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ER alpha monoclonal antibody (sample size)

CUT&Tag grade Abs

ChIP-seq grade Abs

ChIP grade Abs

Negative IgG control

Antibody portal

Antibodies

Catalog Number

Format

Price

C15100066-20

20 µl

$115.00
Bulk order

Other format

C15100066-100

100 µl

Alternative names: ESR, ESR1, ESRA, NR3A1

Monoclonal antibody raised in mouse against human ERalpha (estrogen receptor alpha), using a synthetic peptide.

Lot	007
Concentration	not determined
Species reactivity	Human, mouse
Type	Monoclonal
Purity	Ascites fluid
Host	Mouse
Precautions	This product is for research use only. Not for use in diagnostic or therapeutic procedures.

Applications	Suggested dilution	References
ELISA	1:500 -1:5,000
Western Blotting	1:500 -1:5,000	Ref 3
Gel Supershift	1:10 – 1:20
Immunochemistry	1:500 -1:5,000
Immunoprecipitation	1:200 -1:5,000	Ref 3
ChIP ^*	2.5 μl/ChIP	Fig 1; Ref 1, 2

^* Please note that the optimal antibody amount per IP should be determined by the end-user. We recommend testing 1-5 μl per IP.

Validation data

Figure 1. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against ERalpha
ChIP was performed with the Diagenode monoclonal antibody against ERalpha (cat. No. AC-066-100) on sheared chromatin from MCF7 cells treated for 1 hour with estradiol. The IP’d DNA was analysed with 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. Figure 1 shows the obtained peaks near the TFF1 gene on chromosome 21 (figure 1A), the GREB1 and HAAO genes on chromosome 2 (figure 1B and C), and the ZNF185 gene on the X-chromosome (figure 1D).
Target Description
The estrogen receptor alpha (ERalpha, UniProt/Swiss-Prot entry P03372) belongs to the family of nuclear hormone receptors, which are ligand-activated transcription factors. They are important for the regulation of gene expression, cellular proliferation and differentiation, sexual development and reproductive function. Estrogen receptors are also involved in pathological processes such as breast cancer, and osteoporosis. ERalpha can regulate transcription by direct binding to estrogen response elements (EREs) in the DNA or by interaction with other transcription factors. It may also form a heterodimer with ERbeta.

出版物

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Carnobacterium maltaromaticum boosts intestinal vitamin D production tosuppress colorectal cancer in female mice.
Li Q. et al.
Carnobacterium maltaromaticum was found to be specifically depleted in female patients with colorectal cancer (CRC). Administration of C.Â maltaromaticum reduces intestinal tumor formation in two murine CRC models in a female-specific manner. Estrogen increases the attachment and colonization of C.Â...

27-Hydroxycholesterol, The Estrogen Receptor Modulator, AltersDNA Methylation in Breast Cancer.
Vini Ravindran et al.
27-hydroxycholesterol (27-HC) is the first known endogenous selective estrogen receptor modulator (SERM), and its elevation from normal levels is closely associated with breast cancer. A plethora of evidence suggests that aberrant epigenetic signatures in breast cancer cells can result in differential responses to v...

Epigenetic remodelling of enhancers in response to estrogen deprivationand re-stimulation.
Sklias Athena et al.
Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER), the main nuclear factor mediating estrogen signaling, orchestrates a complex molecular circuitry that is not yet fully elucidated. Here, we investigated genome-wide DNA methylation, histone acetylation and transcriptio...

Estrogen induces dynamic ERα and RING1B recruitment to control gene and enhancer activities in luminal breast cancer
Zhang Yusheng, Chan Ho Lam, Garcia-Martinez Liliana, Karl Daniel L., Weich Natalia, Slingerland Joyce M., Verdun Ramiro E., Morey Lluis
RING1B, a core Polycomb repressive complex 1 subunit, is a histone H2A ubiquitin ligase essential for development. RING1B is overexpressed in patients with luminal breast cancer (BC) and recruited to actively transcribed genes and enhancers co-occupied by the estrogen receptor  (ER). Whether ER-induced transcript...

Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha.
Glont SE, Papachristou EK, Sawle A, Holmes KA, Carroll JS, Siersbaek R
Estrogen Receptor alpha (ERα) plays a major role in most breast cancers, and it is the target of endocrine therapies used in the clinic as standard of care for women with breast cancer expressing this receptor. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapi...

The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer.
Chakravarty D, Sboner A, Nair SS, Giannopoulou E, Li R, Hennig S, Mosquera JM, Pauwels J, Park K, Kossai M, MacDonald TY, Fontugne J, Erho N, Vergara IA, Ghadessi M, Davicioni E, Jenkins RB, Palanisamy N, Chen Z, Nakagawa S, Hirose T, Bander NH, Beltran H
The androgen receptor (AR) plays a central role in establishing an oncogenic cascade that drives prostate cancer progression. Some prostate cancers escape androgen dependence and are often associated with an aggressive phenotype. The oestrogen receptor alpha (ERα) is expressed in prostate cancers, independent of AR ...

Estrogen receptor ligands ameliorate fatty liver through a nonclassical estrogen receptor/Liver X receptor pathway in mice.
Han SI, Komatsu Y, Murayama A, Steffensen KR, Nakagawa Y, Nakajima Y, Suzuki M, Oie S, Parini P, Vedin LL, Kishimoto H, Shimano H, Gustafsson JÅ, Yanagisawa J
UNLABELLED: Liver X receptor (LXR) activation stimulates triglyceride (TG) accumulation in the liver. Several lines of evidence indicate that estradiol-17β (E2) reduces TG levels in the liver; however, the molecular mechanism underlying the E2 effect remains unclear. Here, we show that administration of E2 attenuate...

Functional Genomic Methods to Study Estrogen Receptor Activity.
Gilfillan S, Fiorito E, Hurtado A
Estrogen Receptor (ER) is a nuclear receptor that mediates the actions of estrogen and tamoxifen. ER is expressed in a major fraction of human breast cancers. Recently, genomic maps for estrogen- and tamoxifen-ER have been published. Interestingly, estrogen and tamoxifen induce similar genomic interactions and both ...

ChIP-Seq of ERalpha and RNA polymerase II defines genes differentially responding to ligands.
Welboren WJ, van Driel MA, et al.,
We used ChIP-Seq to map ERa-binding sites and to profile changes in RNA polymerase II (RNAPII) occupancy in MCF-7 cells in response to estradiol (E2), tamoxifen or fulvestrant. We identify 10 205 high confidence ERa-binding sites in response to E2 of which 68% contain an estrogen response element (ERE) and only 7% c...

