833',
			'name' => 'Extensive NEUROG3 occupancy in the human pancreatic endocrine generegulatory network.',
			'authors' => 'Schreiber  V. et al.',
			'description' => '<p>OBJECTIVE: Mice lacking the bHLH transcription factor (TF) Neurog3 do not form pancreatic islet cells, including insulin-secreting beta cells, the absence of which leads to diabetes. In humans, homozygous mutations of NEUROG3 manifest with neonatal or childhood diabetes. Despite this critical role in islet cell development, the precise function of and downstream genetic programs regulated directly by NEUROG3 remain elusive. Therefore, we mapped genome-wide NEUROG3 occupancy in human induced pluripotent stem cell (hiPSC)-derived endocrine progenitors and determined NEUROG3 dependency of associated genes to uncover direct targets. METHODS: We generated a novel hiPSC line (NEUROG3-HA-P2A-Venus) where NEUROG3 is HA-tagged and fused to a self-cleaving fluorescent VENUS reporter. We used the CUT\&amp;RUN technique to map NEUROG3 occupancy and epigenetic marks in pancreatic endocrine progenitors (PEP) that were differentiated from this hiPSC line. We integrated NEUROG3 occupancy data with chromatin status and gene expression in PEPs as well as their NEUROG3-dependence. In addition, we investigated whether NEUROG3 binds type 2 diabetes mellitus (T2DM)-associated variants at the PEP stage. RESULTS: CUT\&amp;RUN revealed a total of 863 NEUROG3 binding sites assigned to 1263 unique genes. NEUROG3 occupancy was found at promoters as well as at distant cis-regulatory elements that frequently overlapped within PEP active enhancers. De novo motif analyses defined a NEUROG3 consensus binding motif and suggested potential co-regulation of NEUROG3 target genes by FOXA or RFX transcription factors. We found that 22\% of the genes downregulated in NEUROG3 PEPs, and 10\% of genes enriched in NEUROG3-Venus positive endocrine cells were bound by NEUROG3 and thus likely to be directly regulated. NEUROG3 binds to 138 transcription factor genes, some with important roles in islet cell development or function, such as NEUROD1, PAX4, NKX2-2, SOX4, MLXIPL, LMX1B, RFX3, and NEUROG3 itself, and many others with unknown islet function. Unexpectedly, we uncovered that NEUROG3 targets genes critical for insulin secretion in beta cells (e.g., GCK, ABCC8/KCNJ11, CACNA1A, CHGA, SCG2, SLC30A8, and PCSK1). Thus, analysis of NEUROG3 occupancy suggests that the transient expression of NEUROG3 not only promotes islet destiny in uncommitted pancreatic progenitors, but could also initiate endocrine programs essential for beta cell function. Lastly, we identified eight T2DM risk SNPs within NEUROG3-bound regions. CONCLUSION: Mapping NEUROG3 genome occupancy in PEPs uncovered unexpectedly broad, direct control of the endocrine genes, raising novel hypotheses on how this master regulator controls islet and beta cell differentiation.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://doi.org/10.1101%2F2021.04.14.439685',
			'doi' => '10.1016/j.molmet.2021.101313',
			'modified' => '2023-08-01 13:46:35',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 40 => array(
			'id' => '4285',
			'name' => 'Alveolar macrophages from persons living with HIV show impairedepigenetic response to Mycobacterium tuberculosis.',
			'authors' => 'Correa-Macedo Wilian et al.',
			'description' => '<p>Persons living with HIV (PLWH) are at increased risk of tuberculosis (TB). HIV-associated TB is often the result of recent infection with Mycobacterium tuberculosis (Mtb) followed by rapid progression to disease. Alveolar macrophages (AM) are the first cells of the innate immune system that engage Mtb, but how HIV and antiretroviral therapy (ART) impact on the anti-mycobacterial response of AM is not known. To investigate the impact of HIV and ART on the transcriptomic and epigenetic response of AM to Mtb, we obtained AM by bronchoalveolar lavage from 20 PLWH receiving ART, 16 control subjects who were HIV-free (HC), and 14 subjects who received ART as pre-exposure prophylaxis (PrEP) to prevent HIV infection. Following in-vitro challenge with Mtb, AM from each group displayed overlapping but distinct profiles of significantly up- and down-regulated genes in response to Mtb. Comparatively, AM isolated from both PLWH and PrEP subjects presented a substantially weaker transcriptional response. In addition, AM from HC subjects challenged with Mtb responded with pronounced chromatin accessibility changes while AM obtained from PLWH and PrEP subjects displayed no significant changes in their chromatin state. Collectively, these results revealed a stronger adverse effect of ART than HIV on the epigenetic landscape and transcriptional responsiveness of AM.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/34473646/',
			'doi' => '10.1172/JCI148013',
			'modified' => '2022-05-24 09:08:39',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 41 => array(
