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ER alpha monoclonal antibody

Catalog # Availability Size / Price Inquiry
AMM00028G 50 μg / $545

ER alpha monoclonal antibody

Brand

Leading Biology

Catalog Number

AMM00028G

Product Type

Monoclonal Antibodies

Field of Research

Product Overview

We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality ER alpha monoclonal antibody.

Molecular Weight

66216 Da

Cellular Localization

Antigen Cellular Localization: Isoform 1: Nucleus {ECO:0000255|PROSITE- ProRule:PRU00407, ECO:0000269|PubMed:12682286}. Cytoplasm. Cell membrane; Peripheral membrane protein; Cytoplasmic side. Note=A minor fraction is associated with the inner membrane Nucleus. Golgi apparatus. Cell membrane. Note=Colocalizes with ZDHHC7 and ZDHHC21 in the Golgi apparatus where most probably palmitoylation occurs. Associated with the plasma membrane when palmitoylated

Host

Mouse

Species Reactivity

Human

Target

ER alpha

GeneID

UniProt ID

Function

Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA- binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF- kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA- binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Isoform 3 is involved in activation of NOS3 and endothelial nitric oxide production. Isoforms lacking one or several functional domains are thought to modulate transcriptional activity by competitive ligand or DNA binding and/or heterodimerization with the full length receptor. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3. Isoform 3 can bind to ERE and inhibit isoform 1.

Summary

Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA- binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF- kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA- binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Isoform 3 is involved in activation of NOS3 and endothelial nitric oxide production. Isoforms lacking one or several functional domains are thought to modulate transcriptional activity by competitive ligand or DNA binding and/or heterodimerization with the full length receptor. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3. Isoform 3 can bind to ERE and inhibit isoform 1.

Form

Liquid

Storage & Stability

Store at +4°C short term. For long-term storage, aliquot and store at -20°C or below. Stable for 12 months at -20°C. Avoid repeated freeze-thaw cycles.

Applications

WB

Images

ChIP using the monoclonal antibody ChIP using the monoclonal antibody against hERα from ChIP assays were performed using MCF7 cells, treated with the ER agonist estradiol for 3 hours prior to harvesting., the monoclonal antibody directed against ER alpha and optimized primer sets for qPCR. Sheared chromatin from 3 million cells and 5 μg of antibody were used per ChIP experiment. Recovery (%: ChIP/input) and occupancy (x fold: +ve/-ve) are shown in figure 1. QPCR was performed with primers for the GREB1 promoter and for exon 2 of the myoglobin gene, used as a negative control. Figure 1 shows the recovery (the relative amount of immunoprecipitated DNA compared to input DNA) and the occupancy (ratio +/- control target). These results demonstrate the occupancy of the GREB1 promoter by ERalpha.

Western blot analysis using the monoclonal antibody against hERα Western blot analysis was performed on 100 fmol ER alpha (ERa) and ER beta (ERb1) recombinant protein with the monoclonal antibody directed against ER alpha at a concentration of 7 μg/ ml. Figure 2 shows the specificity of the antibody for the ER alpha isoform, whereas the ER beta isoform is not recognized.

Immunocytochemistry using the monoclonal antibody against hERα COS-7 cells transiently overexpressing human ERα (left) or ER?1 (right) were labeled with the antibody against ER alpha, used at a concentration of 15 μg/ml, followed by a biotinylated secondary antibody and peroxidase-labeled avidin. Figure 3 shows the specificity of the antibody for the ER alpha isoform.

Specification

Quantity

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