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<p>Monoclonal antibody raised in mouse against human <strong>p300</strong> (<strong>E1A Binding Protein P300</strong>) by DNA immunization in which the C-terminal part of the protein was cloned and expressed.</p>',
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<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed using HeLa cells, the Diagenode monoclonal antibody against p300 (cat. No. C15200211) and optimized PCR primer sets for qPCR. ChIP was performed with the “iDeal ChIP-seq” kit (cat. No. C01010055), using sheared chromatin from 4 million cells. A titration of the antibody consisting of 2, 5 and 10 µg per ChIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. Quantitative PCR was performed with primers for two genomic regions near the ANKRD32 and IRS2 genes, used as positive controls, and for the coding region of the inactive MYOD1 gene and an intergeic region on chromosome 11, used as negative controls. Figure 1 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</p>
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<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed with 5 µg of the Diagenode antibody against p300 (cat. No. C15200211) on sheared chromatin from 4 million HeLa cells as described above. The IP'd DNA was subsequently analysed on an Illumina NovaSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 50 bp tags were aligned to the human genome using the BWA algorithm. Figure 2 shows the peak distribution along the complete sequence and a 3 mb region of chromosome 5 (figure 2A and B) and in two regions surrounding the IRS2 and ANKRD32 (SLF1) positive control genes (figure 2C and D). The position of the amplicon used for ChIP-qPCR is indicated by an arrow.</p>
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<td>Fig 1, 2</td>
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<div class="small-6 columns"><center><img src="https://www.diagenode.com/img/product/antibodies/c15200211-chip.jpg" /></center></div>
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<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed using HeLa cells, the Diagenode monoclonal antibody against p300 (cat. No. C15200211) and optimized PCR primer sets for qPCR. ChIP was performed with the “iDeal ChIP-seq” kit (cat. No. C01010055), using sheared chromatin from 4 million cells. A titration of the antibody consisting of 2, 5 and 10 µg per ChIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. Quantitative PCR was performed with primers for two genomic regions near the ANKRD32 and IRS2 genes, used as positive controls, and for the coding region of the inactive MYOD1 gene and an intergeic region on chromosome 11, used as negative controls. Figure 1 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</p>
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<p style="text-align: center;">A.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-a.jpg" alt="p300 Antibody ChIP-seq Grade" caption="false" width="500" /></p>
<p style="text-align: center;">B.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-b.jpg" alt="p300 Antibody for ChIP-seq" caption="false" width="500" /></p>
<p style="text-align: center;">C.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-c.jpg" alt="p300 Antibody for ChIP-seq assay" caption="false" width="500" /></p>
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<p style="text-align: center;">D.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-d.jpg" alt="p300 Antibody validated in ChIP-seq" caption="false" width="500" /></p>
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<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed with 5 µg of the Diagenode antibody against p300 (cat. No. C15200211) on sheared chromatin from 4 million HeLa cells as described above. The IP'd DNA was subsequently analysed on an Illumina NovaSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 50 bp tags were aligned to the human genome using the BWA algorithm. Figure 2 shows the peak distribution along the complete sequence and a 3 mb region of chromosome 5 (figure 2A and B) and in two regions surrounding the IRS2 and ANKRD32 (SLF1) positive control genes (figure 2C and D). The position of the amplicon used for ChIP-qPCR is indicated by an arrow.</p>
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<p><br />Chromatin immunoprecipitation (<b>ChIP</b>) is a technique to study the associations of proteins with the specific genomic regions in intact cells. One of the most important steps of this protocol is the immunoprecipitation of targeted protein using the antibody specifically recognizing it. The quality of antibodies used in ChIP is essential for the success of the experiment. Diagenode offers extensively validated ChIP-grade antibodies, confirmed for their specificity, and high level of performance in ChIP. Each batch is validated, and batch-specific data are available on the website.</p>
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<p><strong>ChIP results</strong> obtained with the antibody directed against H3K4me3 (Cat. No. <a href="../p/h3k4me3-polyclonal-antibody-premium-50-ug-50-ul">C15410003</a>). </p>
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<p>Our aim at Diagenode is to offer the largest collection of highly specific <strong>ChIP-grade antibodies</strong>. We add new antibodies monthly. Find your ChIP-grade antibody in the list below and check more information about tested applications, extensive validation data, and product information.</p>',
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'description' => '<p><b>Unparalleled ChIP-Seq results with the most rigorously validated antibodies</b></p>
<p><span style="font-weight: 400;">Diagenode provides leading solutions for epigenetic research. Because ChIP-seq is a widely-used technique, we validate our antibodies in ChIP and ChIP-seq experiments (in addition to conventional methods like Western blot, Dot blot, ELISA, and immunofluorescence) to provide the highest quality antibody. We standardize our validation and production to guarantee high product quality without technical bias. Diagenode guarantees ChIP-seq grade antibody performance under our suggested conditions.</span></p>
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<div class="small-12 medium-9 large-9 columns">
<p><strong>ChIP-seq profile</strong> of active (H3K4me3 and H3K36me3) and inactive (H3K27me3) marks using Diagenode antibodies.</p>
<img src="https://www.diagenode.com/img/categories/antibodies/chip-seq-grade-antibodies.png" /></div>
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<p><small> ChIP was performed on sheared chromatin from 100,000 K562 cells using iDeal ChIP-seq kit for Histones (cat. No. C01010051) with 1 µg of the Diagenode antibodies against H3K27me3 (cat. No. C15410195) and H3K4me3 (cat. No. C15410003), and 0.5 µg of the antibody against H3K36me3 (cat. No. C15410192). The IP'd DNA was subsequently analysed on an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. The figure shows the signal distribution along the complete sequence of human chromosome 3, a zoomin to a 10 Mb region and a further zoomin to a 1.5 Mb region. </small></p>
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<p>Diagenode’s highly validated antibodies:</p>
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<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
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<li>100% satisfaction guarantee</li>
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'description' => '<h1><strong>Validated epigenetics antibodies</strong> – care for a sample?<br /> </h1>
<p>Diagenode has partnered with leading epigenetics experts and numerous epigenetics consortiums to bring to you a validated and comprehensive collection of epigenetic antibodies. As an expert in epigenetics, we are committed to offering highly-specific antibodies validated for ChIP/ChIP-seq and many other applications. All batch-specific validation data is available on our website.<br /><a href="../categories/antibodies">Read about our expertise in antibody production</a>.</p>
<ul>
