期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 24, 期 12, 页码 5332-5339出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.24.12.5332-5339.2004
关键词
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资金
- NCI NIH HHS [T32 CA009361, P01-CA50661, P01 CA050661, R01-CA63113, F32CA81745, F32 CA081745, 2T32CA09361, R01 CA063113] Funding Source: Medline
Although the link between transcription and DNA repair is well established, defects in the core transcriptional complex itself have not been shown to elicit a DNA damage response. Here we show that a cell line with a temperature-sensitive defect in TBP-associated factor 1 (TAF1), a component of the TFIID general transcription complex, exhibits hallmarks of an ATR-mediated DNA damage response. Upon inactivation of TAF1, ATR rapidly localized to subnuclear foci and contributed to the phosphorylation of several downstream targets, including p53 and Chk1, resulting in cell cycle arrest. The increase in p53 expression and the G, phase arrest could be blocked by caffeine, an inhibitor of ATR. In addition, dominant negative forms of ATR but not ATM were able to override the arrest in G(1). These results suggest that a defect in TAF1 can elicit a DNA damage response.
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