Journal
BIOCHEMICAL JOURNAL
Volume 423, Issue -, Pages 157-168Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BJ20090942
Keywords
double-strand break (DSB); double-strand break repair (DSB repair); homologous recombination; mammalian DNA repair; non-homologous end-joining (NHEJ)
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Funding
- National Institutes of Health [CA095175, GM073894]
- Leukemia and Lymphoma Society
- Bloom's Syndrome Foundation
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DNA chromosomal DSBs (double-strand breaks) are potentially hazardous DNA lesions, and their accurate repair is essential for the successful maintenance and propagation of genetic information. Two major pathways have evolved to repair DSBs: HR (homologous recombination) and NHEJ (non-homologous end-joining). Depending on the context in which the break is encountered, HR and NHEJ may either compete or co-operate to fix DSBs in eukaryotic cells. Defects in either pathway are strongly associated with human disease, including immunodeficiency and cancer predisposition. Here we review the current knowledge of how NHEJ and HR are controlled in somatic mammalian cells, and discuss the role of the chromatin context in regulating each pathway. We also review evidence for both co-operation and competition between the two pathways.
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