Non-homologous end-joining, a sticky affair

作者：van Gent D C^*; van der Burg M

来源：Oncogene, 2007, 26(56): 7731-7740.

DOI：10.1038/sj.onc.1210871

• DNA repair
• V(D)J recombination
• DNA double-strand break repair
• severe combined immuno-deficiency
• DNA damage response
• chromosomal instability

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.

• 出版日期2007-12-10