			'id' => '4297',
			'name' => 'INTS11 regulates hematopoiesis by promoting PRC2 function.',
			'authors' => 'Zhang Peng et al.',
			'description' => '<p>INTS11, the catalytic subunit of the Integrator (INT) complex, is crucial for the biogenesis of small nuclear RNAs and enhancer RNAs. However, the role of INTS11 in hematopoietic stem and progenitor cell (HSPC) biology is unknown. Here, we report that INTS11 is required for normal hematopoiesis and hematopoietic-specific genetic deletion of leads to cell cycle arrest and impairment of fetal and adult HSPCs. We identified a novel INTS11-interacting protein complex, Polycomb repressive complex 2 (PRC2), that maintains HSPC functions. Loss of INTS11 destabilizes the PRC2 complex, decreases the level of histone H3 lysine 27 trimethylation (H3K27me3), and derepresses PRC2 target genes. Reexpression of INTS11 or PRC2 proteins in -deficient HSPCs restores the levels of PRC2 and H3K27me3 as well as HSPC functions. Collectively, our data demonstrate that INTS11 is an essential regulator of HSPC homeostasis through the INTS11-PRC2 axis.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34516911',
			'doi' => '10.1126/sciadv.abh1684',
			'modified' => '2022-05-30 09:31:00',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 42 => array(
			'id' => '4304',
			'name' => 'The related coactivator complexes SAGA and ATAC control embryonicstem cell self-renewal through acetyltransferase-independent mechanisms',
			'authors' => 'Fischer Veronique et al.',
			'description' => '<p>SUMMARY SAGA (Spt-Ada-Gcn5 acetyltransferase) and ATAC (Ada-two-A-containing) are two related coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development, but the role of these complexes in RNA polymerase II transcription is less understood. To determine whether SAGA and ATAC have redundant or specific functions, we compare the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC are required for complex assembly and mouse ESC growth and self-renewal. Surprisingly, depletion of HAT module subunits causes a global decrease in histone H3K9 acetylation, but does not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for self-renewal of mouse ESCs by regulating transcription through different pathways in a HAT-independent manner.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34433046',
			'doi' => '10.1016/j.celrep.2021.109598',
			'modified' => '2022-05-30 09:57:39',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 43 => array(
			'id' => '4345',
			'name' => 'Altered Chromatin States Drive Cryptic Transcription in AgingMammalian Stem Cells.',
			'authors' => 'McCauley Brenna S et al.',
			'description' => '<p>A repressive chromatin state featuring trimethylated lysine 36 on histone H3 (H3K36me3) and DNA methylation suppresses cryptic transcription in embryonic stem cells. Cryptic transcription is elevated with age in yeast and nematodes, and reducing it extends yeast lifespan, though whether this occurs in mammals is unknown. We show that cryptic transcription is elevated in aged mammalian stem cells, including murine hematopoietic stem cells (mHSCs) and neural stem cells (NSCs) and human mesenchymal stem cells (hMSCs). Precise mapping allowed quantification of age-associated cryptic transcription in hMSCs aged . Regions with significant age-associated cryptic transcription have a unique chromatin signature: decreased H3K36me3 and increased H3K4me1, H3K4me3, and H3K27ac with age. Genomic regions undergoing such changes resemble known promoter sequences and are bound by TBP even in young cells. Hence, the more permissive chromatin state at intragenic cryptic promoters likely underlies increased cryptic transcription in aged mammalian stem cells.</p>',
			'date' => '2021-08-01',
			'pmid' => 'https://doi.org/10.1038%2Fs43587-021-00091-x',
			'doi' => '10.1038/s43587-021-00091-x',
			'modified' => '2022-06-22 12:30:19',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 44 => array(
			'id' => '4333',
			'name' => 'Metabolically controlled histone H4K5 acylation/acetylation ratiodrives BRD4 genomic distribution.',
			'authors' => 'Gao M. et al.',
			'description' => '<p>In addition to acetylation, histones are modified by a series of competing longer-chain acylations. Most of these acylation marks are enriched and co-exist with acetylation on active gene regulatory elements. Their seemingly redundant functions hinder our understanding of histone acylations' specific roles. Here, by using an acute lymphoblastic leukemia (ALL) cell model and blasts from individuals with B-precusor ALL (B-ALL), we demonstrate a role of mitochondrial activity in controlling the histone acylation/acetylation ratio, especially at histone H4 lysine 5 (H4K5). An increase in the ratio of non-acetyl acylations (crotonylation or butyrylation) over acetylation on H4K5 weakens bromodomain containing protein 4 (BRD4) bromodomain-dependent chromatin interaction and enhances BRD4 nuclear mobility and availability for binding transcription start site regions of active genes. Our data suggest that the metabolism-driven control of the histone acetylation/longer-chain acylation(s) ratio could be a common mechanism regulating the bromodomain factors' functional genomic distribution.</p>',
