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Nucleic Acids Research Advance Access originally published online on January 12, 2009
Nucleic Acids Research 2009 37(5):1363-1377; doi:10.1093/nar/gkn1071
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Nucleic Acids Research, 2009, Vol. 37, No. 5 1363-1377
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Chromatin remodeling finds its place in the DNA double-strand break response

Tej K. Pandita1,* and Christine Richardson2

1Department of Radiation Oncology, Washington University School of Medicine, St Louis, MO 63108 and 2Department of Biology, University of North Carolina at Charlotte, Charlotte, NC 28223, USA

*To whom correspondence should be addressed. Tel: +1 314 747 5461; Fax: +1 314 362 9790; Email: pandita{at}wustl.edu

Received December 19, 2008. Accepted December 20, 2008.

The accurate repair of chromosomal double-strand breaks (DSBs) arising from exposure to exogenous agents, such as ionizing radiation (IR) and radiomimetic drugs is crucial in maintaining genomic integrity, cellular viability and the prevention of tumorigenesis. Eukaryotic cells have evolved efficient mechanisms that sense and respond to DSBs. The DNA DSB response is facilitated by hierarchical signaling networks that orchestrate chromatin structural changes, cell-cycle checkpoints and multiple enzymatic activities to repair the broken DNA ends. Sensors and transducers signal to numerous downstream cellular effectors which function primarily by substrate posttranslational modifications including phosphorylation, acetylation, methylation and ubiquitylation. In particular, the past several years have provided important insight into the role of chromatin remodeling and histones-specific modifications to control DNA damage detection, signaling and repair. This review summarizes recently identified factors that influence this complex process and the repair of DNA DSBs in eukaryotic cells.


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