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Non-homologous end-joining, a sticky affair

Abstract

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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Acknowledgements

We thank Drs PO Mari, SP Perseng and NGJ Jaspers for useful comments. Research in our laboratories is supported by the European Union (Projects ‘RISC-RAD’ and ‘DNA Repair’) and the Dutch Organization for Scientific Research (NWO/ZonMw veni grant 916.56.107).

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van Gent, D., van der Burg, M. Non-homologous end-joining, a sticky affair. Oncogene 26, 7731–7740 (2007). https://doi.org/10.1038/sj.onc.1210871

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