			'date' => '2021-07-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.celrep.2021.109460',
			'doi' => '10.1016/j.celrep.2021.109460',
			'modified' => '2022-08-03 16:14:09',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 45 => array(
			'id' => '4343',
			'name' => 'The SAM domain-containing protein 1 (SAMD1) acts as a repressivechromatin regulator at unmethylated CpG islands',
			'authors' => 'Stielow B. et al. ',
			'description' => '<p>CpG islands (CGIs) are key regulatory DNA elements at most promoters, but how they influence the chromatin status and transcription remains elusive. Here, we identify and characterize SAMD1 (SAM domain-containing protein 1) as an unmethylated CGI-binding protein. SAMD1 has an atypical winged-helix domain that directly recognizes unmethylated CpG-containing DNA via simultaneous interactions with both the major and the minor groove. The SAM domain interacts with L3MBTL3, but it can also homopolymerize into a closed pentameric ring. At a genome-wide level, SAMD1 localizes to H3K4me3-decorated CGIs, where it acts as a repressor. SAMD1 tethers L3MBTL3 to chromatin and interacts with the KDM1A histone demethylase complex to modulate H3K4me2 and H3K4me3 levels at CGIs, thereby providing a mechanism for SAMD1-mediated transcriptional repression. The absence of SAMD1 impairs ES cell differentiation processes, leading to misregulation of key biological pathways. Together, our work establishes SAMD1 as a newly identified chromatin regulator acting at unmethylated CGIs.</p>',
			'date' => '2021-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33980486',
			'doi' => '10.1126/sciadv.abf2229',
			'modified' => '2022-08-03 16:34:24',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 46 => array(
			'id' => '4192',
			'name' => 'Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-inducedprogrammed cell death in Arabidopsis.',
			'authors' => 'Dvořák Tomaštíková E. et al.',
			'description' => '<p>The Polycomb Repressive Complex 2 (PRC2) is well-known for its role in controlling developmental transitions by suppressing the premature expression of key developmental regulators. Previous work revealed that PRC2 also controls the onset of senescence, a form of developmental programmed cell death (PCD) in plants. Whether the induction of PCD in response to stress is similarly suppressed by the PRC2 remained largely unknown. In this study, we explored whether PCD triggered in response to immunity- and disease-promoting pathogen effectors is associated with changes in the distribution of the PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) modification in Arabidopsis thaliana. We furthermore tested the distribution of the heterochromatic histone mark H3K9me2, which is established, to a large extent, by the H3K9 methyltransferase KRYPTONITE, and occupies chromatin regions generally not targeted by PRC2. We report that effector-induced PCD caused major changes in the distribution of both repressive epigenetic modifications and that both modifications have a regulatory role and impact on the onset of PCD during pathogen infection. Our work highlights that the transition to pathogen-induced PCD is epigenetically controlled, revealing striking similarities to developmental PCD.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33566101',
			'doi' => '10.1093/plphys/kiab035',
			'modified' => '2022-01-06 14:12:23',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 47 => array(
			'id' => '4273',
			'name' => 'An integrated multi-omics analysis identifies prognostic molecularsubtypes of non-muscle-invasive bladder cancer',
			'authors' => 'Lindskrog Sia Viborg et al.',
			'description' => '<p>The molecular landscape in non-muscle-invasive bladder cancer (NMIBC) is characterized by large biological heterogeneity with variable clinical outcomes. Here, we perform an integrative multi-omics analysis of patients diagnosed with NMIBC (n&thinsp;=&thinsp;834). Transcriptomic analysis identifies four classes (1, 2a, 2b and 3) reflecting tumor biology and disease aggressiveness. Both transcriptome-based subtyping and the level of chromosomal instability provide independent prognostic value beyond established prognostic clinicopathological parameters. High chromosomal instability, p53-pathway disruption and APOBEC-related mutations are significantly associated with transcriptomic class 2a and poor outcome. RNA-derived immune cell infiltration is associated with chromosomally unstable tumors and enriched in class 2b. Spatial proteomics analysis confirms the higher infiltration of class 2b tumors and demonstrates an association between higher immune cell infiltration and lower recurrence rates. Finally, the independent prognostic value of the transcriptomic classes is documented in 1228 validation samples using a single sample classification tool. The classifier provides a framework for biomarker discovery and for optimizing treatment and surveillance in next-generation clinical trials.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33863885',
