Progesterone Receptor Antibody

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]