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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</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>
<div class="small-12 medium-3 large-3 columns">
<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 &micro;g of the Diagenode antibodies against H3K27me3 (cat. No. C15410195) and H3K4me3 (cat. No. C15410003), and 0.5 &micro;g 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>
</div>
</div>
<p>Diagenode&rsquo;s highly validated antibodies:</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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<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Highly sensitive and specific</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Cost-effective (requires less antibody per reaction)</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Batch-specific data is available on the website</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Expert technical support</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Sample sizes available</span></li>
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			'description' => '<h1><strong>Validated epigenetics antibodies</strong>&nbsp;&ndash; care for a sample?<br />&nbsp;</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> -&nbsp;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>&nbsp;with rigorous QC and validation</li>
<li><strong>Classified</strong>&nbsp;based on level of validation for flexibility of application</li>
</ul>
<p>Existing sample sizes are listed below. We will soon expand our collection. &nbsp;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&rsquo;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&rsquo;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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			'name' => 'ChIP-grade antibodies',
			'description' => '<div class="row">
<div class="small-12 columns"><center></center>
<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>
<p></p>
</div>
</div>
<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>).&nbsp;</p>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><img src="https://www.diagenode.com/img/product/antibodies/C15410003-fig1-ChIP.jpg" alt="" width="400" height="315" />&nbsp;</div>
<div class="small-12 medium-6 large-6 columns">
<p></p>
<p></p>
<p></p>
</div>
</div>
<p></p>
<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 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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			'description' => '<p>Carnobacterium maltaromaticum was found to be specifically depleted in female patients with colorectal cancer (CRC). Administration of C.&Acirc;&nbsp;maltaromaticum reduces intestinal tumor formation in two murine CRC models in a female-specific manner. Estrogen increases the attachment and colonization of C.&Acirc;&nbsp;maltaromaticum via increasing the colonic expression of SLC3A2 that binds to DD-CPase of this bacterium. Metabolomic and transcriptomic&Acirc;&nbsp;profiling unveils the increased gut abundance of vitamin D-related metabolites and the mucosal activation of vitamin D receptor (VDR) signaling in C.&Acirc;&nbsp;maltaromaticum-gavaged mice in a gut microbiome- and VDR-dependent manner. In&Acirc;&nbsp;vitro fermentation system confirms the metabolic cross-feeding of&Acirc;&nbsp;C.&Acirc;&nbsp;maltaromaticum with Faecalibacterium prausnitzii to convert C.&Acirc;&nbsp;maltaromaticum-produced 7-dehydrocholesterol into vitamin D for activating the host VDR signaling. Overall, C.&Acirc;&nbsp;maltaromaticum colonizes the gut in an estrogen-dependent manner and acts along with other microbes to augment the intestinal vitamin D production to activate the host VDR for suppressing CRC.</p>',
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			'description' => '<p>27-hydroxycholesterol (27-HC) is the first known endogenous selective estrogen receptor modulator (SERM), and its elevation from normal levels is closely associated with breast cancer. A plethora of evidence suggests that aberrant epigenetic signatures in breast cancer cells can result in differential responses to various chemotherapeutics and often leads to the development of resistant cancer cells. Such aberrant epigenetic changes are mostly dictated by the microenvironment. The local concentration of oxygen and metabolites in the microenvironment of breast cancer are known to influence the development of breast cancer. Hence, we hypothesized that 27-HC, an oxysterol, which has been shown to induce breast cancer progression estrogen receptor alpha (ER&alpha;) and liver X receptor (LXR) and by modulating immune cells, may also induce epigenetic changes. For deciphering the same, we treated the estrogen receptor-positive cells with 27-HC and identified DNA hypermethylation on a subset of genes by performing DNA bisulfite sequencing. The genes that showed significant DNA hypermethylation were and . Furthermore, we found that 27-HC weakens the DNMT3B association with the ER&alpha; in MCF-7 cells. This study reports that 27-HC induces aberrant DNA methylation changes on the promoters of a subset of genes through modulation of ER&alpha; and DNMT3B complexes to induce the local DNA methylation changes, which may dictate drug responses and breast cancer development.</p>',
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			'name' => 'Epigenetic remodelling of enhancers in response to estrogen deprivationand re-stimulation.',
			'authors' => 'Sklias Athena et al.',
			'description' => '<p>Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER), the main nuclear factor mediating estrogen signaling, orchestrates a complex molecular circuitry that is not yet fully elucidated. Here, we investigated genome-wide DNA methylation, histone acetylation and transcription after estradiol (E2) deprivation and re-stimulation to better characterize the ability of ER to coordinate gene regulation. We found that E2 deprivation mostly resulted in DNA hypermethylation and histone deacetylation in enhancers. Transcriptome analysis revealed that E2 deprivation leads to a global down-regulation in gene expression, and more specifically of TET2 demethylase that may be involved in the DNA hypermethylation following short-term E2 deprivation. Further enrichment analysis of transcription factor (TF) binding and motif occurrence highlights the importance of ER connection mainly with two partner TF families, AP-1 and FOX. These interactions take place in the proximity of E2 deprivation-mediated differentially methylated and histone acetylated enhancers. Finally, while most deprivation-dependent epigenetic changes were reversed following E2 re-stimulation, DNA hypermethylation and H3K27 deacetylation at certain enhancers were partially retained. Overall, these results show that inactivation of ER mediates rapid and mostly reversible epigenetic changes at enhancers, and bring new insight into early events, which may ultimately lead to endocrine resistance.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://doi.org/10.1093%2Fnar%2Fgkab697',
			'doi' => '10.1093/nar/gkab697',
			'modified' => '2022-06-22 09:25:09',
			'created' => '2022-05-19 10:41:50',
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		(int) 3 => array(
			'id' => '3961',
			'name' => 'Estrogen induces dynamic ERα and RING1B recruitment to control gene and enhancer activities in luminal breast cancer',
			'authors' => 'Zhang Yusheng, Chan Ho Lam, Garcia-Martinez Liliana, Karl Daniel L., Weich Natalia, Slingerland Joyce M., Verdun Ramiro E., Morey Lluis',
			'description' => '<p>RING1B, a core Polycomb repressive complex 1 subunit, is a histone H2A ubiquitin ligase essential for development. RING1B is overexpressed in patients with luminal breast cancer (BC) and recruited to actively transcribed genes and enhancers co-occupied by the estrogen receptor  (ER). Whether ER-induced transcriptional programs are mediated by RING1B is not understood. We show that prolonged estrogen administration induces transcriptional output and chromatin landscape fluctuations. RING1B loss impairs full estrogen-mediated gene expression and chromatin accessibility for key BC transcription factors. These effects were mediated, in part, by RING1B enzymatic activity and nucleosome binding functions. RING1B is recruited in a cyclic manner to ER, FOXA1, and GRHL2 cobound sites and regulates estrogen-induced enhancers and ER recruitment. Last, ChIP exo revealed multiple binding events of these factors at single-nucleotide resolution, including RING1B occupancy approximately 10 base pairs around ER bound sites. We propose RING1B as a key regulator of the dynamic, liganded-ER transcriptional regulatory circuit in luminal BC.</p>',
			'date' => '2020-06-12',
			'pmid' => 'https://advances.sciencemag.org/content/6/23/eaaz7249.full',
			'doi' => '10.1126/sciadv.aaz7249',
			'modified' => '2020-08-12 09:48:21',
			'created' => '2020-08-10 12:12:25',
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		(int) 4 => array(
			'id' => '3705',
			'name' => 'Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha.',
			'authors' => 'Glont SE, Papachristou EK, Sawle A, Holmes KA, Carroll JS, Siersbaek R',
			'description' => '<p>Estrogen Receptor alpha (ER&alpha;) plays a major role in most breast cancers, and it is the target of endocrine therapies used in the clinic as standard of care for women with breast cancer expressing this receptor. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ER&alpha; function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used against the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ER&alpha; have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ER&alpha; in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.</p>',
			'date' => '2019-01-01',
			'pmid' => 'http://www.pubmed.gov/30970003',
			'doi' => '10.1371/journal.',
			'modified' => '2019-07-05 14:39:11',
			'created' => '2019-07-04 10:42:34',
			'ProductsPublication' => array(
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		),
		(int) 5 => array(
			'id' => '2367',
			'name' => 'The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer.',
			'authors' => 'Chakravarty D, Sboner A, Nair SS, Giannopoulou E, Li R, Hennig S, Mosquera JM, Pauwels J, Park K, Kossai M, MacDonald TY, Fontugne J, Erho N, Vergara IA, Ghadessi M, Davicioni E, Jenkins RB, Palanisamy N, Chen Z, Nakagawa S, Hirose T, Bander NH, Beltran H',
			'description' => 'The androgen receptor (AR) plays a central role in establishing an oncogenic cascade that drives prostate cancer progression. Some prostate cancers escape androgen dependence and are often associated with an aggressive phenotype. The oestrogen receptor alpha (ERα) is expressed in prostate cancers, independent of AR status. However, the role of ERα remains elusive. Using a combination of chromatin immunoprecipitation (ChIP) and RNA-sequencing data, we identified an ERα-specific non-coding transcriptome signature. Among putatively ERα-regulated intergenic long non-coding RNAs (lncRNAs), we identified nuclear enriched abundant transcript 1 (NEAT1) as the most significantly overexpressed lncRNA in prostate cancer. Analysis of two large clinical cohorts also revealed that NEAT1 expression is associated with prostate cancer progression. Prostate cancer cells expressing high levels of NEAT1 were recalcitrant to androgen or AR antagonists. Finally, we provide evidence that NEAT1 drives oncogenic growth by altering the epigenetic landscape of target gene promoters to favour transcription.',
			'date' => '2014-10-21',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/25415230',
			'doi' => '',
			'modified' => '2015-07-24 15:39:04',
			'created' => '2015-07-24 15:39:04',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '2446',
			'name' => 'Estrogen receptor ligands ameliorate fatty liver through a nonclassical estrogen receptor/Liver X receptor pathway in mice.',
			'authors' => 'Han SI, Komatsu Y, Murayama A, Steffensen KR, Nakagawa Y, Nakajima Y, Suzuki M, Oie S, Parini P, Vedin LL, Kishimoto H, Shimano H, Gustafsson JÅ, Yanagisawa J',
