17-603
ChIPAb+ Estrogen Receptor α - ChIP Validated Antibody and Primer Set
ascites fluid, from mouse
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About This Item
biological source
mouse
antibody form
ascites fluid
clone
monoclonal
species reactivity
mouse, human
manufacturer/tradename
ChIPAb+
Upstate®
technique(s)
ChIP: suitable
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
Gene Information
human ... ESR1(2099)
Related Categories
General description
The qPCR primers included flank the ERα binding site in human pS2 promoter.
Immunogen
Application
Sonicated chromatin, prepared from 3x106 MCF7 cells that are either estrogen starved or b-estradiol treated (100 nM, 45 min.) was subjected to chromatin
immunoprecipitation using 4 mL anti-ERa and the Magna ChIP® G (Cat.# 17-611) kit Standard Protocol. Successful enrichment of ER associated DNA fragments was verified by qPCR using ChIP Primers TFF1 (pS2) flanking the human TFF1 promoter that contains an ER binding site (Please see figures).
Please refer to the EZ-Magna ChIP G (Cat.# 17-409) or EZ-ChIP (Cat.# 17-371) kit protocols for experimental details.
Western Blot Analysis:
MCF7cell lysate was resolved by electrophoresis, transferred to nitrocellulose and probed with anti-ERa (1:1000 dilution). Proteins were visualized using a goat anti-mouse secondary antibody conjugated to HRP and a chemiluminescence detection system (Please see figures).
Epigenetics & Nuclear Function
Chromatin Biology
Biochem/physiol Actions
Packaging
Physical form
ChIP primers TFF1 (pS2). 1 vial containing 75 mL of 5 μM of each control primer specific for human TFF1 (pS2) promoter. Store at -20°C.
FOR: CCG GCC ATC TCT CAC TAT GAA
REV: CCT TCC CGC CAG GGT AAA TAC
Preparation Note
Analysis Note
Sonicated chromatin prepared from 3x106 MCF7 cells that were treated with b-estradiol (100 nM, 45 min.) was subjected to chromatin immunoprecipitation using 4 mL anti-ERα and beads only control.
Successful enrichment of ERα associated DNA fragments was verified by qPCR using ChIP Primers TFF1 (pS2) flanking the human TFF1 promoter that contains an ER binding site (Please see figures).
Please refer to the EZ-Magna ChIP G (Cat.# 17- 409) or EZ-ChIP (Cat.# 17-371) kit protocols for experimental details.
Includes control primers specific for human TFF1 (pS2) promoter.
Legal Information
Disclaimer
Storage Class Code
10 - Combustible liquids
Certificates of Analysis (COA)
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Related Content
Signaling Product Guide: Antibodies, small molecule inhibitors, kits, assays and proteins for signaling research.
Epigenetics describes heritable changes in gene expression caused by non-genetic mechanisms. Epigenetic regulation allows a cell to vary its response based on its biological and environmental contexts. Epigenetic changes can effect transcriptional and post-transcriptional regulation via mechanisms such as histone modification, chromatin and nucleosome remodeling, DNA methylation, and small and non-coding RNA-mediated regulation. These mechanisms, in cooperation with transcription factors and other nucleic acid-binding proteins, regulate gene expression. Epigenetic mechanisms of gene regulation impacts diverse areas of research—from agriculture to human health. Common epigenetic assays such as chromatin immunoprecipitation (ChIP) and RNA immunoprecipitation (RIP) rely on high quality antibodies that recognize specific epigenetic modifications for accurate results. EMD Millipore offers over 100 ChIPAb+™ and RIPAb+™ validated antibody kits that are quality tested on ChIP/RIP assays and are conveniently provided with control qPCR primers and negative control antibodies to ensure first time ChIP/RIP success.
"Epigenetics describes heritable changes in gene expression caused by non-genetic mechanisms instead of by alterations in DNA sequence. These changes can be cell- or tissue-specific, and can be passed on to multiple generations. Epigenetic regulation enriches DNAbased information, allowing a cell to vary its response across diverse biological and environmental contexts. Although epigenetic mechanisms are primarily centered in the nucleus, these mechanisms can be induced by environmental signals such as hormones, nutrients, stress, and cellular damage, pointing to the involvement of cytoplasmic and extracellular factors in epigenetic regulation."
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