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.
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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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。
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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。
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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。
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