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激活诱导的胞苷脱氨酶和载脂蛋白B mRNA编辑酶催化多肽样蛋白3G对靶向DNA的胞嘧啶脱氨作用引发免疫和逆转录病毒反应的生化基础

Biochemical basis of immunological and retroviral responses to DNA-targeted cytosine deamination by activation-induced cytidine deaminase and APOBEC3G.

作者信息

Chelico Linda, Pham Phuong, Petruska John, Goodman Myron F

机构信息

Department of Biological Sciences, Molecular and Computational Biology Section, University of Southern California, Los Angeles, California 90089-2910.

Department of Biological Sciences, Molecular and Computational Biology Section, University of Southern California, Los Angeles, California 90089-2910.

出版信息

J Biol Chem. 2009 Oct 9;284(41):27761-27765. doi: 10.1074/jbc.R109.052449. Epub 2009 Aug 13.

DOI:10.1074/jbc.R109.052449
PMID:19684020
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2788826/
Abstract

Activation-induced cytidine deaminase (AID) and APOBEC3G catalyze deamination of cytosine to uracil on single-stranded DNA, thereby setting in motion a regulated hypermutagenic process essential for human well-being. However, if regulation fails, havoc ensues. AID plays a central role in the synthesis of high affinity antibodies, and APOBEC3G inactivates human immunodeficiency virus-1. This minireview highlights biochemical and structural properties of AID and APOBEC3G, showing how studies using the purified enzymes provide valuable insight into the considerably more complex biology governing antibody generation and human immunodeficiency virus inactivation.

摘要

激活诱导的胞苷脱氨酶（AID）和载脂蛋白B mRNA编辑酶催化多肽样3G（APOBEC3G）可催化单链DNA上的胞嘧啶脱氨生成尿嘧啶，从而启动一个对人类健康至关重要的受调控的高突变过程。然而，如果调控失败，就会引发严重问题。AID在高亲和力抗体的合成中起核心作用，而APOBEC3G可使人类免疫缺陷病毒1型失活。这篇小型综述重点介绍了AID和APOBEC3G的生化及结构特性，展示了如何利用纯化酶进行的研究为调控抗体产生和人类免疫缺陷病毒失活的复杂得多的生物学机制提供有价值的见解。

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Biochemical basis of immunological and retroviral responses to DNA-targeted cytosine deamination by activation-induced cytidine deaminase and APOBEC3G.激活诱导的胞苷脱氨酶和载脂蛋白B mRNA编辑酶催化多肽样蛋白3G对靶向DNA的胞嘧啶脱氨作用引发免疫和逆转录病毒反应的生化基础
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2
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本文引用的文献

1
The concerted action of Msh2 and UNG stimulates somatic hypermutation at A . T base pairs.Msh2和UNG的协同作用刺激A.T碱基对处的体细胞超突变。
Mol Cell Biol. 2009 Sep;29(18):5148-57. doi: 10.1128/MCB.00647-09. Epub 2009 Jul 13.
2
A portable hot spot recognition loop transfers sequence preferences from APOBEC family members to activation-induced cytidine deaminase.一种便携式热点识别环将序列偏好从载脂蛋白B mRNA编辑酶催化多肽样家族成员转移至激活诱导的胞嘧啶脱氨酶。
J Biol Chem. 2009 Aug 21;284(34):22898-904. doi: 10.1074/jbc.M109.025536. Epub 2009 Jun 26.
3
The current structural and functional understanding of APOBEC deaminases.目前对载脂蛋白B mRNA编辑酶催化多肽样蛋白（APOBEC）脱氨酶的结构和功能的理解。
Cell Mol Life Sci. 2009 Oct;66(19):3137-47. doi: 10.1007/s00018-009-0070-y. Epub 2009 Jun 23.
4
AID upmutants isolated using a high-throughput screen highlight the immunity/cancer balance limiting DNA deaminase activity.通过高通量筛选分离出的AID上调突变体突出了限制DNA脱氨酶活性的免疫/癌症平衡。
Nat Struct Mol Biol. 2009 Jul;16(7):769-76. doi: 10.1038/nsmb.1623. Epub 2009 Jun 21.
5
AID constrains germinal center size by rendering B cells susceptible to apoptosis.活化诱导的胞苷脱氨酶（AID）通过使B细胞易于凋亡来限制生发中心的大小。
Blood. 2009 Jul 16;114(3):547-54. doi: 10.1182/blood-2009-03-211763. Epub 2009 May 28.
6
V-region mutation in vitro, in vivo, and in silico reveal the importance of the enzymatic properties of AID and the sequence environment.体外、体内和计算机模拟的V区突变揭示了AID酶活性及序列环境的重要性。
Proc Natl Acad Sci U S A. 2009 May 26;106(21):8629-34. doi: 10.1073/pnas.0903803106. Epub 2009 May 14.
7
An extended structure of the APOBEC3G catalytic domain suggests a unique holoenzyme model.载脂蛋白B编辑酶催化多肽样蛋白3G（APOBEC3G）催化结构域的扩展结构提示了一种独特的全酶模型。
J Mol Biol. 2009 Jun 26;389(5):819-32. doi: 10.1016/j.jmb.2009.04.031. Epub 2009 Apr 21.
8
The activation-induced cytidine deaminase (AID) efficiently targets DNA in nucleosomes but only during transcription.激活诱导的胞苷脱氨酶（AID）可有效靶向核小体中的DNA，但仅在转录过程中才会如此。
J Exp Med. 2009 May 11;206(5):1057-71. doi: 10.1084/jem.20082678. Epub 2009 Apr 20.
9
Interference of mismatch and base excision repair during the processing of adjacent U/G mispairs may play a key role in somatic hypermutation.在相邻U/G错配处理过程中，错配修复和碱基切除修复的干扰可能在体细胞高频突变中起关键作用。
Proc Natl Acad Sci U S A. 2009 Apr 7;106(14):5593-8. doi: 10.1073/pnas.0901726106. Epub 2009 Mar 23.
10
Restriction of HIV-1 by APOBEC3G is cytidine deaminase-dependent.载脂蛋白B mRNA编辑酶催化多肽样蛋白3G（APOBEC3G）对HIV-1的限制作用依赖于胞苷脱氨酶。
Virology. 2009 May 10;387(2):313-21. doi: 10.1016/j.virol.2009.02.026. Epub 2009 Mar 21.