<li><strong>Focused</strong> - Diagenode's selection of antibodies is exclusively dedicated for epigenetic research. <a title="See the full collection." href="../categories/all-antibodies">See the full collection.</a></li>
<li><strong>Strict quality standards</strong> with rigorous QC and validation</li>
<li><strong>Classified</strong> based on level of validation for flexibility of application</li>
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<p>Existing sample sizes are listed below. We will soon expand our collection. Are you looking for a sample size of another antibody? Just <a href="mailto:agnieszka.zelisko@diagenode.com?Subject=Sample%20Size%20Request" target="_top">Contact us</a>.</p>',
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'description' => '<p><span style="font-weight: 400;">All Diagenode’s antibodies are listed below. Please, use our Quick search field to find the antibody of interest by target name, application, purity.</span></p>
<p><span style="font-weight: 400;">Diagenode’s highly validated antibodies:</span></p>
<ul>
<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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'meta_title' => 'Diagenode's selection of Antibodies is exclusively dedicated for Epigenetic Research | Diagenode',
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'description' => '<p><span style="font-weight: 400;">Diagenode’s large range of highly validated antibodies includes the antibodies to study chromatin-associated proteins. These antibodies have been thoroughly validated for many applications (ChIP, ChIP-seq, WB, IF, ELISA, Dot blot, IHC, IP). Check out all of our highly sensitive and specific antibodies for chromatin-associated proteins studies below.</span></p>
<p><span style="font-weight: 400;">Diagenode’s highly validated antibodies:</span></p>
<ul>
<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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'description' => '<p style="text-align: justify;"><span>Epigenetic research tools have evolved over time from endpoint PCR to qPCR to the analyses of large sets of genome-wide sequencing data. ChIP sequencing (ChIP-seq) has now become the gold standard method for chromatin studies, given the accuracy and coverage scale of the approach over other methods. Successful ChIP-seq, however, requires a higher level of experimental accuracy and consistency in all steps of ChIP than ever before. Particularly crucial is the quality of ChIP antibodies. </span></p>',
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'name' => 'Datasheet p300 C15200211',
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'authors' => 'Sylvestre M. et al.',
'description' => '<p><span>Mature lymphoid stromal cells (LSCs) are key organizers of immune responses within secondary lymphoid organs. Similarly, inflammation-driven tertiary lymphoid structures depend on immunofibroblasts producing lymphoid cytokines and chemokines. Recent studies have explored the origin and heterogeneity of LSC/immunofibroblasts, yet the molecular and epigenetic mechanisms involved in their commitment are still unknown. This study explored the transcriptomic and epigenetic reprogramming underlying LSC/immunofibroblast commitment. We identified the induction of lysine demethylase 6B (KDM6B) as the primary epigenetic driver of early immunofibroblast differentiation. In addition, we observed an enrichment for KDM6B gene signature in murine inflammatory fibroblasts and pathogenic stroma of patients with autoimmune diseases. Last, KDM6B was required for the acquisition of LSC/immunofibroblast functional properties, including the up-regulation of CCL2 and the resulting recruitment of monocytes. Overall, our results reveal epigenetic mechanisms that participate in the early commitment and immune properties of immunofibroblasts and support the use of epigenetic modifiers as fibroblast-targeting strategies in chronic inflammation.</span></p>',
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'description' => '<p>Spalt-like transcription factor 1 (SALL1) is a critical regulator of organogenesis and microglia identity. Here we demonstrate that disruption of a conserved microglia-specific super-enhancer interacting with the Sall1 promoter results in complete and specific loss of Sall1 expression in microglia. By determining the genomic binding sites of SALL1 and leveraging Sall1 enhancer knockout mice, we provide evidence for functional interactions between SALL1 and SMAD4 required for microglia-specific gene expression. SMAD4 binds directly to the Sall1 super-enhancer and is required for Sall1 expression, consistent with an evolutionarily conserved requirement of the TGFβ and SMAD homologs Dpp and Mad for cell-specific expression of Spalt in the Drosophila wing. Unexpectedly, SALL1 in turn promotes binding and function of SMAD4 at microglia-specific enhancers while simultaneously suppressing binding of SMAD4 to enhancers of genes that become inappropriately activated in enhancer knockout microglia, thereby enforcing microglia-specific functions of the TGFβ-SMAD signaling axis.</p>',
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'description' => '<p>The glucocorticoid (GR) and androgen (AR) receptors execute unique functions in vivo, yet have nearly identical DNA binding specificities. To identify mechanisms that facilitate functional diversification among these transcription factor paralogs, we studied them in an equivalent cellular context. Analysis of chromatin and sequence suggest that divergent binding, and corresponding gene regulation, are driven by different abilities of AR and GR to interact with relatively inaccessible chromatin. Divergent genomic binding patterns can also be the result of subtle differences in DNA binding preference between AR and GR. Furthermore, the sequence composition of large regions (>10 kb) surrounding selectively occupied binding sites differs significantly, indicating a role for the sequence environment in guiding AR and GR to distinct binding sites. The comparison of binding sites that are shared shows that the specificity paradox can also be resolved by differences in the events that occur downstream of receptor binding. Specifically, shared binding sites display receptor-specific enhancer activity, cofactor recruitment and changes in histone modifications. Genomic deletion of shared binding sites demonstrates their contribution to directing receptor-specific gene regulation. Together, these data suggest that differences in genomic occupancy as well as divergence in the events that occur downstream of receptor binding direct functional diversification among transcription factor paralogs.</p>',
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'name' => 'Niche-Specific Reprogramming of Epigenetic Landscapes Drives Myeloid Cell Diversity in Nonalcoholic Steatohepatitis.',
'authors' => 'Seidman JS, Troutman TD, Sakai M, Gola A, Spann NJ, Bennett H, Bruni CM, Ouyang Z, Li RZ, Sun X, Vu BT, Pasillas MP, Ego KM, Gosselin D, Link VM, Chong LW, Evans RM, Thompson BM, McDonald JG, Hosseini M, Witztum JL, Germain RN, Glass CK',
'description' => '<p>Tissue-resident and recruited macrophages contribute to both host defense and pathology. Multiple macrophage phenotypes are represented in diseased tissues, but we lack deep understanding of mechanisms controlling diversification. Here, we investigate origins and epigenetic trajectories of hepatic macrophages during diet-induced non-alcoholic steatohepatitis (NASH). The NASH diet induced significant changes in Kupffer cell enhancers and gene expression, resulting in partial loss of Kupffer cell identity, induction of Trem2 and Cd9 expression, and cell death. Kupffer cell loss was compensated by gain of adjacent monocyte-derived macrophages that exhibited convergent epigenomes, transcriptomes, and functions. NASH-induced changes in Kupffer cell enhancers were driven by AP-1 and EGR that reprogrammed LXR functions required for Kupffer cell identity and survival to instead drive a scar-associated macrophage phenotype. These findings reveal mechanisms by which disease-associated environmental signals instruct resident and recruited macrophages to acquire distinct gene expression programs and corresponding functions.</p>',
