van Gent D C, van der Burg M
Department of Cell Biology and Genetics, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Oncogene. 2007 Dec 10;26(56):7731-40. doi: 10.1038/sj.onc.1210871.
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.
断裂染色体的重新连接对于细胞存活和预防恶性转化至关重要。大多数哺乳动物细胞主要依靠DNA双链断裂（DSB）修复的非同源末端连接途径来完成这项任务。本综述聚焦于由DNA依赖性蛋白激酶和连接酶IV/XRCC4复合物组成的核心非同源末端连接机制，以及促进一部分DSB重新连接的辅助因子。我们讨论了ATM蛋白激酶和Mre11/Rad50/Nbs1复合物在DSB修复中可能发挥的作用，以及电离辐射诱导灶在这一过程中可能扮演的角色。
