Mechanisms of Programmed DNA Lesions and Genomic Instability in the Immune System

被引：369

作者：

Alt, Frederick W. ^{[1
,2
,3
,4
]}

Zhang, Yu ^{[1
,2
,3
,4
]}

Meng, Fei-Long ^{[1
,2
,3
,4
]}

Guo, Chunguang ^{[1
,2
,3
,4
]}

Schwer, Bjoern ^{[1
,2
,3
,4
]}

机构：

[1] Howard Hughes Med Inst, Boston, MA 02115 USA

[2] Boston Childrens Hosp, Program Cellular & Mol Med, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA

[4] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA

来源：

CELL | 2013年 / 152卷 / 03期

关键词：

CLASS SWITCH RECOMBINATION; B-CELL DEVELOPMENT; CHROMOSOMAL TRANSLOCATIONS; IGH LOCUS; HOMOLOGOUS RECOMBINATION; ANTISENSE TRANSCRIPTION; V(D)J RECOMBINATION; SEQUENCING REVEALS; BREAK REPAIR; END;

D O I：

10.1016/j.cell.2013.01.007

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：

Chromosomal translocations involving antigen receptor loci are common in lymphoid malignancies. Translocations require DNA double-strand breaks (DSBs) at two chromosomal sites, their physical juxtaposition, and their fusion by end-joining. Ability of lymphocytes to generate diverse repertoires of antigen receptors and effector antibodies derives from programmed genomic alterations that produce DSBs. We discuss these lymphocyte-specific processes, with a focus on mechanisms that provide requisite DSB target specificity and mechanisms that suppress DSB translocation. We also discuss recent work that provides new insights into DSB repair pathways and the influences of three-dimensional genome organization on physiological processes and cancer genomes.

引用

页码：417 / 429

页数：13

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