Abstract
In mammals, a single gene encodes the receptor for the steroid reproductive hormone progesterone, but the protein exists in two forms, progesterone receptor-A (PR-A) and PR-B, that result from alternative starting points for transcription and translation. Mulac-Jericevic et al . describe mice in which a mutation selectively prevents expression of PR-A. Acting alone, PR-B regulated only a subset of known progesterone-responsive genes in the uterus. Progesterone normally antagonizes estrogen-induced proliferation in the uterine epithelium, yet interactions with PR-B promoted proliferation. The separation of distinct physiological functions for PR-A and PR-B raises the possibility that selective modulators of the PR isoforms could provide more specific therapeutic effects. Mulac-Jericevic, B., Mullinax, R.A., DeMayo, F.J., Lydon, J.P., and Conneely, O.M. (2000) Subgroup of reproductive functions of progesterone mediated by progesterone receptor-B isoform. Science 289 : 1751-1754. [Abstract] [Full Text]
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