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Research Papers

Co-localization of elements required for phorbol ester stimulation and glucocorticoid repression of proliferin gene expression.

Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, Illinois 60208.

Abstract

Proliferin (PLF) gene expression provides a model of growth-related transcriptional activation in mouse cells. Transcription from a cloned PLF promoter is inducible by phorbol esters, and this induction involves a region of 31 bp that includes an AP-1 site and a cluster of sites similar to the simian virus 40 (SV40) SphI element. The mutation of either the AP-1 or the SphI sites abolishes phorbol ester induction, and the transfer of this 31-bp sequence to a site upstream of a minimal promoter is sufficient to confer phorbol-ester responsiveness. In contrast to phorbol esters, glucocorticoids repress PLF transcription, which results in a reduced accumulation of PLF mRNA in serum-stimulated cells. Repression is dependent on the glucocorticoid receptor, which binds to the PLF promoter in a region that includes the AP-1 site, and the 31-bp phorbol ester 12-O-tetra decanoylphorbol-13-acetate (TPA)-inducible region is sufficient to mediate glucocorticoid repression. In addition, extracts from glucocorticoid-treated and untreated mouse cells are found to differ in the nature of the protein complexes that interact with the AP-1 site.

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