The role of the non-homologous end-joining pathway in lymphocyte development

被引：178

作者：

Rooney, S

Chaudhuri, J

Alt, FW

机构：

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

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

[3] Ctr Blood Res, Boston, MA 02115 USA

来源：

IMMUNOLOGICAL REVIEWS | 2004年 / 200卷

关键词：

D O I：

10.1111/j.0105-2896.2004.00165.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

One of the most toxic insults a cell can incur is a disruption of its linear DNA in the form of a double-strand break (DSB). Left unrepaired, or repaired improperly, these lesions can result in cell death or neoplastic transformation. Despite these dangers, lymphoid cells purposely introduce DSBs into their genome to maximize the diversity and effector functions of their antigen receptor genes. While the generation of breaks requires distinct lymphoid-specific factors, their resolution requires various ubiquitously expressed DNA-repair proteins, known collectively as the non-homologous end-joining pathway. In this review, we discuss the factors that constitute this pathway as well as the evidence of their involvement in two lymphoid-specific DNA recombination events.

引用

页码：115 / 131

页数：17

共 244 条

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