HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 282, Issue 13, 9678-9687, March 30, 2007

This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 282/13/9678    most recent M609261200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Stauffer, D. Articles by Thayer, M. Search for Related Content PubMed PubMed Citation Articles by Stauffer, D. Articles by Thayer, M. Social Bookmarking                      What's this?

p300/CREB-binding Protein Interacts with ATR and Is Required for the DNA Replication Checkpoint^*

From the Department of Biochemistry, Oregon Health and Sciences University, Portland, Oregon 97201

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.

Received for publication, September 29, 2006 , and in revised form, January 31, 2007.

^* This work was supported by National Institutes of Health Grants CA97021 and CA104693 (to M. T.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Fig. S1.

¹ To whom correspondence should be addressed: 3181 S.W. Sam Jackson Park Rd., Portland, OR 97201. Tel.: 503-494-2247; Fax: 503-494-7368; E-mail: thayerm{at}ohsu.edu.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				S. M. Smolik Heterochromatin-Mediated Gene Silencing Is Not Affected by Drosophila CBP Activity J. Hered., July 1, 2009; 100(4): 465 - 472. [Abstract] [Full Text] [PDF]

				N. Sankar, R.-K. Kadeppagari, and B. Thimmapaya c-Myc-induced Aberrant DNA Synthesis and Activation of DNA Damage Response in p300 Knockdown Cells J. Biol. Chem., May 29, 2009; 284(22): 15193 - 15205. [Abstract] [Full Text] [PDF]