			'description' => 'UNLABELLED: Liver X receptor (LXR) activation stimulates triglyceride (TG) accumulation in the liver. Several lines of evidence indicate that estradiol-17β (E2) reduces TG levels in the liver; however, the molecular mechanism underlying the E2 effect remains unclear. Here, we show that administration of E2 attenuated sterol regulatory element-binding protein (SREBP)-1 expression and TG accumulation induced by LXR activation in mouse liver. In estrogen receptor alpha (ERα) knockout (KO) and liver-specific ERα KO mice, E2 did not affect SREBP-1 expression or TG levels. Molecular analysis revealed that ERα is recruited to the SREBP-1c promoter through direct binding to LXR and inhibits coactivator recruitment to LXR in an E2-dependent manner. Our findings demonstrate the existence of a novel liver-dependent mechanism controlling TG accumulation through the nonclassical ER/LXR pathway. To confirm that a nonclassical ER/LXR pathway regulates ERα-dependent inhibition of LXR activation, we screened ERα ligands that were able to repress LXR activation without enhancing ERα transcriptional activity, and, as a result, we identified the phytoestrogen, phloretin. In mice, phloretin showed no estrogenic activity; however, it did reduce SREBP-1 expression and TG levels in liver of mice fed a high-fat diet to an extent similar to that of E2. CONCLUSION: We propose that ER ligands reduce TG levels in the liver by inhibiting LXR activation through a nonclassical pathway. Our results also indicate that the effects of ER on TG accumulation can be distinguished from its estrogenic effects by a specific ER ligand.',
			'date' => '2014-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/24277692',
			'doi' => '',
			'modified' => '2015-07-24 15:39:04',
			'created' => '2015-07-24 15:39:04',
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		),
		(int) 7 => array(
			'id' => '764',
			'name' => 'Functional Genomic Methods to Study Estrogen Receptor Activity.',
			'authors' => 'Gilfillan S, Fiorito E, Hurtado A',
			'description' => 'Estrogen Receptor (ER) is a nuclear receptor that mediates the actions of estrogen and tamoxifen. ER is expressed in a major fraction of human breast cancers. Recently, genomic maps for estrogen- and tamoxifen-ER have been published. Interestingly, estrogen and tamoxifen induce similar genomic interactions and both ligands have been shown to use co-operating factors. The interactions of these co-operating factors within ER regions have impact both on ER-DNA interactions and gene expression regulated by estrogen and tamoxifen. Moreover, the study of chromatin changes induced by these factors has also provided significant insight into our understanding of ER transcriptional regulation. This methods review describes some functional genomic methods to study the influence of both ER ligands and ER co-operating factors. The analysis of protein-DNA interactions and chromatin changes can be explored by using classical and novel methods such as Chromatin Immunoprecipitation (ChIP) or Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE). This review also explores the properties of each of these methods and the advantages of combining them with high throughput sequencing.',
			'date' => '2012-05-16',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/22588661',
			'doi' => '',
			'modified' => '2015-07-24 15:38:58',
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			'name' => 'ChIP-Seq of ERalpha and RNA polymerase II defines genes differentially responding to ligands.',
			'authors' => 'Welboren WJ, van Driel MA, et al.,',
			'description' => 'We used ChIP-Seq to map ERa-binding sites and to profile changes in RNA polymerase II (RNAPII) occupancy in MCF-7 cells in response to estradiol (E2), tamoxifen or fulvestrant. We identify 10 205 high confidence ERa-binding sites in response to E2 of which 68% contain an estrogen response element (ERE) and only 7% contain a FOXA1 motif. Remarkably, 596 genes change significantly in RNAPII occupancy (59% up and 41% down) already after 1 h of E2 exposure. Although promoter proximal enrichment of RNAPII (PPEP) occurs frequently in MCF- 7 cells (17%), it is only observed on a minority of E2- regulated genes (4%). Tamoxifen and fulvestrant partially reduce ERa DNA binding and prevent RNAPII loading on the promoter and coding body on E2-upregulated genes. Both ligands act differently on E2-downregulated genes: tamoxifen acts as an agonist thus downregulating these genes, whereas fulvestrant antagonizes E2-induced repression and often increases RNAPII occupancy. Furthermore, our data identify genes preferentially regulated by tamoxifen but not by E2 or fulvestrant. Thus (partial) antagonist loaded ERa acts mechanistically different on E2-activated and E2-repressed genes.',
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<p>Monoclonal antibody raised in mouse against human <strong>ERalpha (estrogen receptor alpha)</strong>, using a synthetic peptide.</p>',
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<p><small><strong> Figure 1. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against ERalpha </strong><br />ChIP was performed with the Diagenode monoclonal antibody against ERalpha (cat. No. AC-066-100) on sheared chromatin from MCF7 cells treated for 1 hour with estradiol. The IP&rsquo;d DNA was analysed with an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer&rsquo;s instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. Figure 1 shows the obtained peaks near the TFF1 gene on chromosome 21 (figure 1A), the GREB1 and HAAO genes on chromosome 2 (figure 1B and C), and the ZNF185 gene on the X-chromosome (figure 1D). </small></p>
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<p>Monoclonal antibody raised in mouse against human <strong>ERalpha (estrogen receptor alpha)</strong>, using a synthetic peptide.</p>',
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include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
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
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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</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>
<div class="small-12 medium-3 large-3 columns">
<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 &micro;g of the Diagenode antibodies against H3K27me3 (cat. No. C15410195) and H3K4me3 (cat. No. C15410003), and 0.5 &micro;g 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&rsquo;s highly validated antibodies:</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>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
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<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Highly sensitive and specific</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Cost-effective (requires less antibody per reaction)</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Batch-specific data is available on the website</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Expert technical support</span></li>
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			'description' => '<h1><strong>Validated epigenetics antibodies</strong>&nbsp;&ndash; care for a sample?<br />&nbsp;</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> -&nbsp;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>&nbsp;with rigorous QC and validation</li>
<li><strong>Classified</strong>&nbsp;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. &nbsp;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&rsquo;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&rsquo;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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			'name' => 'ChIP-grade antibodies',
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<div class="small-12 columns"><center></center>
<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>
<p></p>
</div>
</div>
<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>).&nbsp;</p>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><img src="https://www.diagenode.com/img/product/antibodies/C15410003-fig1-ChIP.jpg" alt="" width="400" height="315" />&nbsp;</div>
<div class="small-12 medium-6 large-6 columns">
<p></p>
<p></p>
<p></p>
</div>
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<p></p>
<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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			'name' => '27-Hydroxycholesterol, The Estrogen Receptor Modulator, AltersDNA Methylation in Breast Cancer.',
			'authors' => 'Vini  Ravindran et al.',
			'description' => '<p>27-hydroxycholesterol (27-HC) is the first known endogenous selective estrogen receptor modulator (SERM), and its elevation from normal levels is closely associated with breast cancer. A plethora of evidence suggests that aberrant epigenetic signatures in breast cancer cells can result in differential responses to various chemotherapeutics and often leads to the development of resistant cancer cells. Such aberrant epigenetic changes are mostly dictated by the microenvironment. The local concentration of oxygen and metabolites in the microenvironment of breast cancer are known to influence the development of breast cancer. Hence, we hypothesized that 27-HC, an oxysterol, which has been shown to induce breast cancer progression estrogen receptor alpha (ER&alpha;) and liver X receptor (LXR) and by modulating immune cells, may also induce epigenetic changes. For deciphering the same, we treated the estrogen receptor-positive cells with 27-HC and identified DNA hypermethylation on a subset of genes by performing DNA bisulfite sequencing. The genes that showed significant DNA hypermethylation were and . Furthermore, we found that 27-HC weakens the DNMT3B association with the ER&alpha; in MCF-7 cells. This study reports that 27-HC induces aberrant DNA methylation changes on the promoters of a subset of genes through modulation of ER&alpha; and DNMT3B complexes to induce the local DNA methylation changes, which may dictate drug responses and breast cancer development.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35360070',
			'doi' => '10.3389/fendo.2022.783823',
			'modified' => '2022-11-24 08:58:58',
			'created' => '2022-11-24 08:49:52',
			'ProductsPublication' => array(
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		),
		(int) 2 => array(
			'id' => '4329',
			'name' => 'Epigenetic remodelling of enhancers in response to estrogen deprivationand re-stimulation.',
			'authors' => 'Sklias Athena et al.',
			'description' => '<p>Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER), the main nuclear factor mediating estrogen signaling, orchestrates a complex molecular circuitry that is not yet fully elucidated. Here, we investigated genome-wide DNA methylation, histone acetylation and transcription after estradiol (E2) deprivation and re-stimulation to better characterize the ability of ER to coordinate gene regulation. We found that E2 deprivation mostly resulted in DNA hypermethylation and histone deacetylation in enhancers. Transcriptome analysis revealed that E2 deprivation leads to a global down-regulation in gene expression, and more specifically of TET2 demethylase that may be involved in the DNA hypermethylation following short-term E2 deprivation. Further enrichment analysis of transcription factor (TF) binding and motif occurrence highlights the importance of ER connection mainly with two partner TF families, AP-1 and FOX. These interactions take place in the proximity of E2 deprivation-mediated differentially methylated and histone acetylated enhancers. Finally, while most deprivation-dependent epigenetic changes were reversed following E2 re-stimulation, DNA hypermethylation and H3K27 deacetylation at certain enhancers were partially retained. Overall, these results show that inactivation of ER mediates rapid and mostly reversible epigenetic changes at enhancers, and bring new insight into early events, which may ultimately lead to endocrine resistance.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://doi.org/10.1093%2Fnar%2Fgkab697',
			'doi' => '10.1093/nar/gkab697',
			'modified' => '2022-06-22 09:25:09',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
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		),
		(int) 3 => array(
			'id' => '3961',
			'name' => 'Estrogen induces dynamic ERα and RING1B recruitment to control gene and enhancer activities in luminal breast cancer',
