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Cloning and Characterization of a 5' Regulatory Region of the Prolactin Receptor-Associated Protein/17ß Hydroxysteroid Dehydrogenase 7 Gene

Department of Physiology and Biophysics (M.R., A.S., J.M., C.O.S., J.M.B.-S., G.G.), University of Illinois at Chicago, Chicago, Illinois 60612; and Department of Obstetrics (L.T.G.), Gynecology and Women’s Health, New Jersey Medical School, Newark, New Jersey 07101

Address all correspondence and requests for reprints to: Dr. Geula Gibori, Department of Physiology and Biophysics, University of Illinois at Chicago, 835 South Wolcott (M/C 901), Chicago, Illinois 60612. E-mail: ggibori{at}uic.edu.

Prolactin receptor-associated protein (PRAP) originally cloned in our laboratory was shown to be a novel, luteal isoform of 17ß hydroxysteroid dehydrogenase 7 (17ßHSD7). In this study, we cloned the promoter region of rat PRAP/17ßHSD7 and investigated the mechanisms regulating both basal activity and LH-induced repression of this promoter. Truncated and site-specific mutants of PRAP/17ßHSD7 promoter identified two enhancer regions that contained highly conserved Sp1 binding site and bound Sp1 from nuclear extracts of both corpora lutea and a rat luteal cell line. Repression of PRAP/17ßHSD7 expression and promoter activity by human chorionic gonadotropin/forskolin was localized to a –52-bp proximal segment of the promoter. This region contained a conserved CCAAT site and bound nuclear factor Y; binding of this transcription factor was inhibited by human chorionic gonadotropin in vivo. Furthermore, mutation of the nuclear factor Y site in the –52-bp promoter-reporter construct abolished forskolin-mediated inhibition of the promoter in a rat luteal cell line. In summary, we have identified the promoter elements involved in the basal expression of PRAP/17ßHSD7. We have also found that LH-mediated repression of this gene is at the level of transcription and involves inhibition of nuclear factor YA binding to the CCAAT site within the proximal promoter.

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