Abstract
We present evidence that the glucocorticoid receptor (GR) and transcription factor Jun/AP-1 can reciprocally repress one another's transcriptional activation by a novel mechanism that is Independent of DNA binding. Overexpression of c-Jun prevents the glucocorticoid-induced activation of genes carrying a functional glucocorticoid response element (GRE). Conversely, GR is able to repress AP-1-mediated transcriptional activation. Mutant analysis reveals that the ligand binding and DNA binding domains of GR and the region including the leucine zipper of c-Jun are required for repression. Gel retardation analysis demonstrates that bacterially expressed c-Jun disrupts GR-GRE complexes. These data Indicate that members of two distinct classes of transcription factors can oppose one another's activity through a mechanism likely involving protein-protein interactions.
Original language | English (US) |
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Pages (from-to) | 1217-1226 |
Number of pages | 10 |
Journal | Cell |
Volume | 62 |
Issue number | 6 |
DOIs | |
State | Published - Sep 21 1990 |
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)