Journal
CELL RESEARCH
Volume 18, Issue 1, Pages 114-124Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cr.2008.3
Keywords
DNA-PK; Ku70/80; XRCC4; ligase IV; artemis; XLF; cernunnos; DSB; NHEJ; ATM; non-homologous end-joining; DNA double-strand break; V(D)J recombination
Categories
Funding
- NATIONAL CANCER INSTITUTE [P01CA092584, R37CA050519] Funding Source: NIH RePORTER
- NCI NIH HHS [R37-CA050519, P01-CA92584] Funding Source: Medline
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DNA double-strand breaks (DSBs) are introduced in cells by ionizing radiation and reactive oxygen species. In addition, they are commonly generated during V(D)J recombination, an essential aspect of the developing immune system. Failure to effectively repair these DSBs can result in chromosome breakage, cell death, onset of cancer, and defects in the immune system of higher vertebrates. Fortunately, all mammalian cells possess two enzymatic pathways that mediate the repair of DSBs: homologous recombination and non-homologous end-joining (NHEJ). The NHEJ process utilizes enzymes that capture both ends of the broken DNA molecule, bring them together in a synaptic DNA-protein complex, and finally repair the DNA break. In this review, all the known enzymes that play a role in the NHEJ process are discussed and a working model for the co-operation of these enzymes during DSB repair is presented.
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