p300/CREB-binding protein interacts with ATR and is required for the DNA replication checkpoint

被引：38

作者：

Stauffer, Daniel ^{[1
]}

Chang, Bill ^{[1
]}

Huang, Jing ^{[1
]}

Dunn, Andrew ^{[1
]}

Thayer, Mathew ^{[1
]}

机构：

[1] Oregon Hlth & Sci Univ, Dept Biochem, Portland, OR 97201 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2007年 / 282卷 / 13期

关键词：

D O I：

10.1074/jbc.M609261200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The highly related acetyltransferases, p300 and CREB-binding protein (CBP) are coactivators of signal-responsive transcriptional activation. In addition, recent evidence suggests that p300/CBP also interacts directly with complexes that mediate DNA replication and repair. In this report, we show that loss of p300/CBP in mammalian cells results in a defect in the cell cycle arrest induced by stalled DNA replication. We demonstrate that complexes containing p300/CBP and ATR can be detected in mammalian cells, and that the downstream kinase CHK1 fails to be phosphorylated in response to stalled DNA replication in cells that lack p300/CBP. These observations broaden the roles for the p300/CBP acetyltransferases to include the modulation of chromatin structure and function during DNA metabolic events as well as for transcription.

引用

页码：9678 / 9687

页数：10

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