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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Oncogene: including Oncogene Reviews
Erasmus MC: University Medical Center Rotterdam

van Gent, D., & Burger, C. (2007). Non-homologous end-joining, a sticky affair. Oncogene: including Oncogene Reviews (Vol. 26, pp. 7731–7740). doi:10.1038/sj.onc.1210871