Non-homologous end-joining, a sticky affair

被引：0
|
作者：
D C van Gent
M van der Burg
机构：
[1] Erasmus MC,Department of Cell Biology and Genetics
[2] University Medical Center Rotterdam,Department of Immunology
[3] Erasmus MC,undefined
[4] University Medical Center Rotterdam,undefined
来源：
Oncogene | 2007年 / 26卷
关键词：
DNA repair; V(D)J recombination; DNA double-strand break repair; severe combined immunodeficiency; DNA damage response; chromosomal instability;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
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.
引用
收藏
页码：7731 / 7740
页数：9
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