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"The endless tale of non-homologous end-joining"

Weterings E, Chen DJ



Published Jan. 1, 2008 in Cell Res. volume 18 .

Pubmed ID: 18166980

Abstract:
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.


This publication refers to following REPAIRtoire entries:

Repair activities
Pathways


Last modification of this entry: Oct. 7, 2008

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