Journal
ONCOGENE
Volume 26, Issue 56, Pages 7731-7740Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1210871
Keywords
DNA repair; V(D)J recombination; DNA double-strand break repair; severe combined immuno-deficiency; DNA damage response; chromosomal instability
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Rejoining of broken chromosomes is crucial for cell survival and prevention of malignant transformation. Most mammalian cells rely primarily on the non-homologous end-joining pathway of DNA double-strand break (DSB) repair to accomplish this task. This review focuses both on the core non-homologous end-joining machinery, which consists of DNA-dependent protein kinase and the ligase IV/XRCC4 complex, and on accessory factors that facilitate rejoining of a subset of the DSBs. We discuss how the ATM protein kinase and the Mre11/Rad50/Nbs1 complex might function in DSB repair and what role ionizing radiation-induced foci may play in this process.
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