The glucocorticoid receptor inhibits the human prolactin gene expression by interference with Pit-1 activity.

Glucocorticoids have been shown to inhibit the activity of the human prolactin (hPRL) promoter. Using transient expression experiments in rat pituitary cells, we located the sequence conferring glucocorticoid inhibition to a region which contains Pit-1 binding sites, responsible for pituitary-specific expression, but does not seem to contain a glucocorticoid receptor ...
(GR) binding site. Co-transfection experiments in non-pituitary cell lines, using expression vectors for Pit-1 and different mutants of the human GR show that inhibition of the hPRL gene is seen only in the presence of Pit-1 and GR, and that the DNA binding function of the receptor is not required. Immunoprecipitation studies show that either anti-GR or anti-Pit-1 antibodies are able to co-precipitate GR and Pit-1, suggesting an interaction between these factors. We conclude that the activated GR functionally interferes with the pituitary specific factor Pit-1, thereby leading to the observed transcriptional repression.
Mesh Terms:
Animals, COS Cells, Cyclic AMP, DNA, DNA-Binding Proteins, Gene Expression Regulation, Hela Cells, Humans, Prolactin, Promoter Regions, Genetic, Protein Binding, Rats, Receptors, Glucocorticoid, Transcription Factor Pit-1, Transcription Factors, Tumor Cells, Cultured
Mol. Cell. Endocrinol.
Date: Nov. 15, 1997
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