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1
Regulating the activity of class II transactivator by posttranslational modifications: exploring the possibilities.通过翻译后修饰调节II类反式激活因子的活性：探索可能性
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2
Phosphorylation and ubiquitination of degron proximal residues are essential for class II transactivator (CIITA) transactivation and major histocompatibility class II expression.磷酸化和泛素化降解序列近端残基对于 II 类转录激活因子（CIITA）转录激活和主要组织相容性复合体 II 表达是必需的。
J Biol Chem. 2010 Aug 20;285(34):25893-903. doi: 10.1074/jbc.M110.127746. Epub 2010 Jun 10.
3
Degradation, Promoter Recruitment and Transactivation Mediated by the Extreme N-Terminus of MHC Class II Transactivator CIITA Isoform III.MHC II类反式激活因子CIITA异构体III的极端N端介导的降解、启动子招募和反式激活
PLoS One. 2016 Feb 12;11(2):e0148753. doi: 10.1371/journal.pone.0148753. eCollection 2016.
4
The class II transactivator (CIITA) is regulated by post-translational modification cross-talk between ERK1/2 phosphorylation, mono-ubiquitination and Lys63 ubiquitination.II类反式激活因子（CIITA）受细胞外信号调节激酶1/2（ERK1/2）磷酸化、单泛素化和赖氨酸63（Lys63）泛素化之间的翻译后修饰串扰调控。
Biosci Rep. 2015 Jun 19;35(4):e00233. doi: 10.1042/BSR20150091.
5
HDAC2 deacetylates class II transactivator and suppresses its activity in macrophages and smooth muscle cells.组蛋白去乙酰化酶2使II类反式激活因子去乙酰化，并抑制其在巨噬细胞和平滑肌细胞中的活性。
J Mol Cell Cardiol. 2009 Mar;46(3):292-9. doi: 10.1016/j.yjmcc.2008.10.023. Epub 2008 Nov 7.
6
Phosphorylation of CIITA directs its oligomerization, accumulation and increased activity on MHCII promoters.CIITA的磷酸化引导其寡聚化、积累并增强其在MHCII启动子上的活性。
EMBO J. 2002 Oct 15;21(20):5467-76. doi: 10.1093/emboj/cdf557.
7
The Major Histocompatibility Complex Class II Transactivator CIITA Inhibits the Persistent Activation of NF-κB by the Human T Cell Lymphotropic Virus Type 1 Tax-1 Oncoprotein.主要组织相容性复合体II类反式激活因子CIITA抑制人嗜T细胞病毒1型Tax-1癌蛋白对NF-κB的持续激活。
J Virol. 2016 Jan 20;90(7):3708-21. doi: 10.1128/JVI.03000-15.
8
Expression of MHC II genes.MHC II类基因的表达
Curr Top Microbiol Immunol. 2005;290:147-70. doi: 10.1007/3-540-26363-2_7.
9
CIITA leucine-rich repeats control nuclear localization, in vivo recruitment to the major histocompatibility complex (MHC) class II enhanceosome, and MHC class II gene transactivation.CIITA富含亮氨酸的重复序列控制核定位、体内募集至主要组织相容性复合体（MHC）II类增强体以及MHC II类基因的反式激活。
Mol Cell Biol. 2000 Oct;20(20):7716-25. doi: 10.1128/MCB.20.20.7716-7725.2000.
10
The class II transactivator requires brahma-related gene 1 to activate transcription of major histocompatibility complex class II genes.II类反式激活因子需要与婆罗门相关基因1来激活主要组织相容性复合体II类基因的转录。
Mol Cell Biol. 2002 Jul;22(14):5019-26. doi: 10.1128/MCB.22.14.5019-5026.2002.

