Classical and Alternative End-Joining Pathways for Repair of Lymphocyte-Specific and General DNA Double-Strand Breaks

被引：192

作者：

Boboila, Cristian ^{[1
,2
]}

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

Schwer, Bjoern ^{[1
,2
]}

机构：

[1] Childrens Hosp, Howard Hughes Med Inst, Immune Dis Inst, Program Cellular & Mol Med, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Genet & Pediat, Boston, MA USA

来源：

ADVANCES IN IMMUNOLOGY, VOL 116 | 2012年 / 116卷

关键词：

CLASS-SWITCH RECOMBINATION; DEPENDENT PROTEIN-KINASE; SEVERE COMBINED IMMUNODEFICIENCY; XRCC4-DNA LIGASE-IV; CHROMOSOMAL TRANSLOCATION FORMATION; ANTIBODY DIVERSIFICATION ENZYME; INCREASED GENOMIC INSTABILITY; COMBINED IMMUNE-DEFICIENCY; LEAKY SCID PHENOTYPE; B-CELL LYMPHOMAS;

D O I：

10.1016/B978-0-12-394300-2.00001-6

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Classical nonhomologous end joining (C-NHEJ) is one of the two major known pathways for the repair of DNA double-strand breaks (DSBs) in mammalian cells. Our understanding of C-NHEJ has been derived, in significant part, through studies of programmed physiologic. DNA DSBs formed during V(D)J recombination in the developing immune system. Studies of immunoglobulin heavy-chain (IgH) class-switch recombination (CSR) also have revealed that there is an "alternative" end-joining process (A-EJ) that can function, relatively robustly, in the repair of DSBs in activated mature B lymphocytes. This A-EJ process has also been implicated in the formation of oncogenic translocations found in lymphoid tumors. In this review, we discuss our current understanding of C-NHEJ and A-EJ in the context of V(D)J recombination, CSR, and the formation of chromosomal translocations.

引用

页码：1 / 49

页数：49

共 237 条

[1] XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining [J].