			'authors' => 'Zhang Yusheng, Chan Ho Lam, Garcia-Martinez Liliana, Karl Daniel L., Weich Natalia, Slingerland Joyce M., Verdun Ramiro E., Morey Lluis',
			'description' => '<p>RING1B, a core Polycomb repressive complex 1 subunit, is a histone H2A ubiquitin ligase essential for development. RING1B is overexpressed in patients with luminal breast cancer (BC) and recruited to actively transcribed genes and enhancers co-occupied by the estrogen receptor  (ER). Whether ER-induced transcriptional programs are mediated by RING1B is not understood. We show that prolonged estrogen administration induces transcriptional output and chromatin landscape fluctuations. RING1B loss impairs full estrogen-mediated gene expression and chromatin accessibility for key BC transcription factors. These effects were mediated, in part, by RING1B enzymatic activity and nucleosome binding functions. RING1B is recruited in a cyclic manner to ER, FOXA1, and GRHL2 cobound sites and regulates estrogen-induced enhancers and ER recruitment. Last, ChIP exo revealed multiple binding events of these factors at single-nucleotide resolution, including RING1B occupancy approximately 10 base pairs around ER bound sites. We propose RING1B as a key regulator of the dynamic, liganded-ER transcriptional regulatory circuit in luminal BC.</p>',
			'date' => '2020-06-12',
			'pmid' => 'https://advances.sciencemag.org/content/6/23/eaaz7249.full',
			'doi' => '10.1126/sciadv.aaz7249',
			'modified' => '2020-08-12 09:48:21',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
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		),
		(int) 4 => array(
			'id' => '3705',
			'name' => 'Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha.',
			'authors' => 'Glont SE, Papachristou EK, Sawle A, Holmes KA, Carroll JS, Siersbaek R',
			'description' => '<p>Estrogen Receptor alpha (ER&alpha;) plays a major role in most breast cancers, and it is the target of endocrine therapies used in the clinic as standard of care for women with breast cancer expressing this receptor. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ER&alpha; function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used against the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ER&alpha; have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ER&alpha; in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.</p>',
			'date' => '2019-01-01',
			'pmid' => 'http://www.pubmed.gov/30970003',
			'doi' => '10.1371/journal.',
			'modified' => '2019-07-05 14:39:11',
			'created' => '2019-07-04 10:42:34',
			'ProductsPublication' => array(
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		),
		(int) 5 => array(
			'id' => '2367',
			'name' => 'The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer.',
			'authors' => 'Chakravarty D, Sboner A, Nair SS, Giannopoulou E, Li R, Hennig S, Mosquera JM, Pauwels J, Park K, Kossai M, MacDonald TY, Fontugne J, Erho N, Vergara IA, Ghadessi M, Davicioni E, Jenkins RB, Palanisamy N, Chen Z, Nakagawa S, Hirose T, Bander NH, Beltran H',
			'description' => 'The androgen receptor (AR) plays a central role in establishing an oncogenic cascade that drives prostate cancer progression. Some prostate cancers escape androgen dependence and are often associated with an aggressive phenotype. The oestrogen receptor alpha (ERα) is expressed in prostate cancers, independent of AR status. However, the role of ERα remains elusive. Using a combination of chromatin immunoprecipitation (ChIP) and RNA-sequencing data, we identified an ERα-specific non-coding transcriptome signature. Among putatively ERα-regulated intergenic long non-coding RNAs (lncRNAs), we identified nuclear enriched abundant transcript 1 (NEAT1) as the most significantly overexpressed lncRNA in prostate cancer. Analysis of two large clinical cohorts also revealed that NEAT1 expression is associated with prostate cancer progression. Prostate cancer cells expressing high levels of NEAT1 were recalcitrant to androgen or AR antagonists. Finally, we provide evidence that NEAT1 drives oncogenic growth by altering the epigenetic landscape of target gene promoters to favour transcription.',
			'date' => '2014-10-21',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/25415230',
			'doi' => '',
			'modified' => '2015-07-24 15:39:04',
			'created' => '2015-07-24 15:39:04',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '2446',
			'name' => 'Estrogen receptor ligands ameliorate fatty liver through a nonclassical estrogen receptor/Liver X receptor pathway in mice.',
			'authors' => 'Han SI, Komatsu Y, Murayama A, Steffensen KR, Nakagawa Y, Nakajima Y, Suzuki M, Oie S, Parini P, Vedin LL, Kishimoto H, Shimano H, Gustafsson JÅ, Yanagisawa J',
			'description' => 'UNLABELLED: Liver X receptor (LXR) activation stimulates triglyceride (TG) accumulation in the liver. Several lines of evidence indicate that estradiol-17β (E2) reduces TG levels in the liver; however, the molecular mechanism underlying the E2 effect remains unclear. Here, we show that administration of E2 attenuated sterol regulatory element-binding protein (SREBP)-1 expression and TG accumulation induced by LXR activation in mouse liver. In estrogen receptor alpha (ERα) knockout (KO) and liver-specific ERα KO mice, E2 did not affect SREBP-1 expression or TG levels. Molecular analysis revealed that ERα is recruited to the SREBP-1c promoter through direct binding to LXR and inhibits coactivator recruitment to LXR in an E2-dependent manner. Our findings demonstrate the existence of a novel liver-dependent mechanism controlling TG accumulation through the nonclassical ER/LXR pathway. To confirm that a nonclassical ER/LXR pathway regulates ERα-dependent inhibition of LXR activation, we screened ERα ligands that were able to repress LXR activation without enhancing ERα transcriptional activity, and, as a result, we identified the phytoestrogen, phloretin. In mice, phloretin showed no estrogenic activity; however, it did reduce SREBP-1 expression and TG levels in liver of mice fed a high-fat diet to an extent similar to that of E2. CONCLUSION: We propose that ER ligands reduce TG levels in the liver by inhibiting LXR activation through a nonclassical pathway. Our results also indicate that the effects of ER on TG accumulation can be distinguished from its estrogenic effects by a specific ER ligand.',
			'date' => '2014-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/24277692',
			'doi' => '',
			'modified' => '2015-07-24 15:39:04',
			'created' => '2015-07-24 15:39:04',
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			)
		),
		(int) 7 => array(
			'id' => '764',
			'name' => 'Functional Genomic Methods to Study Estrogen Receptor Activity.',
			'authors' => 'Gilfillan S, Fiorito E, Hurtado A',
			'description' => 'Estrogen Receptor (ER) is a nuclear receptor that mediates the actions of estrogen and tamoxifen. ER is expressed in a major fraction of human breast cancers. Recently, genomic maps for estrogen- and tamoxifen-ER have been published. Interestingly, estrogen and tamoxifen induce similar genomic interactions and both ligands have been shown to use co-operating factors. The interactions of these co-operating factors within ER regions have impact both on ER-DNA interactions and gene expression regulated by estrogen and tamoxifen. Moreover, the study of chromatin changes induced by these factors has also provided significant insight into our understanding of ER transcriptional regulation. This methods review describes some functional genomic methods to study the influence of both ER ligands and ER co-operating factors. The analysis of protein-DNA interactions and chromatin changes can be explored by using classical and novel methods such as Chromatin Immunoprecipitation (ChIP) or Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE). This review also explores the properties of each of these methods and the advantages of combining them with high throughput sequencing.',
			'date' => '2012-05-16',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/22588661',
			'doi' => '',
			'modified' => '2015-07-24 15:38:58',
			'created' => '2015-07-24 15:38:58',
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		),
		(int) 8 => array(
			'id' => '67',
			'name' => 'ChIP-Seq of ERalpha and RNA polymerase II defines genes differentially responding to ligands.',
			'authors' => 'Welboren WJ, van Driel MA, et al.,',
			'description' => 'We used ChIP-Seq to map ERa-binding sites and to profile changes in RNA polymerase II (RNAPII) occupancy in MCF-7 cells in response to estradiol (E2), tamoxifen or fulvestrant. We identify 10 205 high confidence ERa-binding sites in response to E2 of which 68% contain an estrogen response element (ERE) and only 7% contain a FOXA1 motif. Remarkably, 596 genes change significantly in RNAPII occupancy (59% up and 41% down) already after 1 h of E2 exposure. Although promoter proximal enrichment of RNAPII (PPEP) occurs frequently in MCF- 7 cells (17%), it is only observed on a minority of E2- regulated genes (4%). Tamoxifen and fulvestrant partially reduce ERa DNA binding and prevent RNAPII loading on the promoter and coding body on E2-upregulated genes. Both ligands act differently on E2-downregulated genes: tamoxifen acts as an agonist thus downregulating these genes, whereas fulvestrant antagonizes E2-induced repression and often increases RNAPII occupancy. Furthermore, our data identify genes preferentially regulated by tamoxifen but not by E2 or fulvestrant. Thus (partial) antagonist loaded ERa acts mechanistically different on E2-activated and E2-repressed genes.',
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<p>Monoclonal antibody raised in mouse against human <strong>ERalpha (estrogen receptor alpha)</strong>, using a synthetic peptide.</p>',
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<p><small><strong> Figure 1. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against ERalpha </strong><br />ChIP was performed with the Diagenode monoclonal antibody against ERalpha (cat. No. AC-066-100) on sheared chromatin from MCF7 cells treated for 1 hour with estradiol. The IP&rsquo;d DNA was analysed with an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer&rsquo;s instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. Figure 1 shows the obtained peaks near the TFF1 gene on chromosome 21 (figure 1A), the GREB1 and HAAO genes on chromosome 2 (figure 1B and C), and the ZNF185 gene on the X-chromosome (figure 1D). </small></p>
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<p>Monoclonal antibody raised in mouse against human <strong>ERalpha (estrogen receptor alpha)</strong>, using a synthetic peptide.</p>',
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<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-B-CHIP.png" alt="ER Antibody for ChIP-seq " caption="false" width="284" height="42" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-C-CHIP.png" alt="ER Antibody for ChIP-seq assay" caption="false" width="284" height="46" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-D-CHIP.png" alt="ER Antibody validated in ChIP-seq" caption="false" width="284" height="62" /></p>
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<div class="small-8 columns">
<p><small><strong> Figure 1. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against ERalpha </strong><br />ChIP was performed with the Diagenode monoclonal antibody against ERalpha (cat. No. AC-066-100) on sheared chromatin from MCF7 cells treated for 1 hour with estradiol. The IP&rsquo;d DNA was analysed with an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer&rsquo;s instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. Figure 1 shows the obtained peaks near the TFF1 gene on chromosome 21 (figure 1A), the GREB1 and HAAO genes on chromosome 2 (figure 1B and C), and the ZNF185 gene on the X-chromosome (figure 1D). </small></p>
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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</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><small> ChIP was performed on sheared chromatin from 100,000 K562 cells using iDeal ChIP-seq kit for Histones (cat. No. C01010051) with 1 &micro;g of the Diagenode antibodies against H3K27me3 (cat. No. C15410195) and H3K4me3 (cat. No. C15410003), and 0.5 &micro;g 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&rsquo;s highly validated antibodies:</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>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
