Abstract:
:The estrogen receptor (ER) is a ligand-dependent transcription factor which regulates growth, development, differentiation and reproduction. To test the hypothesis that the diverse effects of the ER could be mediated by interacting with other transcription factors/oncogenes, the present study assessed its interaction with the tumor suppressor p53. p53 is a transcription factor which is involved in cell cycle regulation and apoptosis. We found that the wild-type p53 physically interacted with ER in vivo and repressed the estrogen-activated transcriptional activity. However, p53 mutants had no or reduced repression effect, depending on the sites of mutation. These findings suggest that p53 can cross talk with the ER in hormone-activated signaling pathways in cells.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Yu CL,Driggers P,Barrera-Hernandez G,Nunez SB,Segars JH,Cheng Sdoi
10.1006/bbrc.1997.7522subject
Has Abstractpub_date
1997-10-20 00:00:00pages
617-20issue
2eissn
0006-291Xissn
1090-2104pii
S0006291X97975227journal_volume
239pub_type
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