			'doi' => '10.1038/s41467-021-22465-w',
			'modified' => '2022-05-23 09:49:43',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 48 => array(
			'id' => '4109',
			'name' => 'VPRBP functions downstream of the androgen receptor and OGT to restrict p53 activation in prostate cancer ',
			'authors' => 'Poulose N. et al. ',
			'description' => '<p>Androgen receptor (AR) is a major driver of prostate cancer (PCa) initiation and progression. O-GlcNAc transferase (OGT), the enzyme that catalyses the covalent addition of UDP-N-acetylglucosamine (UDP-GlcNAc) to serine and threonine residues of proteins, is often up-regulated in PCa with its expression correlated with high Gleason score. In this study we have identified an AR and OGT co-regulated factor, VPRBP/DCAF1. We show that VPRBP is regulated by the AR at the transcript level, and by OGT at the protein level. In human tissue samples, VPRBP protein expression correlated with AR amplification, OGT overexpression and poor prognosis. VPRBP knockdown in prostate cancer cells led to a significant decrease in cell proliferation, p53 stabilization, nucleolar fragmentation and increased p53 recruitment to the chromatin. In conclusion, we have shown that VPRBP/DCAF1 promotes prostate cancer cell proliferation by restraining p53 activation under the influence of the AR and OGT.</p>',
			'date' => '2021-02-21',
			'pmid' => 'https://www.biorxiv.org/content/10.1101/2021.02.28.433236v1',
			'doi' => '',
			'modified' => '2021-07-07 11:59:15',
			'created' => '2021-07-07 11:59:15',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 49 => array(
			'id' => '4124',
			'name' => 'JAZF1, A Novel p400/TIP60/NuA4 Complex Member, Regulates H2A.ZAcetylation at Regulatory Regions.',
			'authors' => 'Procida, Tara and Friedrich, Tobias and Jack, Antonia P M and Peritore,Martina and Bönisch, Clemens and Eberl, H Christian and Daus, Nadine andKletenkov, Konstantin and Nist, Andrea and Stiewe, Thorsten and Borggrefe,Tilman and Mann, Matthias and Bartk',
			'description' => '<p>Histone variants differ in amino acid sequence, expression timing and genomic localization sites from canonical histones and convey unique functions to eukaryotic cells. Their tightly controlled spatial and temporal deposition into specific chromatin regions is accomplished by dedicated chaperone and/or remodeling complexes. While quantitatively identifying the chaperone complexes of many human H2A variants by using mass spectrometry, we also found additional members of the known H2A.Z chaperone complexes p400/TIP60/NuA4 and SRCAP. We discovered JAZF1, a nuclear/nucleolar protein, as a member of a p400 sub-complex containing MBTD1 but excluding ANP32E. Depletion of JAZF1 results in transcriptome changes that affect, among other pathways, ribosome biogenesis. To identify the underlying molecular mechanism contributing to JAZF1's function in gene regulation, we performed genome-wide ChIP-seq analyses. Interestingly, depletion of JAZF1 leads to reduced H2A.Z acetylation levels at &gt; 1000 regulatory sites without affecting H2A.Z nucleosome positioning. Since JAZF1 associates with the histone acetyltransferase TIP60, whose depletion causes a correlated H2A.Z deacetylation of several JAZF1-targeted enhancer regions, we speculate that JAZF1 acts as chromatin modulator by recruiting TIP60's enzymatic activity. Altogether, this study uncovers JAZF1 as a member of a TIP60-containing p400 chaperone complex orchestrating H2A.Z acetylation at regulatory regions controlling the expression of genes, many of which are involved in ribosome biogenesis.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33445503',
			'doi' => '10.3390/ijms22020678',
			'modified' => '2021-12-07 10:00:44',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 50 => array(
			'id' => '4179',
			'name' => 'Histone demethylase JMJD2B/KDM4B regulates transcriptional program viadistinctive epigenetic targets and protein interactors for the maintenanceof trophoblast stem cells.',
			'authors' => 'Mak, Kylie Hin-Man et al.',
