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) |
|---|---|
| Pages (from-to) | 1217-1226 |
| Number of pages | 10 |
| Journal | Cell |
| Volume | 62 |
| Issue number | 6 |
| DOIs | |
| State | Published - Sep 21 1990 |
Fingerprint
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
Cite this
Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor. / Schüle, Roland; Rangarajan, Pundl; Kliewer, Steven; Ransone, Lynn J.; Bolado, Jack; Yang, Na; Verma, Inder M.; Evans, Ronald M.
In: Cell, Vol. 62, No. 6, 21.09.1990, p. 1217-1226.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor
AU - Schüle, Roland
AU - Rangarajan, Pundl
AU - Kliewer, Steven
AU - Ransone, Lynn J.
AU - Bolado, Jack
AU - Yang, Na
AU - Verma, Inder M.
AU - Evans, Ronald M.
PY - 1990/9/21
Y1 - 1990/9/21
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0025130179&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025130179&partnerID=8YFLogxK
U2 - 10.1016/0092-8674(90)90397-W
DO - 10.1016/0092-8674(90)90397-W
M3 - Article
C2 - 2169353
AN - SCOPUS:0025130179
VL - 62
SP - 1217
EP - 1226
JO - Cell
JF - Cell
SN - 0092-8674
IS - 6
ER -