Mechanism and regulation of human non-homologous DNA end-joining

被引：762

作者：

Lieber, MR

Ma, YM

Pannicke, U

Schwarz, K

机构：

[1] Univ So Calif, Dept Pathol, Kenneth Norris Jr Comprehens Canc Ctr, Sch Med, Los Angeles, CA 90089 USA

[2] Univ So Calif, Sch Med, Dept Biochem & Mol Biol, Los Angeles, CA 90089 USA

[3] Univ So Calif, Sch Med, Dept Microbiol, Los Angeles, CA 90089 USA

[4] Univ So Calif, Sch Med, Dept Biol, Los Angeles, CA 90089 USA

[5] Univ Ulm, Dept Transfus Med, Inst Clin Transfus Med & Immunogenet, D-89081 Ulm, Germany

来源：

NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2003年 / 4卷 / 09期

关键词：

D O I：

10.1038/nrm1202

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Non-homologous DNA end-joining (NHEJ) - the main pathway for repairing double-stranded DNA breaks - functions throughout the cell cycle to repair such lesions. Defects in NHEJ result in marked sensitivity to ionizing radiation and ablation of lymphocytes, which rely on NHEJ to complete the rearrangement of antigen-receptor genes. NHEJ is typically imprecise, a characteristic that is useful for immune diversification in lymphocytes, but which might also contribute to some of the genetic changes that underlie cancer and ageing.

引用

页码：712 / 720

页数：9

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