Steroid Receptor Coactivator-1 and Its Family Members Differentially Regulate Transactivation by the Tumor Suppressor Protein p53
Author(s) -
SooKyung Lee,
HanJong Kim,
Jung Ho Kim,
Jae Woon Lee
Publication year - 1999
Publication title -
molecular endocrinology
Language(s) - English
Resource type - Journals
eISSN - 1944-9917
pISSN - 0888-8809
DOI - 10.1210/mend.13.11.0365
Subject(s) - transactivation , biology , coactivator , nuclear receptor coactivator 3 , transcription factor , nuclear receptor , nuclear receptor coactivator 1 , microbiology and biotechnology , cancer research , genetics , gene
The tumor suppressor protein p53 exerts its cell cycle-regulatory effects through its ability to function as a sequence-specific DNA-binding transcription factor. Herein, we show that p53 physically interacts with specific subregions of steroid receptor coactivator-1 (SRC-1) and its family members, p/CIP (p300/CBP interacting protein), xSRC-3, and AIB1 (amplified in breast cancer), originally isolated as transcription coactivators of nuclear receptors, as demonstrated by the yeast and mammalian two-hybrid tests as well as glutathione S-transferase pull-down assays. Interestingly, cotransfection of HeLa cells with SRC-1- or p/CIP expression vector potentiated the p53-mediated transactivation, whereas AIB1 and xSRC-3 were repressive. All of these SRC-1 members, however, similarly stimulated transactivation mediated by nuclear receptors and AP-1, as previously described. These results suggest that SRC-1 and its family members may differentially modulate the p53 transactivation in vivo.
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