'date' => '2020-04-28',
'pmid' => 'http://www.pubmed.gov/32362324',
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'name' => 'The TGF-β profibrotic cascade targets ecto-5'-nucleotidase gene in proximal tubule epithelial cells and is a traceable marker of progressive diabetic kidney disease.',
'authors' => 'Cappelli C, Tellez A, Jara C, Alarcón S, Torres A, Mendoza P, Podestá L, Flores C, Quezada C, Oyarzún C, Martín RS',
'description' => '<p>Progressive diabetic nephropathy (DN) and loss of renal function correlate with kidney fibrosis. Crosstalk between TGF-β and adenosinergic signaling contributes to the phenotypic transition of cells and to renal fibrosis in DN models. We evaluated the role of TGF-β on NT5E gene expression coding for the ecto-5`-nucleotidase CD73, the limiting enzyme in extracellular adenosine production. We showed that high d-glucose may predispose HK-2 cells towards active transcription of the proximal promoter region of the NT5E gene while additional TGF-β results in full activation. The epigenetic landscape of the NT5E gene promoter was modified by concurrent TGF-β with occupancy by the p300 co-activator and the phosphorylated forms of the Smad2/3 complex and RNA Pol II. Transcriptional induction at NT5E in response to TGF-β was earlier compared to the classic responsiveness genes PAI-1 and Fn1. CD73 levels and AMPase activity were concomitantly increased by TGF-β in HK-2 cells. Interestingly, we found increased CD73 content in urinary extracellular vesicles only in diabetic patients with renal repercussions. Further, CD73-mediated AMPase activity was increased in the urinary sediment of DN patients. We conclude that the NT5E gene is a target of the profibrotic TGF-β cascade and is a traceable marker of progressive DN.</p>',
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'name' => 'p300 Antibody',
'description' => '<p>Alternative names: <strong>EP300</strong>, <strong>KAT3B</strong>, <strong>RSTS2</strong></p>
<p>Monoclonal antibody raised in mouse against human <strong>p300</strong> (<strong>E1A Binding Protein P300</strong>) by DNA immunization in which the C-terminal part of the protein was cloned and expressed.</p>',
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<div class="small-6 columns"><center><img src="https://www.diagenode.com/img/product/antibodies/c15200211-chip.jpg" /></center></div>
<div class="small-6 columns">
<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed using HeLa cells, the Diagenode monoclonal antibody against p300 (cat. No. C15200211) and optimized PCR primer sets for qPCR. ChIP was performed with the “iDeal ChIP-seq” kit (cat. No. C01010055), using sheared chromatin from 4 million cells. A titration of the antibody consisting of 2, 5 and 10 µg per ChIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. Quantitative PCR was performed with primers for two genomic regions near the ANKRD32 and IRS2 genes, used as positive controls, and for the coding region of the inactive MYOD1 gene and an intergeic region on chromosome 11, used as negative controls. Figure 1 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</p>
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<div class="row">
<div class="small-12 columns"><center>
<p style="text-align: center;">A.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-a.jpg" alt="p300 Antibody ChIP-seq Grade" caption="false" width="500" /></p>
<p style="text-align: center;">B.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-b.jpg" alt="p300 Antibody for ChIP-seq" caption="false" width="500" /></p>
<p style="text-align: center;">C.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-c.jpg" alt="p300 Antibody for ChIP-seq assay" caption="false" width="500" /></p>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<p style="text-align: center;">D.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-d.jpg" alt="p300 Antibody validated in ChIP-seq" caption="false" width="500" /></p>
</center></div>
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<div class="row">
<div class="small-12 columns">
<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed with 5 µg of the Diagenode antibody against p300 (cat. No. C15200211) on sheared chromatin from 4 million HeLa cells as described above. The IP'd DNA was subsequently analysed on an Illumina NovaSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 50 bp tags were aligned to the human genome using the BWA algorithm. Figure 2 shows the peak distribution along the complete sequence and a 3 mb region of chromosome 5 (figure 2A and B) and in two regions surrounding the IRS2 and ANKRD32 (SLF1) positive control genes (figure 2C and D). The position of the amplicon used for ChIP-qPCR is indicated by an arrow.</p>
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'info2' => '<p>p300 (UniProt/Swiss-Prot entry Q09472) is a histone acetyltransferase that regulates transcription via chromatin remodelling. As such it is important for cell proliferation and differentiation. p300 is able to acetylate all four core histones in nucleosomes. Acetylation of histones is associated with transcriptional activation. p300 also acetylates non-histone proteins such as HDAC1 leading to its inactivation and modulation of transcription. It has also been identified as a co-activator of HIF1A (hypoxiainducible factor 1 alpha), and thus plays a role in the stimulation of hypoxia-induced genes such as VEGF. Defects in the p300 gene are a cause of Rubinstein-Taybi syndrome and may also play a role in epithelial cancer.</p>',
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<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
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'meta_title' => 'p300 monoclonal antibody (sample size)',
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'description' => 'p300 (UniProt/Swiss-Prot entry Q09472) is a histone acetyltransferase that regulates transcription via chromatin remodelling. As such it is important for cell proliferation and differentiation. p300 is able to acetylate all four core histones in nucleosomes. Acetylation of histones is associated with transcriptional activation. p300 also acetylates non-histone proteins such as HDAC1 leading to its inactivation and modulation of transcription. It has also been identified as a co-activator of HIF1A (hypoxia- inducible factor 1 alpha), and thus plays a role in the stimulation of hypoxia-induced genes such as VEGF. Defects in the p300 gene are a cause of Rubinstein-Taybi syndrome and may also play a role in epithelial cancer.',
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'isotype' => ' IgG3',
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'concentration' => '1.8 µg/µl',
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'type' => 'Monoclonal',
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<thead>
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<th>Applications</th>
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<th>References</th>
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<td>ChIP/ChIP-seq <sup>*</sup></td>
<td>2-5 μg/ChIP</td>
<td>Fig 1, 2</td>
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<tr>
<td>Western Blotting</td>
<td>Not Recommended</td>
<td></td>
</tr>
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<p><small><sup>*</sup> Please note that the optimal antibody amount per IP should be determined by the end-user. We recommend testing 1-10 μg per IP.</small></p>',
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'description' => '<p>Alternative names: <strong>EP300</strong>, <strong>KAT3B</strong>, <strong>RSTS2</strong></p>
<p>Monoclonal antibody raised in mouse against human <strong>p300</strong> (<strong>E1A Binding Protein P300</strong>) by DNA immunization in which the C-terminal part of the protein was cloned and expressed.</p>',
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<div class="small-6 columns"><center><img src="https://www.diagenode.com/img/product/antibodies/c15200211-chip.jpg" /></center></div>
<div class="small-6 columns">
