AID targeting: old mysteries and new challenges

被引：49

作者：

Chandra, Vivek ^{[1
]}

Bortnick, Alexandra ^{[1
]}

Murre, Cornelis ^{[1
]}

机构：

[1] Univ Calif San Diego, Dept Mol Biol, Div Biol Sci, La Jolla, CA 92093 USA

来源：

TRENDS IN IMMUNOLOGY | 2015年 / 36卷 / 09期

基金：

美国国家卫生研究院;

关键词：

INDUCED CYTIDINE DEAMINASE; CLASS-SWITCH RECOMBINATION; RNA-POLYMERASE-II; ACTIVATION-INDUCED DEAMINASE; TRANSCRIPTION FACTOR E2A; 5 NONCODING REGION; B-CELL LYMPHOMA; NON-IG GENES; SOMATIC HYPERMUTATION; C-MYC;

D O I：

10.1016/j.it.2015.07.003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Activation-induced cytidine deaminase (AID) mediates cytosine deamination and underlies two central processes in antibody diversification: somatic hypermutation and class-switch recombination. AID deamination is not exclusive to immunoglobulin loci; it can instigate DNA lesions in non-immunoglobulin genes and thus stringent checks are in place to constrain and restrict its activity. Recent findings have provided new insights into the mechanisms that target AID activity to specific genomic regions, revealing an involvement for noncoding RNAs associated with polymerase pausing and with enhancer transcription as well as genomic architecture. We review these findings and integrate them into a model for multilevel regulation of AID expression and targeting in immunoglobulin and non-immunoglobulin loci. Within this framework we discuss gaps in understanding, and outline important areas of further research.

引用

页码：527 / 535

页数：9

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