The mechanism of vertebrate nonhomologous DNA end joining and its role in V(D)J recombination

被引：187

作者：

Lieber, MR

Ma, YM

Pannicke, U

Schwarz, K

机构：

[1] Univ So Calif, Keck Sch Med, USC Norris Comprehens Canc Ctr, Dept Pathol, Los Angeles, CA 90033 USA

[2] Univ So Calif, Keck Sch Med, USC Norris Comprehens Canc Ctr, Dept Biochem & Mol Biol, Los Angeles, CA 90033 USA

[3] Univ So Calif, Keck Sch Med, USC Norris Comprehens Canc Ctr, Dept Mol Microbiol & Immunol, Los Angeles, CA 90033 USA

[4] Univ So Calif, Keck Sch Med, USC Norris Comprehens Canc Ctr, Dept Biol Sci, Los Angeles, CA 90033 USA

[5] Univ Ulm, Dept Transfus Med, D-89081 Ulm, Germany

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

来源：

DNA REPAIR | 2004年 / 3卷 / 8-9期

关键词：

double-strand break repair; immunoglobulin gene recombination; V(D)J recombination; artemis; DNA-dependent protein kinase; DNA-PKcs; Ku; Ku86; K70; XRCC4; DNA ligase IV; genetic recombination; recombination activating genes; RAG-1; RAG-2; severe combined immune deficiency;

D O I：

10.1016/j.dnarep.2004.03.015

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

The vertebrate immune system generates double-strand DNA (dsDNA) breaks to generate the antigen receptor repertoire of lymphocytes. After those double-strand breaks have been created, the DNA joinings required to complete the process are carried out by the nonhomologous DNA end joining pathway, or NHEJ. The NHEJ pathway is present not only in lymphocytes, but in all eukaryotic cells ranging from yeast to humans. The NHEJ pathway is needed to repair these physiologic breaks, as well as challenging pathologic breaks that arise from ionizing radiation and oxidative damage to DNA. (C) 2004 Elsevier B.V. All rights reserved.

引用

页码：817 / 826

页数：10

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