DNA double-strand break repair: A relentless hunt uncovers new prey

被引：47

作者：

Sekiguchi, JM

Ferguson, DO

机构：

[1] Univ Michigan, Sch Med, Ctr Comprehens Canc, Dept Internal Med, Ann Arbor, MI 48109 USA

[2] Univ Michigan, Sch Med, Ctr Comprehens Canc, Dept Human Genet, Ann Arbor, MI 48109 USA

[3] Univ Michigan, Sch Med, Ctr Comprehens Canc, Dept Pathol, Ann Arbor, MI 48109 USA

来源：

CELL | 2006年 / 124卷 / 02期

关键词：

D O I：

10.1016/j.cell.2006.01.010

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

A major pathway for repair of DNA double-strand breaks is nonhomologous end-joining (NHEJ). In this issue of Cell, Buck et al. (2006a) and Ahnesorg et al. (2006) report the discovery of a new NHEJ factor called Cernunnos-XLF. Both groups report that this protein is mutated in a rare inherited human syndrome characterized by severe immunodeficiency, developmental delay, and hypersensitivity to agents that cause DNA double-strand breaks.

引用

收藏

页码：260 / 262

页数：3

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