Regulation of activation-induced cytidine deaminase DNA deamination activity in B-cells by Ser38 phosphorylation

被引：12
作者：
Basu, Uttiya [1 ,2 ,3 ]
Franklin, Andrew [1 ,2 ,3 ]
Schwer, Bjoern [1 ,2 ,3 ]
Cheng, Hwei-Ling [1 ,2 ,3 ]
Chaudhuri, Jayanta [4 ]
Alt, Frederick W. [1 ,2 ,3 ]
机构：
[1] Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA
[3] Immune Dis Inst, Boston, MA 02115 USA
[4] Mem Sloan Kettering Canc Ctr, Program Immunol, New York, NY 10021 USA
来源：
BIOCHEMICAL SOCIETY TRANSACTIONS | 2009年 / 37卷
关键词：
activation-induced cytidine deaminase (AID); class switch recombination; evolution; phosphorylation; somatic hypermutation; CLASS-SWITCH RECOMBINATION; SINGLE-STRANDED-DNA; SOMATIC HYPERMUTATION; ANTIBODY DIVERSIFICATION; MUTATION SPECTRA; C-MYC; AID; TRANSCRIPTION; EXPRESSION; EVOLUTION;
D O I：
10.1042/BST0370561
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：
Human and mouse Ig genes are diversified in mature B-cells by distinct processes known as Ig heavy-chain CSR (class switch recombination) and Ig variable-region exon SHM (somatic hypermutation). These DNA-modification processes are initiated by AID (activation-induced cytidine deaminase), a DNA cytidine deaminase predominantly expressed in activated B-cells. AID is post-transcriptionally regulated via multiple mechanisms, including microRNA regulation, nucleocytoplasmic shuttling, ubiquitination and phosphorylation. Among these regulatory processes, AID phosphorylation at Ser(38) has been a focus of particularly intense study and debate. In the present paper, we discuss recent biochemical and mouse genetic studies that begin to elucidate the functional significance of AID Ser(38) phosphorylation in the context of the evolution of this mode of AID regulation and the potential roles that it may play in activated B-cells during a normal immune response.
引用
收藏
页码：561 / 568
页数：8
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