<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed using HeLa cells, the Diagenode monoclonal antibody against p300 (cat. No. C15200211) and optimized PCR primer sets for qPCR. ChIP was performed with the “iDeal ChIP-seq” kit (cat. No. C01010055), using sheared chromatin from 4 million cells. A titration of the antibody consisting of 2, 5 and 10 µg per ChIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. Quantitative PCR was performed with primers for two genomic regions near the ANKRD32 and IRS2 genes, used as positive controls, and for the coding region of the inactive MYOD1 gene and an intergeic region on chromosome 11, used as negative controls. Figure 1 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</p>
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<div class="row">
<div class="small-12 columns"><center>
<p style="text-align: center;">A.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-a.jpg" alt="p300 Antibody ChIP-seq Grade" caption="false" width="500" /></p>
<p style="text-align: center;">B.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-b.jpg" alt="p300 Antibody for ChIP-seq" caption="false" width="500" /></p>
<p style="text-align: center;">C.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-c.jpg" alt="p300 Antibody for ChIP-seq assay" caption="false" width="500" /></p>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<p style="text-align: center;">D.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-d.jpg" alt="p300 Antibody validated in ChIP-seq" caption="false" width="500" /></p>
</center></div>
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<div class="row">
<div class="small-12 columns">
<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed with 5 µg of the Diagenode antibody against p300 (cat. No. C15200211) on sheared chromatin from 4 million HeLa cells as described above. The IP'd DNA was subsequently analysed on an Illumina NovaSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 50 bp tags were aligned to the human genome using the BWA algorithm. Figure 2 shows the peak distribution along the complete sequence and a 3 mb region of chromosome 5 (figure 2A and B) and in two regions surrounding the IRS2 and ANKRD32 (SLF1) positive control genes (figure 2C and D). The position of the amplicon used for ChIP-qPCR is indicated by an arrow.</p>
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<p><br />Chromatin immunoprecipitation (<b>ChIP</b>) is a technique to study the associations of proteins with the specific genomic regions in intact cells. One of the most important steps of this protocol is the immunoprecipitation of targeted protein using the antibody specifically recognizing it. The quality of antibodies used in ChIP is essential for the success of the experiment. Diagenode offers extensively validated ChIP-grade antibodies, confirmed for their specificity, and high level of performance in ChIP. Each batch is validated, and batch-specific data are available on the website.</p>
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<p><strong>ChIP results</strong> obtained with the antibody directed against H3K4me3 (Cat. No. <a href="../p/h3k4me3-polyclonal-antibody-premium-50-ug-50-ul">C15410003</a>). </p>
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<p>Our aim at Diagenode is to offer the largest collection of highly specific <strong>ChIP-grade antibodies</strong>. We add new antibodies monthly. Find your ChIP-grade antibody in the list below and check more information about tested applications, extensive validation data, and product information.</p>',
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<p><span style="font-weight: 400;">Diagenode provides leading solutions for epigenetic research. Because ChIP-seq is a widely-used technique, we validate our antibodies in ChIP and ChIP-seq experiments (in addition to conventional methods like Western blot, Dot blot, ELISA, and immunofluorescence) to provide the highest quality antibody. We standardize our validation and production to guarantee high product quality without technical bias. Diagenode guarantees ChIP-seq grade antibody performance under our suggested conditions.</span></p>
<div class="row">
<div class="small-12 medium-9 large-9 columns">
<p><strong>ChIP-seq profile</strong> of active (H3K4me3 and H3K36me3) and inactive (H3K27me3) marks using Diagenode antibodies.</p>
<img src="https://www.diagenode.com/img/categories/antibodies/chip-seq-grade-antibodies.png" /></div>
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<p><small> ChIP was performed on sheared chromatin from 100,000 K562 cells using iDeal ChIP-seq kit for Histones (cat. No. C01010051) with 1 µg of the Diagenode antibodies against H3K27me3 (cat. No. C15410195) and H3K4me3 (cat. No. C15410003), and 0.5 µg of the antibody against H3K36me3 (cat. No. C15410192). The IP'd DNA was subsequently analysed on an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. The figure shows the signal distribution along the complete sequence of human chromosome 3, a zoomin to a 10 Mb region and a further zoomin to a 1.5 Mb region. </small></p>
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<p>Diagenode’s highly validated antibodies:</p>
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<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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<p>Diagenode has partnered with leading epigenetics experts and numerous epigenetics consortiums to bring to you a validated and comprehensive collection of epigenetic antibodies. As an expert in epigenetics, we are committed to offering highly-specific antibodies validated for ChIP/ChIP-seq and many other applications. All batch-specific validation data is available on our website.<br /><a href="../categories/antibodies">Read about our expertise in antibody production</a>.</p>
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<li><strong>Focused</strong> - Diagenode's selection of antibodies is exclusively dedicated for epigenetic research. <a title="See the full collection." href="../categories/all-antibodies">See the full collection.</a></li>
<li><strong>Strict quality standards</strong> with rigorous QC and validation</li>
<li><strong>Classified</strong> based on level of validation for flexibility of application</li>
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<p>Existing sample sizes are listed below. We will soon expand our collection. Are you looking for a sample size of another antibody? Just <a href="mailto:agnieszka.zelisko@diagenode.com?Subject=Sample%20Size%20Request" target="_top">Contact us</a>.</p>',
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<p><span style="font-weight: 400;">Diagenode’s highly validated antibodies:</span></p>
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<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
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<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
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'name' => 'KDM6B drives epigenetic reprogramming associated with lymphoid stromal cell early commitment and immune properties',
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'description' => '<p><span>Mature lymphoid stromal cells (LSCs) are key organizers of immune responses within secondary lymphoid organs. Similarly, inflammation-driven tertiary lymphoid structures depend on immunofibroblasts producing lymphoid cytokines and chemokines. Recent studies have explored the origin and heterogeneity of LSC/immunofibroblasts, yet the molecular and epigenetic mechanisms involved in their commitment are still unknown. This study explored the transcriptomic and epigenetic reprogramming underlying LSC/immunofibroblast commitment. We identified the induction of lysine demethylase 6B (KDM6B) as the primary epigenetic driver of early immunofibroblast differentiation. In addition, we observed an enrichment for KDM6B gene signature in murine inflammatory fibroblasts and pathogenic stroma of patients with autoimmune diseases. Last, KDM6B was required for the acquisition of LSC/immunofibroblast functional properties, including the up-regulation of CCL2 and the resulting recruitment of monocytes. Overall, our results reveal epigenetic mechanisms that participate in the early commitment and immune properties of immunofibroblasts and support the use of epigenetic modifiers as fibroblast-targeting strategies in chronic inflammation.</span></p>',