			'description' => '<p>Trophoblast stem cell (TSC) is crucial to the formation of placenta in mammals. Histone demethylase JMJD2 (also known as KDM4) family proteins have been previously shown to support self-renewal and differentiation of stem cells. However, their roles in the context of the trophoblast lineage remain unclear. Here, we find that knockdown of Jmjd2b resulted in differentiation of TSCs, suggesting an indispensable role of JMJD2B/KDM4B in maintaining the stemness. Through the integration of transcriptome and ChIP-seq profiling data, we show that JMJD2B is associated with a loss of H3K36me3 in a subset of embryonic lineage genes which are marked by H3K9me3 for stable repression. By characterizing the JMJD2B binding motifs and other transcription factor binding datasets, we discover that JMJD2B forms a protein complex with AP-2 family transcription factor TFAP2C and histone demethylase LSD1. The JMJD2B-TFAP2C-LSD1 complex predominantly occupies active gene promoters, whereas the TFAP2C-LSD1 complex is located at putative enhancers, suggesting that these proteins mediate enhancer-promoter interaction for gene regulation. We conclude that JMJD2B is vital to the TSC transcriptional program and safeguards the trophoblast cell fate via distinctive protein interactors and epigenetic targets.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33441614',
			'doi' => '10.1038/s41598-020-79601-7',
			'modified' => '2021-12-21 16:43:16',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 51 => array(
			'id' => '4210',
			'name' => 'Trans- and cis-acting effects of Firre on epigenetic features of theinactive X chromosome.',
			'authors' => 'Fang, He and Bonora, Giancarlo and Lewandowski, Jordan P and Thakur,Jitendra and Filippova, Galina N and Henikoff, Steven and Shendure, Jay andDuan, Zhijun and Rinn, John L and Deng, Xinxian and Noble, William S andDisteche, Christine M',
			'description' => '<p>Firre encodes a lncRNA involved in nuclear organization. Here, we show that Firre RNA expressed from the active X chromosome maintains histone H3K27me3 enrichment on the inactive X chromosome (Xi) in somatic cells. This trans-acting effect involves SUZ12, reflecting interactions between Firre RNA and components of the Polycomb repressive complexes. Without Firre RNA, H3K27me3 decreases on the Xi and the&nbsp;Xi-perinucleolar location is disrupted, possibly due to decreased CTCF binding on the Xi. We also observe widespread gene dysregulation, but not on the Xi. These effects are measurably rescued by ectopic expression of mouse or human Firre/FIRRE transgenes, supporting conserved trans-acting roles. We also find that the compact 3D structure of the Xi partly depends on the Firre locus and its RNA. In common lymphoid progenitors and T-cells Firre exerts a cis-acting effect on maintenance of H3K27me3 in a 26&thinsp;Mb region around the locus, demonstrating cell type-specific trans- and cis-acting roles of this lncRNA.</p>',
			'date' => '2020-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33247132',
			'doi' => '10.1038/s41467-020-19879-3',
			'modified' => '2022-01-13 15:03:45',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 52 => array(
			'id' => '4206',
			'name' => 'H2A.Z is dispensable for both basal and activated transcription inpost-mitotic mouse muscles.',
			'authors' => 'Belotti E. et al.',
			'description' => '<p>While the histone variant H2A.Z is known to be required for mitosis, it is also enriched in nucleosomes surrounding the transcription start site of active promoters, implicating H2A.Z in transcription. However, evidence obtained so far mainly rely on correlational data generated in actively dividing cells. We have exploited a paradigm in which transcription is uncoupled from the cell cycle by developing an in vivo system to inactivate H2A.Z in terminally differentiated post-mitotic muscle cells. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is a marker but not an active driver of transcription.</p>',
			'date' => '2020-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/32266374',
			'doi' => '10.1093/nar/gkaa157',
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<li><a href="https://www.diagenode.com/en/p/24-dual-indexes-for-microplex-kit-v3-48-rxns">C05010003 - 24 Dual indexes for MicroPlex Kit v3 /48 rxns</a></li>
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<li><a href="https://www.diagenode.com/en/p/96-dual-indexes-for-microplex-kit-v3-set-4">C05010007 - 96 Dual indexes for MicroPlex Kit v3 &ndash; Set IV /96 rxns</a></li>
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<p style="padding-left: 30px;">NEW! Unique dual indexes :</p>
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<li><a href="https://www.diagenode.com/en/p/24-unique-dual-indexes-for-microplex-kit-v3-set1">C05010008 - 24 UDI for MicroPlex Kit v3 - Set I</a></li>
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<p>Read more about<span>&nbsp;</span><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq">library preparation for ChIP-seq</a></p>
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