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<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Highly sensitive and specific</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Cost-effective (requires less antibody per reaction)</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Batch-specific data is available on the website</span></li>
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			'description' => '<h1><strong>Validated epigenetics antibodies</strong>&nbsp;&ndash; care for a sample?<br />&nbsp;</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> -&nbsp;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>&nbsp;with rigorous QC and validation</li>
<li><strong>Classified</strong>&nbsp;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. &nbsp;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&rsquo;s highly validated antibodies:</span></p>
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<div class="small-12 columns"><center></center>
<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>
<p></p>
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</div>
<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>).&nbsp;</p>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><img src="https://www.diagenode.com/img/product/antibodies/C15410003-fig1-ChIP.jpg" alt="" width="400" height="315" />&nbsp;</div>
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<p></p>
<p></p>
<p></p>
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<p></p>
<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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			'name' => 'Carnobacterium maltaromaticum boosts intestinal vitamin D production tosuppress colorectal cancer in female mice.',
			'authors' => 'Li  Q. et al.',
			'description' => '<p>Carnobacterium maltaromaticum was found to be specifically depleted in female patients with colorectal cancer (CRC). Administration of C.&Acirc;&nbsp;maltaromaticum reduces intestinal tumor formation in two murine CRC models in a female-specific manner. Estrogen increases the attachment and colonization of C.&Acirc;&nbsp;maltaromaticum via increasing the colonic expression of SLC3A2 that binds to DD-CPase of this bacterium. Metabolomic and transcriptomic&Acirc;&nbsp;profiling unveils the increased gut abundance of vitamin D-related metabolites and the mucosal activation of vitamin D receptor (VDR) signaling in C.&Acirc;&nbsp;maltaromaticum-gavaged mice in a gut microbiome- and VDR-dependent manner. In&Acirc;&nbsp;vitro fermentation system confirms the metabolic cross-feeding of&Acirc;&nbsp;C.&Acirc;&nbsp;maltaromaticum with Faecalibacterium prausnitzii to convert C.&Acirc;&nbsp;maltaromaticum-produced 7-dehydrocholesterol into vitamin D for activating the host VDR signaling. Overall, C.&Acirc;&nbsp;maltaromaticum colonizes the gut in an estrogen-dependent manner and acts along with other microbes to augment the intestinal vitamin D production to activate the host VDR for suppressing CRC.</p>',
			'date' => '2023-07-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37478851',
			'doi' => '10.1016/j.ccell.2023.06.011',
			'modified' => '2023-08-01 13:44:12',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
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		),
		(int) 1 => array(
			'id' => '4567',
			'name' => '27-Hydroxycholesterol, The Estrogen Receptor Modulator, AltersDNA Methylation in Breast Cancer.',
			'authors' => 'Vini  Ravindran et al.',
			'description' => '<p>27-hydroxycholesterol (27-HC) is the first known endogenous selective estrogen receptor modulator (SERM), and its elevation from normal levels is closely associated with breast cancer. A plethora of evidence suggests that aberrant epigenetic signatures in breast cancer cells can result in differential responses to various chemotherapeutics and often leads to the development of resistant cancer cells. Such aberrant epigenetic changes are mostly dictated by the microenvironment. The local concentration of oxygen and metabolites in the microenvironment of breast cancer are known to influence the development of breast cancer. Hence, we hypothesized that 27-HC, an oxysterol, which has been shown to induce breast cancer progression estrogen receptor alpha (ER&alpha;) and liver X receptor (LXR) and by modulating immune cells, may also induce epigenetic changes. For deciphering the same, we treated the estrogen receptor-positive cells with 27-HC and identified DNA hypermethylation on a subset of genes by performing DNA bisulfite sequencing. The genes that showed significant DNA hypermethylation were and . Furthermore, we found that 27-HC weakens the DNMT3B association with the ER&alpha; in MCF-7 cells. This study reports that 27-HC induces aberrant DNA methylation changes on the promoters of a subset of genes through modulation of ER&alpha; and DNMT3B complexes to induce the local DNA methylation changes, which may dictate drug responses and breast cancer development.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35360070',
			'doi' => '10.3389/fendo.2022.783823',
			'modified' => '2022-11-24 08:58:58',
			'created' => '2022-11-24 08:49:52',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 2 => array(
			'id' => '4329',
			'name' => 'Epigenetic remodelling of enhancers in response to estrogen deprivationand re-stimulation.',
			'authors' => 'Sklias Athena et al.',
			'description' => '<p>Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER), the main nuclear factor mediating estrogen signaling, orchestrates a complex molecular circuitry that is not yet fully elucidated. Here, we investigated genome-wide DNA methylation, histone acetylation and transcription after estradiol (E2) deprivation and re-stimulation to better characterize the ability of ER to coordinate gene regulation. We found that E2 deprivation mostly resulted in DNA hypermethylation and histone deacetylation in enhancers. Transcriptome analysis revealed that E2 deprivation leads to a global down-regulation in gene expression, and more specifically of TET2 demethylase that may be involved in the DNA hypermethylation following short-term E2 deprivation. Further enrichment analysis of transcription factor (TF) binding and motif occurrence highlights the importance of ER connection mainly with two partner TF families, AP-1 and FOX. These interactions take place in the proximity of E2 deprivation-mediated differentially methylated and histone acetylated enhancers. Finally, while most deprivation-dependent epigenetic changes were reversed following E2 re-stimulation, DNA hypermethylation and H3K27 deacetylation at certain enhancers were partially retained. Overall, these results show that inactivation of ER mediates rapid and mostly reversible epigenetic changes at enhancers, and bring new insight into early events, which may ultimately lead to endocrine resistance.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://doi.org/10.1093%2Fnar%2Fgkab697',
			'doi' => '10.1093/nar/gkab697',
			'modified' => '2022-06-22 09:25:09',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
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		),
		(int) 3 => array(
			'id' => '3961',
			'name' => 'Estrogen induces dynamic ERα and RING1B recruitment to control gene and enhancer activities in luminal breast cancer',
			'authors' => 'Zhang Yusheng, Chan Ho Lam, Garcia-Martinez Liliana, Karl Daniel L., Weich Natalia, Slingerland Joyce M., Verdun Ramiro E., Morey Lluis',
			'description' => '<p>RING1B, a core Polycomb repressive complex 1 subunit, is a histone H2A ubiquitin ligase essential for development. RING1B is overexpressed in patients with luminal breast cancer (BC) and recruited to actively transcribed genes and enhancers co-occupied by the estrogen receptor  (ER). Whether ER-induced transcriptional programs are mediated by RING1B is not understood. We show that prolonged estrogen administration induces transcriptional output and chromatin landscape fluctuations. RING1B loss impairs full estrogen-mediated gene expression and chromatin accessibility for key BC transcription factors. These effects were mediated, in part, by RING1B enzymatic activity and nucleosome binding functions. RING1B is recruited in a cyclic manner to ER, FOXA1, and GRHL2 cobound sites and regulates estrogen-induced enhancers and ER recruitment. Last, ChIP exo revealed multiple binding events of these factors at single-nucleotide resolution, including RING1B occupancy approximately 10 base pairs around ER bound sites. We propose RING1B as a key regulator of the dynamic, liganded-ER transcriptional regulatory circuit in luminal BC.</p>',
			'date' => '2020-06-12',
			'pmid' => 'https://advances.sciencemag.org/content/6/23/eaaz7249.full',
			'doi' => '10.1126/sciadv.aaz7249',
			'modified' => '2020-08-12 09:48:21',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
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		),
		(int) 4 => array(
			'id' => '3705',
			'name' => 'Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha.',
			'authors' => 'Glont SE, Papachristou EK, Sawle A, Holmes KA, Carroll JS, Siersbaek R',
			'description' => '<p>Estrogen Receptor alpha (ER&alpha;) plays a major role in most breast cancers, and it is the target of endocrine therapies used in the clinic as standard of care for women with breast cancer expressing this receptor. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ER&alpha; function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used against the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ER&alpha; have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ER&alpha; in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.</p>',
			'date' => '2019-01-01',
			'pmid' => 'http://www.pubmed.gov/30970003',
			'doi' => '10.1371/journal.',
			'modified' => '2019-07-05 14:39:11',
			'created' => '2019-07-04 10:42:34',
			'ProductsPublication' => array(
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			)
		),
		(int) 5 => array(
			'id' => '2367',
			'name' => 'The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer.',
			'authors' => 'Chakravarty D, Sboner A, Nair SS, Giannopoulou E, Li R, Hennig S, Mosquera JM, Pauwels J, Park K, Kossai M, MacDonald TY, Fontugne J, Erho N, Vergara IA, Ghadessi M, Davicioni E, Jenkins RB, Palanisamy N, Chen Z, Nakagawa S, Hirose T, Bander NH, Beltran H',
			'description' => 'The androgen receptor (AR) plays a central role in establishing an oncogenic cascade that drives prostate cancer progression. Some prostate cancers escape androgen dependence and are often associated with an aggressive phenotype. The oestrogen receptor alpha (ERα) is expressed in prostate cancers, independent of AR status. However, the role of ERα remains elusive. Using a combination of chromatin immunoprecipitation (ChIP) and RNA-sequencing data, we identified an ERα-specific non-coding transcriptome signature. Among putatively ERα-regulated intergenic long non-coding RNAs (lncRNAs), we identified nuclear enriched abundant transcript 1 (NEAT1) as the most significantly overexpressed lncRNA in prostate cancer. Analysis of two large clinical cohorts also revealed that NEAT1 expression is associated with prostate cancer progression. Prostate cancer cells expressing high levels of NEAT1 were recalcitrant to androgen or AR antagonists. Finally, we provide evidence that NEAT1 drives oncogenic growth by altering the epigenetic landscape of target gene promoters to favour transcription.',
			'date' => '2014-10-21',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/25415230',
			'doi' => '',
			'modified' => '2015-07-24 15:39:04',
			'created' => '2015-07-24 15:39:04',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '2446',
			'name' => 'Estrogen receptor ligands ameliorate fatty liver through a nonclassical estrogen receptor/Liver X receptor pathway in mice.',
			'authors' => 'Han SI, Komatsu Y, Murayama A, Steffensen KR, Nakagawa Y, Nakajima Y, Suzuki M, Oie S, Parini P, Vedin LL, Kishimoto H, Shimano H, Gustafsson JÅ, Yanagisawa J',