'date' => '2023-11-29',
'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/38019914/',
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'description' => '<p>Spalt-like transcription factor 1 (SALL1) is a critical regulator of organogenesis and microglia identity. Here we demonstrate that disruption of a conserved microglia-specific super-enhancer interacting with the Sall1 promoter results in complete and specific loss of Sall1 expression in microglia. By determining the genomic binding sites of SALL1 and leveraging Sall1 enhancer knockout mice, we provide evidence for functional interactions between SALL1 and SMAD4 required for microglia-specific gene expression. SMAD4 binds directly to the Sall1 super-enhancer and is required for Sall1 expression, consistent with an evolutionarily conserved requirement of the TGFβ and SMAD homologs Dpp and Mad for cell-specific expression of Spalt in the Drosophila wing. Unexpectedly, SALL1 in turn promotes binding and function of SMAD4 at microglia-specific enhancers while simultaneously suppressing binding of SMAD4 to enhancers of genes that become inappropriately activated in enhancer knockout microglia, thereby enforcing microglia-specific functions of the TGFβ-SMAD signaling axis.</p>',
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'url' => 'files/SDS/p300/SDS-C15200211-p300_Antibody-ES-es-GHS_2_0.pdf',
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'description' => '<p>Progressive diabetic nephropathy (DN) and loss of renal function correlate with kidney fibrosis. Crosstalk between TGF-β and adenosinergic signaling contributes to the phenotypic transition of cells and to renal fibrosis in DN models. We evaluated the role of TGF-β on NT5E gene expression coding for the ecto-5`-nucleotidase CD73, the limiting enzyme in extracellular adenosine production. We showed that high d-glucose may predispose HK-2 cells towards active transcription of the proximal promoter region of the NT5E gene while additional TGF-β results in full activation. The epigenetic landscape of the NT5E gene promoter was modified by concurrent TGF-β with occupancy by the p300 co-activator and the phosphorylated forms of the Smad2/3 complex and RNA Pol II. Transcriptional induction at NT5E in response to TGF-β was earlier compared to the classic responsiveness genes PAI-1 and Fn1. CD73 levels and AMPase activity were concomitantly increased by TGF-β in HK-2 cells. Interestingly, we found increased CD73 content in urinary extracellular vesicles only in diabetic patients with renal repercussions. Further, CD73-mediated AMPase activity was increased in the urinary sediment of DN patients. We conclude that the NT5E gene is a target of the profibrotic TGF-β cascade and is a traceable marker of progressive DN.</p>',
'date' => '2020-04-11',
'pmid' => 'http://www.pubmed.gov/32289379',
'doi' => '10.1016/j.bbadis.2020.165796',
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<p><strong>ChIP results</strong> obtained with the antibody directed against H3K4me3 (Cat. No. <a href="../p/h3k4me3-polyclonal-antibody-premium-50-ug-50-ul">C15410003</a>). </p>
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<p>Our aim at Diagenode is to offer the largest collection of highly specific <strong>ChIP-grade antibodies</strong>. We add new antibodies monthly. Find your ChIP-grade antibody in the list below and check more information about tested applications, extensive validation data, and product information.</p>',
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'description' => '<p><b>Unparalleled ChIP-Seq results with the most rigorously validated antibodies</b></p>
<p><span style="font-weight: 400;">Diagenode provides leading solutions for epigenetic research. Because ChIP-seq is a widely-used technique, we validate our antibodies in ChIP and ChIP-seq experiments (in addition to conventional methods like Western blot, Dot blot, ELISA, and immunofluorescence) to provide the highest quality antibody. We standardize our validation and production to guarantee high product quality without technical bias. Diagenode guarantees ChIP-seq grade antibody performance under our suggested conditions.</span></p>
<div class="row">
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<p><strong>ChIP-seq profile</strong> of active (H3K4me3 and H3K36me3) and inactive (H3K27me3) marks using Diagenode antibodies.</p>
<img src="https://www.diagenode.com/img/categories/antibodies/chip-seq-grade-antibodies.png" /></div>
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<p><small> ChIP was performed on sheared chromatin from 100,000 K562 cells using iDeal ChIP-seq kit for Histones (cat. No. C01010051) with 1 µg of the Diagenode antibodies against H3K27me3 (cat. No. C15410195) and H3K4me3 (cat. No. C15410003), and 0.5 µg of the antibody against H3K36me3 (cat. No. C15410192). The IP'd DNA was subsequently analysed on an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. The figure shows the signal distribution along the complete sequence of human chromosome 3, a zoomin to a 10 Mb region and a further zoomin to a 1.5 Mb region. </small></p>
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<p>Diagenode’s highly validated antibodies:</p>
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<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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'description' => '<h1><strong>Validated epigenetics antibodies</strong> – care for a sample?<br /> </h1>
<p>Diagenode has partnered with leading epigenetics experts and numerous epigenetics consortiums to bring to you a validated and comprehensive collection of epigenetic antibodies. As an expert in epigenetics, we are committed to offering highly-specific antibodies validated for ChIP/ChIP-seq and many other applications. All batch-specific validation data is available on our website.<br /><a href="../categories/antibodies">Read about our expertise in antibody production</a>.</p>
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<li><strong>Focused</strong> - Diagenode's selection of antibodies is exclusively dedicated for epigenetic research. <a title="See the full collection." href="../categories/all-antibodies">See the full collection.</a></li>
<li><strong>Strict quality standards</strong> with rigorous QC and validation</li>
<li><strong>Classified</strong> based on level of validation for flexibility of application</li>
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<p>Existing sample sizes are listed below. We will soon expand our collection. Are you looking for a sample size of another antibody? Just <a href="mailto:agnieszka.zelisko@diagenode.com?Subject=Sample%20Size%20Request" target="_top">Contact us</a>.</p>',
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'description' => '<p><span style="font-weight: 400;">All Diagenode’s antibodies are listed below. Please, use our Quick search field to find the antibody of interest by target name, application, purity.</span></p>
<p><span style="font-weight: 400;">Diagenode’s highly validated antibodies:</span></p>
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<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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<p><span style="font-weight: 400;">Diagenode’s highly validated antibodies:</span></p>
