例如:"lncRNA", "apoptosis", "WRKY"

Cloning and characterization of a 5' regulatory region of the prolactin receptor-associated protein/17{beta} hydroxysteroid dehydrogenase 7 gene.

Endocrinology. 2005 Jun;146(6):2807-16. Epub 2005 Feb 24
Michael Risk 1 , Aurora Shehu , Jifang Mao , Carlos O Stocco , Laura T Goldsmith , Jennifer M Bowen-Shauver , Geula Gibori
Michael Risk 1 , Aurora Shehu , Jifang Mao , Carlos O Stocco , Laura T Goldsmith , Jennifer M Bowen-Shauver , Geula Gibori
+ et al

[No authors listed]

Author information
  • 1 Department of Physiology and Biophysics, University of Illinois at Chicago, 835 South Wolcott (M/C 901), Chicago, Illinois 60612, USA.

摘要


Prolactin receptor-associated protein (PRAP) originally cloned in our laboratory was shown to be a novel, luteal isoform of 17beta hydroxysteroid dehydrogenase 7 (17betaHSD7). In this study, we cloned the promoter region of rat PRAP/17betaHSD7 and investigated the mechanisms regulating both basal activity and LH-induced repression of this promoter. Truncated and site-specific mutants of PRAP/17betaHSD7 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/17betaHSD7 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/17betaHSD7. 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.