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

Daniel Stauffer, Bill Chang, Jing Huang, Andrew Dunn, Mathew Thayer

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)9678-9687
Number of pages10
JournalJournal of Biological Chemistry
Volume282
Issue number13
DOIs
StatePublished - Mar 30 2007

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ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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