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<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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'description' => '<p>Tissue-resident and recruited macrophages contribute to both host defense and pathology. Multiple macrophage phenotypes are represented in diseased tissues, but we lack deep understanding of mechanisms controlling diversification. Here, we investigate origins and epigenetic trajectories of hepatic macrophages during diet-induced non-alcoholic steatohepatitis (NASH). The NASH diet induced significant changes in Kupffer cell enhancers and gene expression, resulting in partial loss of Kupffer cell identity, induction of Trem2 and Cd9 expression, and cell death. Kupffer cell loss was compensated by gain of adjacent monocyte-derived macrophages that exhibited convergent epigenomes, transcriptomes, and functions. NASH-induced changes in Kupffer cell enhancers were driven by AP-1 and EGR that reprogrammed LXR functions required for Kupffer cell identity and survival to instead drive a scar-associated macrophage phenotype. These findings reveal mechanisms by which disease-associated environmental signals instruct resident and recruited macrophages to acquire distinct gene expression programs and corresponding functions.</p>',
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'description' => '<p>Alternative names: <strong>EP300</strong>, <strong>KAT3B</strong>, <strong>RSTS2</strong></p>
<p>Monoclonal antibody raised in mouse against human <strong>p300</strong> (<strong>E1A Binding Protein P300</strong>) by DNA immunization in which the C-terminal part of the protein was cloned and expressed.</p>',
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<div class="small-6 columns"><center><img src="https://www.diagenode.com/img/product/antibodies/c15200211-chip.jpg" /></center></div>
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<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
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<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
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<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed using HeLa cells, the Diagenode monoclonal antibody against p300 (cat. No. C15200211) and optimized PCR primer sets for qPCR. ChIP was performed with the “iDeal ChIP-seq” kit (cat. No. C01010055), using sheared chromatin from 4 million cells. A titration of the antibody consisting of 2, 5 and 10 µg per ChIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. Quantitative PCR was performed with primers for two genomic regions near the ANKRD32 and IRS2 genes, used as positive controls, and for the coding region of the inactive MYOD1 gene and an intergeic region on chromosome 11, used as negative controls. Figure 1 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</p>
</div>
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<div class="row">
<div class="small-12 columns"><center>
<p style="text-align: center;">A.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-a.jpg" alt="p300 Antibody ChIP-seq Grade" caption="false" width="500" /></p>
<p style="text-align: center;">B.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-b.jpg" alt="p300 Antibody for ChIP-seq" caption="false" width="500" /></p>
<p style="text-align: center;">C.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-c.jpg" alt="p300 Antibody for ChIP-seq assay" caption="false" width="500" /></p>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<p style="text-align: center;">D.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-d.jpg" alt="p300 Antibody validated in ChIP-seq" caption="false" width="500" /></p>
</center></div>
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<div class="row">
<div class="small-12 columns">
<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed with 5 µg of the Diagenode antibody against p300 (cat. No. C15200211) on sheared chromatin from 4 million HeLa cells as described above. The IP'd DNA was subsequently analysed on an Illumina NovaSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 50 bp tags were aligned to the human genome using the BWA algorithm. Figure 2 shows the peak distribution along the complete sequence and a 3 mb region of chromosome 5 (figure 2A and B) and in two regions surrounding the IRS2 and ANKRD32 (SLF1) positive control genes (figure 2C and D). The position of the amplicon used for ChIP-qPCR is indicated by an arrow.</p>
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<td>ChIP/ChIP-seq <sup>*</sup></td>
<td>2-5 μg/ChIP</td>
<td>Fig 1, 2</td>
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<td>Western Blotting</td>
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<p><small><sup>*</sup> Please note that the optimal antibody amount per IP should be determined by the end-user. We recommend testing 1-10 μg per IP.</small></p>',
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<p>Monoclonal antibody raised in mouse against human <strong>p300</strong> (<strong>E1A Binding Protein P300</strong>) by DNA immunization in which the C-terminal part of the protein was cloned and expressed.</p>',
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<div class="small-6 columns"><center><img src="https://www.diagenode.com/img/product/antibodies/c15200211-chip.jpg" /></center></div>
<div class="small-6 columns">
<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed using HeLa cells, the Diagenode monoclonal antibody against p300 (cat. No. C15200211) and optimized PCR primer sets for qPCR. ChIP was performed with the “iDeal ChIP-seq” kit (cat. No. C01010055), using sheared chromatin from 4 million cells. A titration of the antibody consisting of 2, 5 and 10 µg per ChIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. Quantitative PCR was performed with primers for two genomic regions near the ANKRD32 and IRS2 genes, used as positive controls, and for the coding region of the inactive MYOD1 gene and an intergeic region on chromosome 11, used as negative controls. Figure 1 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</p>
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<p style="text-align: center;">A.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-a.jpg" alt="p300 Antibody ChIP-seq Grade" caption="false" width="500" /></p>
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<p style="text-align: center;">C.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-c.jpg" alt="p300 Antibody for ChIP-seq assay" caption="false" width="500" /></p>
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<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed with 5 µg of the Diagenode antibody against p300 (cat. No. C15200211) on sheared chromatin from 4 million HeLa cells as described above. The IP'd DNA was subsequently analysed on an Illumina NovaSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 50 bp tags were aligned to the human genome using the BWA algorithm. Figure 2 shows the peak distribution along the complete sequence and a 3 mb region of chromosome 5 (figure 2A and B) and in two regions surrounding the IRS2 and ANKRD32 (SLF1) positive control genes (figure 2C and D). The position of the amplicon used for ChIP-qPCR is indicated by an arrow.</p>
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<p><br />Chromatin immunoprecipitation (<b>ChIP</b>) is a technique to study the associations of proteins with the specific genomic regions in intact cells. One of the most important steps of this protocol is the immunoprecipitation of targeted protein using the antibody specifically recognizing it. The quality of antibodies used in ChIP is essential for the success of the experiment. Diagenode offers extensively validated ChIP-grade antibodies, confirmed for their specificity, and high level of performance in ChIP. Each batch is validated, and batch-specific data are available on the website.</p>
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<p><strong>ChIP results</strong> obtained with the antibody directed against H3K4me3 (Cat. No. <a href="../p/h3k4me3-polyclonal-antibody-premium-50-ug-50-ul">C15410003</a>). </p>
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<p>Our aim at Diagenode is to offer the largest collection of highly specific <strong>ChIP-grade antibodies</strong>. We add new antibodies monthly. Find your ChIP-grade antibody in the list below and check more information about tested applications, extensive validation data, and product information.</p>',
