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- Email: info@nsjbio.com
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As demonstrated in PR-deficient mice, the physiological effects of progesterone depend completely on the presence of its receptor (hPR), a member of the steroid-receptor superfamily of nuclear receptors. The single-copy hPR gene uses separate promoters and translational start sites to produce two isoforms, hPR-A and -B, which are identical except for an additional 165 amino acids present only in the N terminus of -B. Although hPR-B shares many important structural domains as -A, they are in fact two functionally distinct transcription factors, mediating their own response genes and physiological effects with little overlap. Selective ablation of PR-A in a mouse model, resulting in exclusive production of -B, unexpectedly revealed that -B contributes to, rather than inhibits, epithelial cell proliferation both in response to estrogen alone and in the presence of progesterone and estrogen. These results suggest that in the uterus, the PR-A isoform is necessary to oppose estrogen-induced proliferation as well as -B-dependent proliferation. [Wiki]
Titration of the Progesterone Receptor antibody may be required due to differences in protocols and secondary/substrate sensitivity.
A portion of amino acids 349-377 from the human protein was used as the immunogen for this Progesterone Receptor antibody.
Aliquot the Progesterone Receptor antibody and store frozen at -20oC or colder. Avoid repeated freeze-thaw cycles.
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