			'description' => 'UNLABELLED: Liver X receptor (LXR) activation stimulates triglyceride (TG) accumulation in the liver. Several lines of evidence indicate that estradiol-17β (E2) reduces TG levels in the liver; however, the molecular mechanism underlying the E2 effect remains unclear. Here, we show that administration of E2 attenuated sterol regulatory element-binding protein (SREBP)-1 expression and TG accumulation induced by LXR activation in mouse liver. In estrogen receptor alpha (ERα) knockout (KO) and liver-specific ERα KO mice, E2 did not affect SREBP-1 expression or TG levels. Molecular analysis revealed that ERα is recruited to the SREBP-1c promoter through direct binding to LXR and inhibits coactivator recruitment to LXR in an E2-dependent manner. Our findings demonstrate the existence of a novel liver-dependent mechanism controlling TG accumulation through the nonclassical ER/LXR pathway. To confirm that a nonclassical ER/LXR pathway regulates ERα-dependent inhibition of LXR activation, we screened ERα ligands that were able to repress LXR activation without enhancing ERα transcriptional activity, and, as a result, we identified the phytoestrogen, phloretin. In mice, phloretin showed no estrogenic activity; however, it did reduce SREBP-1 expression and TG levels in liver of mice fed a high-fat diet to an extent similar to that of E2. CONCLUSION: We propose that ER ligands reduce TG levels in the liver by inhibiting LXR activation through a nonclassical pathway. Our results also indicate that the effects of ER on TG accumulation can be distinguished from its estrogenic effects by a specific ER ligand.',
			'date' => '2014-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/24277692',
			'doi' => '',
			'modified' => '2015-07-24 15:39:04',
			'created' => '2015-07-24 15:39:04',
			'ProductsPublication' => array(
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			)
		),
		(int) 7 => array(
			'id' => '764',
			'name' => 'Functional Genomic Methods to Study Estrogen Receptor Activity.',
			'authors' => 'Gilfillan S, Fiorito E, Hurtado A',
			'description' => 'Estrogen Receptor (ER) is a nuclear receptor that mediates the actions of estrogen and tamoxifen. ER is expressed in a major fraction of human breast cancers. Recently, genomic maps for estrogen- and tamoxifen-ER have been published. Interestingly, estrogen and tamoxifen induce similar genomic interactions and both ligands have been shown to use co-operating factors. The interactions of these co-operating factors within ER regions have impact both on ER-DNA interactions and gene expression regulated by estrogen and tamoxifen. Moreover, the study of chromatin changes induced by these factors has also provided significant insight into our understanding of ER transcriptional regulation. This methods review describes some functional genomic methods to study the influence of both ER ligands and ER co-operating factors. The analysis of protein-DNA interactions and chromatin changes can be explored by using classical and novel methods such as Chromatin Immunoprecipitation (ChIP) or Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE). This review also explores the properties of each of these methods and the advantages of combining them with high throughput sequencing.',
			'date' => '2012-05-16',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/22588661',
			'doi' => '',
			'modified' => '2015-07-24 15:38:58',
			'created' => '2015-07-24 15:38:58',
			'ProductsPublication' => array(
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		),
		(int) 8 => array(
			'id' => '67',
			'name' => 'ChIP-Seq of ERalpha and RNA polymerase II defines genes differentially responding to ligands.',
			'authors' => 'Welboren WJ, van Driel MA, et al.,',
			'description' => 'We used ChIP-Seq to map ERa-binding sites and to profile changes in RNA polymerase II (RNAPII) occupancy in MCF-7 cells in response to estradiol (E2), tamoxifen or fulvestrant. We identify 10 205 high confidence ERa-binding sites in response to E2 of which 68% contain an estrogen response element (ERE) and only 7% contain a FOXA1 motif. Remarkably, 596 genes change significantly in RNAPII occupancy (59% up and 41% down) already after 1 h of E2 exposure. Although promoter proximal enrichment of RNAPII (PPEP) occurs frequently in MCF- 7 cells (17%), it is only observed on a minority of E2- regulated genes (4%). Tamoxifen and fulvestrant partially reduce ERa DNA binding and prevent RNAPII loading on the promoter and coding body on E2-upregulated genes. Both ligands act differently on E2-downregulated genes: tamoxifen acts as an agonist thus downregulating these genes, whereas fulvestrant antagonizes E2-induced repression and often increases RNAPII occupancy. Furthermore, our data identify genes preferentially regulated by tamoxifen but not by E2 or fulvestrant. Thus (partial) antagonist loaded ERa acts mechanistically different on E2-activated and E2-repressed genes.',
			'date' => '0000-00-00',
			'pmid' => '',
			'doi' => '',
			'modified' => '2015-07-24 15:38:56',
			'created' => '2015-07-24 15:38:56',
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		'name' => 'ERalpha Antibody',
		'description' => '<p>Alternative names: <strong>ESR</strong>, <strong>ESR1</strong>, <strong>ESRA</strong>, <strong>NR3A1</strong></p>
<p>Monoclonal antibody raised in mouse against human <strong>ERalpha (estrogen receptor alpha)</strong>, using a synthetic peptide.</p>',
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<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-A-CHIP.png" alt="ER Antibody ChIP-seq Grade" caption="false" width="284" height="50" /></p>
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<p><small><strong> Figure 1. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against ERalpha </strong><br />ChIP was performed with the Diagenode monoclonal antibody against ERalpha (cat. No. AC-066-100) on sheared chromatin from MCF7 cells treated for 1 hour with estradiol. The IP&rsquo;d DNA was analysed with an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer&rsquo;s instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. Figure 1 shows the obtained peaks near the TFF1 gene on chromosome 21 (figure 1A), the GREB1 and HAAO genes on chromosome 2 (figure 1B and C), and the ZNF185 gene on the X-chromosome (figure 1D). </small></p>
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		'modified' => '2021-12-23 12:20:58',
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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
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		'select_label' => '66 - ER alpha monoclonal antibody (007 - not determined - Human, mouse - Ascites fluid - Mouse)'
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			'antibody_id' => '66',
			'name' => 'ERalpha Antibody',
			'description' => '<p>Alternative names: <strong>ESR</strong>, <strong>ESR1</strong>, <strong>ESRA</strong>, <strong>NR3A1</strong></p>
<p>Monoclonal antibody raised in mouse against human <strong>ERalpha (estrogen receptor alpha)</strong>, using a synthetic peptide.</p>',
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<div class="small-4 columns">
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-A-CHIP.png" alt="ER Antibody ChIP-seq Grade" caption="false" width="284" height="50" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-B-CHIP.png" alt="ER Antibody for ChIP-seq " caption="false" width="284" height="42" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-C-CHIP.png" alt="ER Antibody for ChIP-seq assay" caption="false" width="284" height="46" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-D-CHIP.png" alt="ER Antibody validated in ChIP-seq" caption="false" width="284" height="62" /></p>
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<div class="small-8 columns">
<p><small><strong> Figure 1. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against ERalpha </strong><br />ChIP was performed with the Diagenode monoclonal antibody against ERalpha (cat. No. AC-066-100) on sheared chromatin from MCF7 cells treated for 1 hour with estradiol. The IP&rsquo;d DNA was analysed with an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer&rsquo;s instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. Figure 1 shows the obtained peaks near the TFF1 gene on chromosome 21 (figure 1A), the GREB1 and HAAO genes on chromosome 2 (figure 1B and C), and the ZNF185 gene on the X-chromosome (figure 1D). </small></p>
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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</p>',
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			'meta_description' => 'Diagenode offers a wide range of antibodies and technical support for ChIP Sequencing applications',
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			'meta_description' => 'Diagenode offers a wide range of antibodies and technical support for ChIP-qPCR applications',
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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">
<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>
<div class="small-12 medium-3 large-3 columns">
<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 &micro;g of the Diagenode antibodies against H3K27me3 (cat. No. C15410195) and H3K4me3 (cat. No. C15410003), and 0.5 &micro;g 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>
</div>
</div>
<p>Diagenode&rsquo;s highly validated antibodies:</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><span style="font-weight: 400;">The list of Diagenode&rsquo;s highly specific antibodies for transcription studies includes the antibodies against many transcription factors and nuclear receptors. &nbsp;Check the list below to see our targets.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Highly sensitive and specific</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Cost-effective (requires less antibody per reaction)</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Batch-specific data is available on the website</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Expert technical support</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Sample sizes available</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; 100% satisfaction guarantee</span></li>
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			'description' => '<h1><strong>Validated epigenetics antibodies</strong>&nbsp;&ndash; care for a sample?<br />&nbsp;</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> -&nbsp;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>&nbsp;with rigorous QC and validation</li>
<li><strong>Classified</strong>&nbsp;based on level of validation for flexibility of application</li>
</ul>
<p>Existing sample sizes are listed below. We will soon expand our collection. &nbsp;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&rsquo;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&rsquo;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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			'name' => 'ChIP-grade antibodies',
			'description' => '<div class="row">
<div class="small-12 columns"><center></center>
<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>
<p></p>
</div>
</div>
<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>).&nbsp;</p>
<div class="row">
<div class="small-12 medium-6 large-6 columns"><img src="https://www.diagenode.com/img/product/antibodies/C15410003-fig1-ChIP.jpg" alt="" width="400" height="315" />&nbsp;</div>
<div class="small-12 medium-6 large-6 columns">
<p></p>
<p></p>
<p></p>
</div>
</div>
<p></p>
<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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			'meta_description' => 'Diagenode Offers Extensively Validated ChIP-Grade Antibodies, Confirmed for their Specificity, and high level of Performance in Chromatin Immunoprecipitation ChIP',
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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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			'url' => 'files/products/antibodies/Datasheet_hERalpha_C15100066.pdf',
			'slug' => 'datasheet-heralpha-C15100066',
			'meta_keywords' => '',
			'meta_description' => '',
			'modified' => '2015-11-20 17:15:38',