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<p><span style="font-weight: 400;">Diagenode provides leading solutions for epigenetic research. Because ChIP-seq is a widely-used technique, we validate our antibodies in ChIP and ChIP-seq experiments (in addition to conventional methods like Western blot, Dot blot, ELISA, and immunofluorescence) to provide the highest quality antibody. We standardize our validation and production to guarantee high product quality without technical bias. Diagenode guarantees ChIP-seq grade antibody performance under our suggested conditions.</span></p>
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<p><strong>ChIP-seq profile</strong> of active (H3K4me3 and H3K36me3) and inactive (H3K27me3) marks using Diagenode antibodies.</p>
<img src="https://www.diagenode.com/img/categories/antibodies/chip-seq-grade-antibodies.png" /></div>
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<p>Diagenode’s highly validated antibodies:</p>
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<p>Diagenode has partnered with leading epigenetics experts and numerous epigenetics consortiums to bring to you a validated and comprehensive collection of epigenetic antibodies. As an expert in epigenetics, we are committed to offering highly-specific antibodies validated for ChIP/ChIP-seq and many other applications. All batch-specific validation data is available on our website.<br /><a href="../categories/antibodies">Read about our expertise in antibody production</a>.</p>
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<li><strong>Focused</strong> - Diagenode's selection of antibodies is exclusively dedicated for epigenetic research. <a title="See the full collection." href="../categories/all-antibodies">See the full collection.</a></li>
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<p><span style="font-weight: 400;">Diagenode’s highly validated antibodies:</span></p>
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'name' => 'KDM6B drives epigenetic reprogramming associated with lymphoid stromal cell early commitment and immune properties',
'authors' => 'Sylvestre M. et al.',
'description' => '<p><span>Mature lymphoid stromal cells (LSCs) are key organizers of immune responses within secondary lymphoid organs. Similarly, inflammation-driven tertiary lymphoid structures depend on immunofibroblasts producing lymphoid cytokines and chemokines. Recent studies have explored the origin and heterogeneity of LSC/immunofibroblasts, yet the molecular and epigenetic mechanisms involved in their commitment are still unknown. This study explored the transcriptomic and epigenetic reprogramming underlying LSC/immunofibroblast commitment. We identified the induction of lysine demethylase 6B (KDM6B) as the primary epigenetic driver of early immunofibroblast differentiation. In addition, we observed an enrichment for KDM6B gene signature in murine inflammatory fibroblasts and pathogenic stroma of patients with autoimmune diseases. Last, KDM6B was required for the acquisition of LSC/immunofibroblast functional properties, including the up-regulation of CCL2 and the resulting recruitment of monocytes. Overall, our results reveal epigenetic mechanisms that participate in the early commitment and immune properties of immunofibroblasts and support the use of epigenetic modifiers as fibroblast-targeting strategies in chronic inflammation.</span></p>',
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'description' => '<p>Spalt-like transcription factor 1 (SALL1) is a critical regulator of organogenesis and microglia identity. Here we demonstrate that disruption of a conserved microglia-specific super-enhancer interacting with the Sall1 promoter results in complete and specific loss of Sall1 expression in microglia. By determining the genomic binding sites of SALL1 and leveraging Sall1 enhancer knockout mice, we provide evidence for functional interactions between SALL1 and SMAD4 required for microglia-specific gene expression. SMAD4 binds directly to the Sall1 super-enhancer and is required for Sall1 expression, consistent with an evolutionarily conserved requirement of the TGFβ and SMAD homologs Dpp and Mad for cell-specific expression of Spalt in the Drosophila wing. Unexpectedly, SALL1 in turn promotes binding and function of SMAD4 at microglia-specific enhancers while simultaneously suppressing binding of SMAD4 to enhancers of genes that become inappropriately activated in enhancer knockout microglia, thereby enforcing microglia-specific functions of the TGFβ-SMAD signaling axis.</p>',
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'description' => '<p>The glucocorticoid (GR) and androgen (AR) receptors execute unique functions in vivo, yet have nearly identical DNA binding specificities. To identify mechanisms that facilitate functional diversification among these transcription factor paralogs, we studied them in an equivalent cellular context. Analysis of chromatin and sequence suggest that divergent binding, and corresponding gene regulation, are driven by different abilities of AR and GR to interact with relatively inaccessible chromatin. Divergent genomic binding patterns can also be the result of subtle differences in DNA binding preference between AR and GR. Furthermore, the sequence composition of large regions (>10 kb) surrounding selectively occupied binding sites differs significantly, indicating a role for the sequence environment in guiding AR and GR to distinct binding sites. The comparison of binding sites that are shared shows that the specificity paradox can also be resolved by differences in the events that occur downstream of receptor binding. Specifically, shared binding sites display receptor-specific enhancer activity, cofactor recruitment and changes in histone modifications. Genomic deletion of shared binding sites demonstrates their contribution to directing receptor-specific gene regulation. Together, these data suggest that differences in genomic occupancy as well as divergence in the events that occur downstream of receptor binding direct functional diversification among transcription factor paralogs.</p>',
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'authors' => 'Seidman JS, Troutman TD, Sakai M, Gola A, Spann NJ, Bennett H, Bruni CM, Ouyang Z, Li RZ, Sun X, Vu BT, Pasillas MP, Ego KM, Gosselin D, Link VM, Chong LW, Evans RM, Thompson BM, McDonald JG, Hosseini M, Witztum JL, Germain RN, Glass CK',
'description' => '<p>Tissue-resident and recruited macrophages contribute to both host defense and pathology. Multiple macrophage phenotypes are represented in diseased tissues, but we lack deep understanding of mechanisms controlling diversification. Here, we investigate origins and epigenetic trajectories of hepatic macrophages during diet-induced non-alcoholic steatohepatitis (NASH). The NASH diet induced significant changes in Kupffer cell enhancers and gene expression, resulting in partial loss of Kupffer cell identity, induction of Trem2 and Cd9 expression, and cell death. Kupffer cell loss was compensated by gain of adjacent monocyte-derived macrophages that exhibited convergent epigenomes, transcriptomes, and functions. NASH-induced changes in Kupffer cell enhancers were driven by AP-1 and EGR that reprogrammed LXR functions required for Kupffer cell identity and survival to instead drive a scar-associated macrophage phenotype. These findings reveal mechanisms by which disease-associated environmental signals instruct resident and recruited macrophages to acquire distinct gene expression programs and corresponding functions.</p>',
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'description' => '<p>Progressive diabetic nephropathy (DN) and loss of renal function correlate with kidney fibrosis. Crosstalk between TGF-β and adenosinergic signaling contributes to the phenotypic transition of cells and to renal fibrosis in DN models. We evaluated the role of TGF-β on NT5E gene expression coding for the ecto-5`-nucleotidase CD73, the limiting enzyme in extracellular adenosine production. We showed that high d-glucose may predispose HK-2 cells towards active transcription of the proximal promoter region of the NT5E gene while additional TGF-β results in full activation. The epigenetic landscape of the NT5E gene promoter was modified by concurrent TGF-β with occupancy by the p300 co-activator and the phosphorylated forms of the Smad2/3 complex and RNA Pol II. Transcriptional induction at NT5E in response to TGF-β was earlier compared to the classic responsiveness genes PAI-1 and Fn1. CD73 levels and AMPase activity were concomitantly increased by TGF-β in HK-2 cells. Interestingly, we found increased CD73 content in urinary extracellular vesicles only in diabetic patients with renal repercussions. Further, CD73-mediated AMPase activity was increased in the urinary sediment of DN patients. We conclude that the NT5E gene is a target of the profibrotic TGF-β cascade and is a traceable marker of progressive DN.</p>',
