REACTIVITY | H M R Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 52, 55, 63 |
SOURCE | Rabbit |
Product Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
NOTE: Please refer to primary antibody product webpage for recommended antibody dilution.
From sample preparation to detection, the reagents you need for your Western Blot are now in one convenient kit: #12957 Western Blotting Application Solutions Kit
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalent grade water.
Load 20 µl onto SDS-PAGE gel (10 cm x 10 cm).
NOTE: Loading of prestained molecular weight markers (#59329, 10 µl/lane) to verify electrotransfer and biotinylated protein ladder (#7727, 10 µl/lane) to determine molecular weights are recommended.
NOTE: Volumes are for 10 cm x 10 cm (100 cm2) of membrane; for different sized membranes, adjust volumes accordingly.
* Avoid repeated exposure to skin.
posted June 2005
revised June 2020
Protocol Id: 10
Human, Mouse, Rat, Monkey
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human Estrogen Receptor β1 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Estrogen Receptor β (ER β) is a member of the nuclear receptor superfamily of transcription factors and was discovered to be encoded by a gene (ESR2) distinct from that encoding Estrogen Receptor α (ER α) (1,2). While studies have revealed that alternative splicing generates mutiple isoforms of ER β that differ at their respective C-termini and in tissue distribution, ER β1 is believed to be the longest and only fully functional isoform (3,4). Indeed, it has been reported that shorter isoforms of ER β (ER β2, β4, and β5) can heterodimerize with ER β1 and enhance its transcriptional activity in an estradiol-dependent manner (4). ER β is expressed in a wide range of normal and malignant tissues, many of which coexpress ER α. It is proposed that ER β has an antiproliferative role, perhaps through heterodimerization with ER α and repression of its transcriptional activity at estrogen response elements (5,6). Recent studies have revealed that expression of ESR2 is subject to epigenetic regulation and that loss of ER β expression positively contributes to epithelial-mesenchymal transition and enhanced invasiveness in prostate cancer (7,8). ER β has also been found to be negatively regulated at the posttranslational level through phosphorylation of its AF-1 domain, which promotes its ubiquitin-dependent proteasomal degradation (9,10).
Explore pathways related to this product.
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