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We attempted to elucidate molecular mechanisms of gonadotropin-releasing hormone (GnRH) gene regulation by the protein kinase C (PKC) pathway in GT1-1 cells. Activation of PKC with 12-tetra-decanoylphorbol-13-acetate (TPA) or inhibition with staurosporine or calphostin C down-regulated GnRH mRNA levels. A serial deletion mutant analysis revealed that this suppression was mediated by the proximal region (-187/-69) of the mouse GnRH promoter. TPA transiently induced c-fos mRNA, whereas staurosporine or calphostin C failed to do so. However, PKC inhibitors blocked the TPA-evoked c-fos induction. Over-expression of PKC alpha down-regulated GnRH promoter activity, indicating that PKC activation was sufficient to inhibit GnRH gene expression. These results suggest that both activation and inhibition of PKC decrease the GnRH gene expression in the GT1-1 cells probably through different signal cascade mechanisms.
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
October 1997,
Brain research. Molecular brain research,
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
November 2005,
Molecular endocrinology (Baltimore, Md.),
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
February 1998,
Brain research. Molecular brain research,
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
January 2006,
Neuroendocrinology,
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
February 1995,
Cellular and molecular neurobiology,
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
May 2003,
Molecular and cellular endocrinology,
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
March 1998,
Endocrinology,
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
January 2012,
Brain research,
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
March 2011,
Molecular endocrinology (Baltimore, Md.),
W Sun, and
Y S Choe, and
Y J Lee, and
K Kim
September 2006,
The Journal of endocrinology,