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<p>Monoclonal antibody raised in mouse against human <strong>p300</strong> (<strong>E1A Binding Protein P300</strong>) by DNA immunization in which the C-terminal part of the protein was cloned and expressed.</p>',
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<div class="small-6 columns"><center><img src="https://www.diagenode.com/img/product/antibodies/c15200211-chip.jpg" /></center></div>
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<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
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<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed with 5 µg of the Diagenode antibody against p300 (cat. No. C15200211) on sheared chromatin from 4 million HeLa cells as described above. The IP'd DNA was subsequently analysed on an Illumina NovaSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 50 bp tags were aligned to the human genome using the BWA algorithm. Figure 2 shows the peak distribution along the complete sequence and a 3 mb region of chromosome 5 (figure 2A and B) and in two regions surrounding the IRS2 and ANKRD32 (SLF1) positive control genes (figure 2C and D). The position of the amplicon used for ChIP-qPCR is indicated by an arrow.</p>
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<p><strong>Figure 1. ChIP results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed using HeLa cells, the Diagenode monoclonal antibody against p300 (cat. No. C15200211) and optimized PCR primer sets for qPCR. ChIP was performed with the “iDeal ChIP-seq” kit (cat. No. C01010055), using sheared chromatin from 4 million cells. A titration of the antibody consisting of 2, 5 and 10 µg per ChIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. Quantitative PCR was performed with primers for two genomic regions near the ANKRD32 and IRS2 genes, used as positive controls, and for the coding region of the inactive MYOD1 gene and an intergeic region on chromosome 11, used as negative controls. Figure 1 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</p>
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<p style="text-align: center;">A.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-a.jpg" alt="p300 Antibody ChIP-seq Grade" caption="false" width="500" /></p>
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<p style="text-align: center;">C.<img src="https://www.diagenode.com/img/product/antibodies/c15200211-chipseq-c.jpg" alt="p300 Antibody for ChIP-seq assay" caption="false" width="500" /></p>
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<p><strong>Figure 2. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against p300</strong></p>
<p>ChIP was performed with 5 µg of the Diagenode antibody against p300 (cat. No. C15200211) on sheared chromatin from 4 million HeLa cells as described above. The IP'd DNA was subsequently analysed on an Illumina NovaSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. The 50 bp tags were aligned to the human genome using the BWA algorithm. Figure 2 shows the peak distribution along the complete sequence and a 3 mb region of chromosome 5 (figure 2A and B) and in two regions surrounding the IRS2 and ANKRD32 (SLF1) positive control genes (figure 2C and D). The position of the amplicon used for ChIP-qPCR is indicated by an arrow.</p>
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'search_order' => '03-Antibody',
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'meta_title' => 'p300 Antibody - ChIP-seq Grade (C15200211) | Diagenode',
'meta_keywords' => '',
'meta_description' => 'p300 (E1A Binding Protein P300) Monoclonal Antibody validated in ChIP-seq and ChIP-qPCR. Batch-specific data available on the website. Alternative names: EP300, KAT3B, RSTS2. Sample size available',
'modified' => '2024-01-28 12:15:17',
'created' => '2015-06-29 14:08:20'
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'slug' => 'chip-qpcr-antibodies',
'meta_keywords' => 'Chromatin Immunoprecipitation Sequencing,ChIP-Seq,ChIP-seq grade antibodies,DNA purification,qPCR,Shearing of chromatin',
'meta_description' => 'Diagenode offers a wide range of antibodies and technical support for ChIP-qPCR applications',
'meta_title' => 'ChIP Quantitative PCR Antibodies (ChIP-qPCR) | Diagenode',
'modified' => '2016-01-20 11:30:24',
'created' => '2015-10-20 11:45:36',
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'name' => 'ChIP-qPCR (ab)',
'description' => '',
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'online' => true,
'tabular' => true,
'slug' => 'chip-qpcr-antibodies',
'meta_keywords' => 'Chromatin Immunoprecipitation Sequencing,ChIP-Seq,ChIP-seq grade antibodies,DNA purification,qPCR,Shearing of chromatin',
'meta_description' => 'Diagenode offers a wide range of antibodies and technical support for ChIP-qPCR applications',
'meta_title' => 'ChIP Quantitative PCR Antibodies (ChIP-qPCR) | Diagenode',
'modified' => '2016-01-20 11:30:24',
'created' => '2015-10-20 11:45:36',
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$name = 'ChIP-qPCR (ab)'
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'name' => 'Datasheet p300 C15200211',
'description' => 'Datasheet description',
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'type' => 'Datasheet',
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'slug' => 'datasheet-p300-c15200211',
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'modified' => '2015-07-07 11:47:44',
'created' => '2015-07-07 11:47:44',
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'name' => 'The TGF-β profibrotic cascade targets ecto-5'-nucleotidase gene in proximal tubule epithelial cells and is a traceable marker of progressive diabetic kidney disease.',
'authors' => 'Cappelli C, Tellez A, Jara C, Alarcón S, Torres A, Mendoza P, Podestá L, Flores C, Quezada C, Oyarzún C, Martín RS',
'description' => '<p>Progressive diabetic nephropathy (DN) and loss of renal function correlate with kidney fibrosis. Crosstalk between TGF-β and adenosinergic signaling contributes to the phenotypic transition of cells and to renal fibrosis in DN models. We evaluated the role of TGF-β on NT5E gene expression coding for the ecto-5`-nucleotidase CD73, the limiting enzyme in extracellular adenosine production. We showed that high d-glucose may predispose HK-2 cells towards active transcription of the proximal promoter region of the NT5E gene while additional TGF-β results in full activation. The epigenetic landscape of the NT5E gene promoter was modified by concurrent TGF-β with occupancy by the p300 co-activator and the phosphorylated forms of the Smad2/3 complex and RNA Pol II. Transcriptional induction at NT5E in response to TGF-β was earlier compared to the classic responsiveness genes PAI-1 and Fn1. CD73 levels and AMPase activity were concomitantly increased by TGF-β in HK-2 cells. Interestingly, we found increased CD73 content in urinary extracellular vesicles only in diabetic patients with renal repercussions. Further, CD73-mediated AMPase activity was increased in the urinary sediment of DN patients. We conclude that the NT5E gene is a target of the profibrotic TGF-β cascade and is a traceable marker of progressive DN.</p>',
'date' => '2020-04-11',
'pmid' => 'http://www.pubmed.gov/32289379',
'doi' => '10.1016/j.bbadis.2020.165796',
'modified' => '2020-08-17 10:46:30',
'created' => '2020-08-10 12:12:25',
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View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118
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