期刊
MOLECULAR CELL
卷 57, 期 6, 页码 1034-1046出版社
CELL PRESS
DOI: 10.1016/j.molcel.2015.02.015
关键词
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资金
- National Cancer Institute (NCI) [CA77742]
- German-Israeli Foundation for Scientific Research and Development [998/2008]
- Israel Cancer Society
- Israel Cancer Research Foundation
- Weinkselbaum Family Medical Research Fund
DNA binding by numerous transcription factors including the p53 tumor suppressor protein constitutes a vital early step in transcriptional activation. While the role of the central core DNA binding domain (DBD) of p53 in site-specific DNA binding has been established, the contribution of the sequence-independent C-terminal domain (CTD) is still not well understood. We investigated the DNA-binding properties of a series of p53 CTD variants using a combination of in vitro biochemical analyses and in vivo binding experiments. Our results provide several unanticipated and interconnected findings. First, the CTD enables DNA binding in a sequence-dependent manner that is drastically altered by either its modification or deletion. Second, dependence on the CTD correlates with the extent to which the p53 binding site deviates from the canonical consensus sequence. Third, the CTD enables stable formation of p53-DNA complexes to divergent binding sites via DNA-induced conformational changes within the DBD itself.
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