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本文引用的文献

1
A combined nuclear and nucleolar localization motif in activation-induced cytidine deaminase (AID) controls immunoglobulin class switching.激活诱导胞苷脱氨酶(AID)中的核和核仁定位基序的组合控制免疫球蛋白类别转换。
J Mol Biol. 2013 Jan 23;425(2):424-43. doi: 10.1016/j.jmb.2012.11.026. Epub 2012 Nov 23.
2
Regulation of Aicda expression and AID activity.Aicda 表达和 AID 活性的调节。
Autoimmunity. 2013 Mar;46(2):83-101. doi: 10.3109/08916934.2012.749244. Epub 2013 Jan 17.
3
APRIL stimulates NF-κB-mediated HoxC4 induction for AID expression in mouse B cells.APRIL 刺激 NF-κB 介导的 HoxC4 诱导,促进小鼠 B 细胞中 AID 的表达。
Cytokine. 2013 Feb;61(2):608-13. doi: 10.1016/j.cyto.2012.10.018. Epub 2012 Nov 21.
4
Rev1 recruits ung to switch regions and enhances du glycosylation for immunoglobulin class switch DNA recombination.Rev1 招募 ung 以切换区域并增强 du 糖基化,用于免疫球蛋白类别转换 DNA 重组。
Cell Rep. 2012 Nov 29;2(5):1220-32. doi: 10.1016/j.celrep.2012.09.029. Epub 2012 Nov 8.
5
Activation-induced cytidine deaminase alters the subcellular localization of Tet family proteins.激活诱导的胞嘧啶脱氨酶改变 Tet 家族蛋白的亚细胞定位。
PLoS One. 2012;7(9):e45031. doi: 10.1371/journal.pone.0045031. Epub 2012 Sep 17.
6
Chromosome translocation, B cell lymphoma, and activation-induced cytidine deaminase.染色体易位、B 细胞淋巴瘤和激活诱导的胞嘧啶脱氨酶。
Annu Rev Pathol. 2013 Jan 24;8:79-103. doi: 10.1146/annurev-pathol-020712-164004. Epub 2012 Sep 4.
7
IgH partner breakpoint sequences provide evidence that AID initiates t(11;14) and t(8;14) chromosomal breaks in mantle cell and Burkitt lymphomas.IGH 伙伴断裂点序列提供了证据,表明 AID 启动了套细胞淋巴瘤和伯基特淋巴瘤中的 t(11;14)和 t(8;14)染色体断裂。
Blood. 2012 Oct 4;120(14):2864-7. doi: 10.1182/blood-2012-02-412791. Epub 2012 Aug 20.
8
The histone chaperone Spt6 is required for activation-induced cytidine deaminase target determination through H3K4me3 regulation.组蛋白伴侣 Spt6 通过调节 H3K4me3 来确定激活诱导的胞苷脱氨酶的靶标。
J Biol Chem. 2012 Sep 21;287(39):32415-29. doi: 10.1074/jbc.M112.351569. Epub 2012 Jul 26.
9
Immunoglobulin class-switch DNA recombination: induction, targeting and beyond.免疫球蛋白类别转换 DNA 重组:诱导、靶向及其他。
Nat Rev Immunol. 2012 Jun 25;12(7):517-31. doi: 10.1038/nri3216.
10
The DSIF subunits Spt4 and Spt5 have distinct roles at various phases of immunoglobulin class switch recombination.DSIF 亚基 Spt4 和 Spt5 在免疫球蛋白类别转换重组的各个阶段具有不同的作用。
PLoS Genet. 2012;8(4):e1002675. doi: 10.1371/journal.pgen.1002675. Epub 2012 Apr 26.

B 细胞免疫与癌症中的激活诱导胞苷脱氨酶。

Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers.

机构信息

Department of Microbiology, College of Medicine, Konyang University, Daejeon 302-718, Korea.

出版信息

Immune Netw. 2012 Dec;12(6):230-9. doi: 10.4110/in.2012.12.6.230. Epub 2012 Dec 31.

DOI:10.4110/in.2012.12.6.230
PMID:23396757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3566417/
Abstract

Activation-induced cytidine deaminase (AID) is an enzyme that is predominantly expressed in germinal center B cells and plays a pivotal role in immunoglobulin class switch recombination and somatic hypermutation for antibody (Ab) maturation. These two genetic processes endow Abs with protective functions against a multitude of antigens (pathogens) during humoral immune responses. In B cells, AID expression is regulated at the level of either transcriptional activation on AID gene loci or post-transcriptional suppression of AID mRNA. Furthermore, AID stabilization and targeting are determined by post-translational modifications and interactions with other cellular/nuclear factors. On the other hand, aberrant expression of AID causes B cell leukemias and lymphomas, including Burkitt's lymphoma caused by c-myc/IgH translocation. AID is also ectopically expressed in T cells and non-immune cells, and triggers point mutations in relevant DNA loci, resulting in tumorigenesis. Here, I review the recent literatures on the function of AID, regulation of AID expression, stability and targeting in B cells, and AID-related tumor formation.

摘要

激活诱导胞嘧啶脱氨酶(AID)是一种主要在生发中心 B 细胞中表达的酶,在免疫球蛋白类别转换重组和体细胞超突变中发挥关键作用,从而促进抗体(Ab)成熟。这两个遗传过程使 Ab 具有在体液免疫反应中针对多种抗原(病原体)的保护功能。在 B 细胞中,AID 的表达受到 AID 基因座转录激活或 AID mRNA 转录后抑制的调节。此外,AID 的稳定和靶向取决于翻译后修饰以及与其他细胞/核因子的相互作用。另一方面,AID 的异常表达会导致 B 细胞白血病和淋巴瘤,包括由 c-myc/IgH 易位引起的伯基特淋巴瘤。AID 还异位表达于 T 细胞和非免疫细胞中,并在相关 DNA 位点引发点突变,导致肿瘤形成。在这里,我回顾了关于 AID 功能、AID 表达调控、B 细胞中 AID 的稳定性和靶向性以及 AID 相关肿瘤形成的最新文献。