			'created' => '2015-07-07 11:47:43',
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			'id' => '1783',
			'name' => 'product/antibodies/chipseq-grade-ab-icon.png',
			'alt' => 'ChIP-seq Grade',
			'modified' => '2020-11-27 07:04:40',
			'created' => '2018-03-15 15:54:09',
			'ProductsImage' => array(
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	'Promotion' => array(),
	'Protocol' => array(),
	'Publication' => array(
		(int) 0 => array(
			'id' => '4832',
			'name' => 'Carnobacterium maltaromaticum boosts intestinal vitamin D production tosuppress colorectal cancer in female mice.',
			'authors' => 'Li  Q. et al.',
			'description' => '<p>Carnobacterium maltaromaticum was found to be specifically depleted in female patients with colorectal cancer (CRC). Administration of C.&Acirc;&nbsp;maltaromaticum reduces intestinal tumor formation in two murine CRC models in a female-specific manner. Estrogen increases the attachment and colonization of C.&Acirc;&nbsp;maltaromaticum via increasing the colonic expression of SLC3A2 that binds to DD-CPase of this bacterium. Metabolomic and transcriptomic&Acirc;&nbsp;profiling unveils the increased gut abundance of vitamin D-related metabolites and the mucosal activation of vitamin D receptor (VDR) signaling in C.&Acirc;&nbsp;maltaromaticum-gavaged mice in a gut microbiome- and VDR-dependent manner. In&Acirc;&nbsp;vitro fermentation system confirms the metabolic cross-feeding of&Acirc;&nbsp;C.&Acirc;&nbsp;maltaromaticum with Faecalibacterium prausnitzii to convert C.&Acirc;&nbsp;maltaromaticum-produced 7-dehydrocholesterol into vitamin D for activating the host VDR signaling. Overall, C.&Acirc;&nbsp;maltaromaticum colonizes the gut in an estrogen-dependent manner and acts along with other microbes to augment the intestinal vitamin D production to activate the host VDR for suppressing CRC.</p>',
			'date' => '2023-07-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37478851',
			'doi' => '10.1016/j.ccell.2023.06.011',
			'modified' => '2023-08-01 13:44:12',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
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		),
		(int) 1 => array(
			'id' => '4567',
			'name' => '27-Hydroxycholesterol, The Estrogen Receptor Modulator, AltersDNA Methylation in Breast Cancer.',
			'authors' => 'Vini  Ravindran et al.',
			'description' => '<p>27-hydroxycholesterol (27-HC) is the first known endogenous selective estrogen receptor modulator (SERM), and its elevation from normal levels is closely associated with breast cancer. A plethora of evidence suggests that aberrant epigenetic signatures in breast cancer cells can result in differential responses to various chemotherapeutics and often leads to the development of resistant cancer cells. Such aberrant epigenetic changes are mostly dictated by the microenvironment. The local concentration of oxygen and metabolites in the microenvironment of breast cancer are known to influence the development of breast cancer. Hence, we hypothesized that 27-HC, an oxysterol, which has been shown to induce breast cancer progression estrogen receptor alpha (ER&alpha;) and liver X receptor (LXR) and by modulating immune cells, may also induce epigenetic changes. For deciphering the same, we treated the estrogen receptor-positive cells with 27-HC and identified DNA hypermethylation on a subset of genes by performing DNA bisulfite sequencing. The genes that showed significant DNA hypermethylation were and . Furthermore, we found that 27-HC weakens the DNMT3B association with the ER&alpha; in MCF-7 cells. This study reports that 27-HC induces aberrant DNA methylation changes on the promoters of a subset of genes through modulation of ER&alpha; and DNMT3B complexes to induce the local DNA methylation changes, which may dictate drug responses and breast cancer development.</p>',
			'date' => '2022-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35360070',
			'doi' => '10.3389/fendo.2022.783823',
			'modified' => '2022-11-24 08:58:58',
			'created' => '2022-11-24 08:49:52',
			'ProductsPublication' => array(
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		),
		(int) 2 => array(
			'id' => '4329',
			'name' => 'Epigenetic remodelling of enhancers in response to estrogen deprivationand re-stimulation.',
			'authors' => 'Sklias Athena et al.',
			'description' => '<p>Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER), the main nuclear factor mediating estrogen signaling, orchestrates a complex molecular circuitry that is not yet fully elucidated. Here, we investigated genome-wide DNA methylation, histone acetylation and transcription after estradiol (E2) deprivation and re-stimulation to better characterize the ability of ER to coordinate gene regulation. We found that E2 deprivation mostly resulted in DNA hypermethylation and histone deacetylation in enhancers. Transcriptome analysis revealed that E2 deprivation leads to a global down-regulation in gene expression, and more specifically of TET2 demethylase that may be involved in the DNA hypermethylation following short-term E2 deprivation. Further enrichment analysis of transcription factor (TF) binding and motif occurrence highlights the importance of ER connection mainly with two partner TF families, AP-1 and FOX. These interactions take place in the proximity of E2 deprivation-mediated differentially methylated and histone acetylated enhancers. Finally, while most deprivation-dependent epigenetic changes were reversed following E2 re-stimulation, DNA hypermethylation and H3K27 deacetylation at certain enhancers were partially retained. Overall, these results show that inactivation of ER mediates rapid and mostly reversible epigenetic changes at enhancers, and bring new insight into early events, which may ultimately lead to endocrine resistance.</p>',
			'date' => '2021-09-01',
			'pmid' => 'https://doi.org/10.1093%2Fnar%2Fgkab697',
			'doi' => '10.1093/nar/gkab697',
			'modified' => '2022-06-22 09:25:09',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 3 => array(
			'id' => '3961',
			'name' => 'Estrogen induces dynamic ERα and RING1B recruitment to control gene and enhancer activities in luminal breast cancer',
			'authors' => 'Zhang Yusheng, Chan Ho Lam, Garcia-Martinez Liliana, Karl Daniel L., Weich Natalia, Slingerland Joyce M., Verdun Ramiro E., Morey Lluis',
			'description' => '<p>RING1B, a core Polycomb repressive complex 1 subunit, is a histone H2A ubiquitin ligase essential for development. RING1B is overexpressed in patients with luminal breast cancer (BC) and recruited to actively transcribed genes and enhancers co-occupied by the estrogen receptor  (ER). Whether ER-induced transcriptional programs are mediated by RING1B is not understood. We show that prolonged estrogen administration induces transcriptional output and chromatin landscape fluctuations. RING1B loss impairs full estrogen-mediated gene expression and chromatin accessibility for key BC transcription factors. These effects were mediated, in part, by RING1B enzymatic activity and nucleosome binding functions. RING1B is recruited in a cyclic manner to ER, FOXA1, and GRHL2 cobound sites and regulates estrogen-induced enhancers and ER recruitment. Last, ChIP exo revealed multiple binding events of these factors at single-nucleotide resolution, including RING1B occupancy approximately 10 base pairs around ER bound sites. We propose RING1B as a key regulator of the dynamic, liganded-ER transcriptional regulatory circuit in luminal BC.</p>',
			'date' => '2020-06-12',
			'pmid' => 'https://advances.sciencemag.org/content/6/23/eaaz7249.full',
			'doi' => '10.1126/sciadv.aaz7249',
			'modified' => '2020-08-12 09:48:21',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 4 => array(
			'id' => '3705',
			'name' => 'Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha.',
			'authors' => 'Glont SE, Papachristou EK, Sawle A, Holmes KA, Carroll JS, Siersbaek R',
			'description' => '<p>Estrogen Receptor alpha (ER&alpha;) plays a major role in most breast cancers, and it is the target of endocrine therapies used in the clinic as standard of care for women with breast cancer expressing this receptor. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ER&alpha; function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used against the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ER&alpha; have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ER&alpha; in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.</p>',
			'date' => '2019-01-01',
			'pmid' => 'http://www.pubmed.gov/30970003',
			'doi' => '10.1371/journal.',
			'modified' => '2019-07-05 14:39:11',
			'created' => '2019-07-04 10:42:34',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 5 => array(
			'id' => '2367',
			'name' => 'The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer.',
			'authors' => 'Chakravarty D, Sboner A, Nair SS, Giannopoulou E, Li R, Hennig S, Mosquera JM, Pauwels J, Park K, Kossai M, MacDonald TY, Fontugne J, Erho N, Vergara IA, Ghadessi M, Davicioni E, Jenkins RB, Palanisamy N, Chen Z, Nakagawa S, Hirose T, Bander NH, Beltran H',
			'description' => 'The androgen receptor (AR) plays a central role in establishing an oncogenic cascade that drives prostate cancer progression. Some prostate cancers escape androgen dependence and are often associated with an aggressive phenotype. The oestrogen receptor alpha (ERα) is expressed in prostate cancers, independent of AR status. However, the role of ERα remains elusive. Using a combination of chromatin immunoprecipitation (ChIP) and RNA-sequencing data, we identified an ERα-specific non-coding transcriptome signature. Among putatively ERα-regulated intergenic long non-coding RNAs (lncRNAs), we identified nuclear enriched abundant transcript 1 (NEAT1) as the most significantly overexpressed lncRNA in prostate cancer. Analysis of two large clinical cohorts also revealed that NEAT1 expression is associated with prostate cancer progression. Prostate cancer cells expressing high levels of NEAT1 were recalcitrant to androgen or AR antagonists. Finally, we provide evidence that NEAT1 drives oncogenic growth by altering the epigenetic landscape of target gene promoters to favour transcription.',
			'date' => '2014-10-21',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/25415230',
			'doi' => '',
			'modified' => '2015-07-24 15:39:04',
			'created' => '2015-07-24 15:39:04',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '2446',
			'name' => 'Estrogen receptor ligands ameliorate fatty liver through a nonclassical estrogen receptor/Liver X receptor pathway in mice.',
			'authors' => 'Han SI, Komatsu Y, Murayama A, Steffensen KR, Nakagawa Y, Nakajima Y, Suzuki M, Oie S, Parini P, Vedin LL, Kishimoto H, Shimano H, Gustafsson JÅ, Yanagisawa J',
			'description' => 'UNLABELLED: Liver X receptor (LXR) activation stimulates triglyceride (TG) accumulation in the liver. Several lines of evidence indicate that estradiol-17β (E2) reduces TG levels in the liver; however, the molecular mechanism underlying the E2 effect remains unclear. Here, we show that administration of E2 attenuated sterol regulatory element-binding protein (SREBP)-1 expression and TG accumulation induced by LXR activation in mouse liver. In estrogen receptor alpha (ERα) knockout (KO) and liver-specific ERα KO mice, E2 did not affect SREBP-1 expression or TG levels. Molecular analysis revealed that ERα is recruited to the SREBP-1c promoter through direct binding to LXR and inhibits coactivator recruitment to LXR in an E2-dependent manner. Our findings demonstrate the existence of a novel liver-dependent mechanism controlling TG accumulation through the nonclassical ER/LXR pathway. To confirm that a nonclassical ER/LXR pathway regulates ERα-dependent inhibition of LXR activation, we screened ERα ligands that were able to repress LXR activation without enhancing ERα transcriptional activity, and, as a result, we identified the phytoestrogen, phloretin. In mice, phloretin showed no estrogenic activity; however, it did reduce SREBP-1 expression and TG levels in liver of mice fed a high-fat diet to an extent similar to that of E2. CONCLUSION: We propose that ER ligands reduce TG levels in the liver by inhibiting LXR activation through a nonclassical pathway. Our results also indicate that the effects of ER on TG accumulation can be distinguished from its estrogenic effects by a specific ER ligand.',
			'date' => '2014-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/24277692',
			'doi' => '',
			'modified' => '2015-07-24 15:39:04',
			'created' => '2015-07-24 15:39:04',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '764',
			'name' => 'Functional Genomic Methods to Study Estrogen Receptor Activity.',
			'authors' => 'Gilfillan S, Fiorito E, Hurtado A',
			'description' => 'Estrogen Receptor (ER) is a nuclear receptor that mediates the actions of estrogen and tamoxifen. ER is expressed in a major fraction of human breast cancers. Recently, genomic maps for estrogen- and tamoxifen-ER have been published. Interestingly, estrogen and tamoxifen induce similar genomic interactions and both ligands have been shown to use co-operating factors. The interactions of these co-operating factors within ER regions have impact both on ER-DNA interactions and gene expression regulated by estrogen and tamoxifen. Moreover, the study of chromatin changes induced by these factors has also provided significant insight into our understanding of ER transcriptional regulation. This methods review describes some functional genomic methods to study the influence of both ER ligands and ER co-operating factors. The analysis of protein-DNA interactions and chromatin changes can be explored by using classical and novel methods such as Chromatin Immunoprecipitation (ChIP) or Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE). This review also explores the properties of each of these methods and the advantages of combining them with high throughput sequencing.',
			'date' => '2012-05-16',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/22588661',
			'doi' => '',
			'modified' => '2015-07-24 15:38:58',
			'created' => '2015-07-24 15:38:58',
			'ProductsPublication' => array(
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		),
		(int) 8 => array(
			'id' => '67',
			'name' => 'ChIP-Seq of ERalpha and RNA polymerase II defines genes differentially responding to ligands.',
			'authors' => 'Welboren WJ, van Driel MA, et al.,',
			'description' => 'We used ChIP-Seq to map ERa-binding sites and to profile changes in RNA polymerase II (RNAPII) occupancy in MCF-7 cells in response to estradiol (E2), tamoxifen or fulvestrant. We identify 10 205 high confidence ERa-binding sites in response to E2 of which 68% contain an estrogen response element (ERE) and only 7% contain a FOXA1 motif. Remarkably, 596 genes change significantly in RNAPII occupancy (59% up and 41% down) already after 1 h of E2 exposure. Although promoter proximal enrichment of RNAPII (PPEP) occurs frequently in MCF- 7 cells (17%), it is only observed on a minority of E2- regulated genes (4%). Tamoxifen and fulvestrant partially reduce ERa DNA binding and prevent RNAPII loading on the promoter and coding body on E2-upregulated genes. Both ligands act differently on E2-downregulated genes: tamoxifen acts as an agonist thus downregulating these genes, whereas fulvestrant antagonizes E2-induced repression and often increases RNAPII occupancy. Furthermore, our data identify genes preferentially regulated by tamoxifen but not by E2 or fulvestrant. Thus (partial) antagonist loaded ERa acts mechanistically different on E2-activated and E2-repressed genes.',
			'date' => '0000-00-00',
			'pmid' => '',
			'doi' => '',
			'modified' => '2015-07-24 15:38:56',
			'created' => '2015-07-24 15:38:56',
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		'id' => '1953',
		'antibody_id' => '66',
		'name' => 'ERalpha Antibody',
		'description' => '<p>Alternative names: <strong>ESR</strong>, <strong>ESR1</strong>, <strong>ESRA</strong>, <strong>NR3A1</strong></p>
<p>Monoclonal antibody raised in mouse against human <strong>ERalpha (estrogen receptor alpha)</strong>, using a synthetic peptide.</p>',
		'label1' => 'Validation Data',
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<div class="small-4 columns">
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-A-CHIP.png" alt="ER Antibody ChIP-seq Grade" caption="false" width="284" height="50" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-B-CHIP.png" alt="ER Antibody for ChIP-seq " caption="false" width="284" height="42" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-C-CHIP.png" alt="ER Antibody for ChIP-seq assay" caption="false" width="284" height="46" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-D-CHIP.png" alt="ER Antibody validated in ChIP-seq" caption="false" width="284" height="62" /></p>
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<p><small><strong> Figure 1. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against ERalpha </strong><br />ChIP was performed with the Diagenode monoclonal antibody against ERalpha (cat. No. AC-066-100) on sheared chromatin from MCF7 cells treated for 1 hour with estradiol. The IP&rsquo;d DNA was analysed with an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer&rsquo;s instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. Figure 1 shows the obtained peaks near the TFF1 gene on chromosome 21 (figure 1A), the GREB1 and HAAO genes on chromosome 2 (figure 1B and C), and the ZNF185 gene on the X-chromosome (figure 1D). </small></p>
</div>
</div>',
		'label2' => 'Target Description',
		'info2' => '<p>The estrogen receptor alpha (ERalpha, UniProt/Swiss-Prot entry P03372) belongs to the family of nuclear hormone receptors, which are ligand-activated transcription factors. They are important for the regulation of gene expression, cellular proliferation and differentiation, sexual development and reproductive function. Estrogen receptors are also involved in pathological processes such as breast cancer, and osteoporosis. ERalpha can regulate transcription by direct binding to estrogen response elements (EREs) in the DNA or by interaction with other transcription factors. It may also form a heterodimer with ERbeta.</p>',
		'label3' => '',
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		'price_EUR' => '380',
		'price_USD' => '380',
		'price_GBP' => '340',
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		'price_CNY' => '',
		'price_AUD' => '950',
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		'slug' => 'er-alpha-monoclonal-antibody-classic-100-ul',
		'meta_title' => 'ER alpha Antibody - ChIP-seq Grade (C15100066-100) | Diagenode',
		'meta_keywords' => '',
		'meta_description' => 'ER alpha (Estrogen receptor alpha) Monoclonal Antibody validated  in ChIP-seq, ChIP-qPCR, WB, IP, IC, GSA and ELISA. Batch-specific data available on the website. Alternative names: ESR, ESR1, ESRA, NR3A1. Sample size available.',
		'modified' => '2021-12-23 12:20:58',
		'created' => '2015-06-29 14:08:20'
	)
)
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	'description' => '',
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	'label3' => '',
	'info3' => '',
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	'type' => 'FRE',
	'search_order' => '03-Antibody',
	'price_EUR' => '105',
	'price_USD' => '115',
	'price_GBP' => '100',
	'price_JPY' => '16450',
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	'meta_description' => 'ER alpha (Estrogen receptor alpha) Monoclonal Antibody  validated  in ChIP-seq, ChIP-qPCR, ELISA, IP, IC, GSA and WB. Alternative names: ESR, ESR1, ESRA, NR3A1. Sample size available.',
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	'name' => 'ERalpha Antibody',
	'description' => '<p>Alternative names: <strong>ESR</strong>, <strong>ESR1</strong>, <strong>ESRA</strong>, <strong>NR3A1</strong></p>
<p>Monoclonal antibody raised in mouse against human <strong>ERalpha (estrogen receptor alpha)</strong>, using a synthetic peptide.</p>',
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<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-A-CHIP.png" alt="ER Antibody ChIP-seq Grade" caption="false" width="284" height="50" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-B-CHIP.png" alt="ER Antibody for ChIP-seq " caption="false" width="284" height="42" /></p>
<p><img src="https://www.diagenode.com/img/product/antibodies/C15100066-C-CHIP.png" alt="ER Antibody for ChIP-seq assay" caption="false" width="284" height="46" /></p>
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<p><small><strong> Figure 1. ChIP-seq results obtained with the Diagenode monoclonal antibody directed against ERalpha </strong><br />ChIP was performed with the Diagenode monoclonal antibody against ERalpha (cat. No. AC-066-100) on sheared chromatin from MCF7 cells treated for 1 hour with estradiol. The IP&rsquo;d DNA was analysed with an Illumina Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer&rsquo;s instructions. The 36 bp tags were aligned to the human genome using the ELAND algorithm. Figure 1 shows the obtained peaks near the TFF1 gene on chromosome 21 (figure 1A), the GREB1 and HAAO genes on chromosome 2 (figure 1B and C), and the ZNF185 gene on the X-chromosome (figure 1D). </small></p>
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	'info2' => '<p>The estrogen receptor alpha (ERalpha, UniProt/Swiss-Prot entry P03372) belongs to the family of nuclear hormone receptors, which are ligand-activated transcription factors. They are important for the regulation of gene expression, cellular proliferation and differentiation, sexual development and reproductive function. Estrogen receptors are also involved in pathological processes such as breast cancer, and osteoporosis. ERalpha can regulate transcription by direct binding to estrogen response elements (EREs) in the DNA or by interaction with other transcription factors. It may also form a heterodimer with ERbeta.</p>',
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	'format' => '100 µl',
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	'meta_title' => 'ER alpha Antibody - ChIP-seq Grade (C15100066-100) | Diagenode',
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	'meta_description' => 'ER alpha (Estrogen receptor alpha) Monoclonal Antibody validated  in ChIP-seq, ChIP-qPCR, WB, IP, IC, GSA and ELISA. Batch-specific data available on the website. Alternative names: ESR, ESR1, ESRA, NR3A1. Sample size available.',
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	'meta_description' => 'Diagenode offers a wide range of antibodies and technical support for ChIP-qPCR applications',
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	'meta_description' => 'Diagenode offers a wide range of antibodies and technical support for ChIP-qPCR applications',
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	'name' => 'ChIP-Seq of ERalpha and RNA polymerase II defines genes differentially responding to ligands.',
	'authors' => 'Welboren WJ, van Driel MA, et al.,',
	'description' => 'We used ChIP-Seq to map ERa-binding sites and to profile changes in RNA polymerase II (RNAPII) occupancy in MCF-7 cells in response to estradiol (E2), tamoxifen or fulvestrant. We identify 10 205 high confidence ERa-binding sites in response to E2 of which 68% contain an estrogen response element (ERE) and only 7% contain a FOXA1 motif. Remarkably, 596 genes change significantly in RNAPII occupancy (59% up and 41% down) already after 1 h of E2 exposure. Although promoter proximal enrichment of RNAPII (PPEP) occurs frequently in MCF- 7 cells (17%), it is only observed on a minority of E2- regulated genes (4%). Tamoxifen and fulvestrant partially reduce ERa DNA binding and prevent RNAPII loading on the promoter and coding body on E2-upregulated genes. Both ligands act differently on E2-downregulated genes: tamoxifen acts as an agonist thus downregulating these genes, whereas fulvestrant antagonizes E2-induced repression and often increases RNAPII occupancy. Furthermore, our data identify genes preferentially regulated by tamoxifen but not by E2 or fulvestrant. Thus (partial) antagonist loaded ERa acts mechanistically different on E2-activated and E2-repressed genes.',
	'date' => '0000-00-00',
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Antibodies you can trust POSTER Epigenetic research tools have evolved over time from endpoint PCR to qPCR to the analyses of lar...	Download
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