引用本文的文献

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Reply to correspondence on "Novel role of MHC class II transactivator in hepatitis B virus replication and viral counteraction".对关于“MHC II类反式激活因子在乙型肝炎病毒复制及病毒对抗中的新作用”信件的回复
Clin Mol Hepatol. 2024 Oct;30(4):1053-1054. doi: 10.3350/cmh.2024.0572. Epub 2024 Jul 17.
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New Insight in HDACs: Potential Therapeutic Targets for the Treatment of Atherosclerosis.组蛋白去乙酰化酶的新见解：治疗动脉粥样硬化的潜在治疗靶点。
Front Pharmacol. 2022 Apr 21;13:863677. doi: 10.3389/fphar.2022.863677. eCollection 2022.
3
The MHC Class II Transactivator CIITA: Not (Quite) the Odd-One-Out Anymore among NLR Proteins.MHC II 类转录激活因子 CIITA：不再是 NLR 蛋白中的“异类”。
Int J Mol Sci. 2021 Jan 22;22(3):1074. doi: 10.3390/ijms22031074.
4
HADC5 deacetylates MKL1 to dampen TNF-α induced pro-inflammatory gene transcription in macrophages.HADC5使MKL1去乙酰化，以抑制巨噬细胞中肿瘤坏死因子-α诱导的促炎基因转录。
Oncotarget. 2017 Oct 9;8(55):94235-94246. doi: 10.18632/oncotarget.21670. eCollection 2017 Nov 7.
5
Pulling a Ligase out of a "HAT": pCAF Mediates Ubiquitination of the Class II Transactivator.从“帽子”中拉出连接酶：pCAF介导II类反式激活因子的泛素化
Int J Cell Biol. 2017;2017:8093813. doi: 10.1155/2017/8093813. Epub 2017 Feb 12.
6
Protein arginine methyltransferase 1 (PRMT1) represses MHC II transcription in macrophages by methylating CIITA.蛋白质精氨酸甲基转移酶 1（PRMT1）通过甲基化 CIITA 来抑制巨噬细胞中的 MHC II 转录。
Sci Rep. 2017 Jan 17;7:40531. doi: 10.1038/srep40531.
7
Understanding the Impact of ErbB Activating Events and Signal Transduction on Antigen Processing and Presentation: MHC Expression as a Model.了解ErbB激活事件和信号转导对抗原加工和呈递的影响：以MHC表达为模型
Front Pharmacol. 2016 Sep 26;7:327. doi: 10.3389/fphar.2016.00327. eCollection 2016.
8
Class II transactivator (CIITA) mediates transcriptional repression of pdk4 gene by interacting with hypermethylated in cancer 1 (HIC1).II类反式激活因子（CIITA）通过与癌症1中高甲基化蛋白（HIC1）相互作用介导丙酮酸脱氢酶激酶4（pdk4）基因的转录抑制。
J Biomed Res. 2015 Jul;29(4):308-15. doi: 10.7555/JBR.29.20150055. Epub 2015 Jun 30.
9
The class II transactivator (CIITA) is regulated by post-translational modification cross-talk between ERK1/2 phosphorylation, mono-ubiquitination and Lys63 ubiquitination.II类反式激活因子（CIITA）受细胞外信号调节激酶1/2（ERK1/2）磷酸化、单泛素化和赖氨酸63（Lys63）泛素化之间的翻译后修饰串扰调控。
Biosci Rep. 2015 Jun 19;35(4):e00233. doi: 10.1042/BSR20150091.
10
Extracellular matrix synthesis in vascular disease: hypertension, and atherosclerosis.血管疾病中的细胞外基质合成：高血压和动脉粥样硬化。
J Biomed Res. 2014 Jan;28(1):25-39. doi: 10.7555/JBR.27.20130064. Epub 2013 Sep 20.

本文引用的文献

1
CIITA versus IFN-gamma induced MHC class II expression in head and neck cancer cells.CIITA与干扰素-γ在头颈部癌细胞中诱导的MHC II类分子表达
Arch Dermatol Res. 2009 Feb;301(2):189-93. doi: 10.1007/s00403-008-0922-6. Epub 2008 Dec 23.
2
HDAC2 deacetylates class II transactivator and suppresses its activity in macrophages and smooth muscle cells.组蛋白去乙酰化酶2使II类反式激活因子去乙酰化，并抑制其在巨噬细胞和平滑肌细胞中的活性。
J Mol Cell Cardiol. 2009 Mar;46(3):292-9. doi: 10.1016/j.yjmcc.2008.10.023. Epub 2008 Nov 7.
3
Current approaches for global post-translational modification discovery and mass spectrometric analysis.全球翻译后修饰发现与质谱分析的当前方法。
Anal Chim Acta. 2008 Oct 3;627(1):50-61. doi: 10.1016/j.aca.2008.03.032. Epub 2008 Mar 22.
4
SIRT1 regulates circadian clock gene expression through PER2 deacetylation.沉默调节蛋白1通过对周期蛋白2进行去乙酰化作用来调节生物钟基因的表达。
Cell. 2008 Jul 25;134(2):317-28. doi: 10.1016/j.cell.2008.06.050.
5
NLR, the nucleotide-binding domain leucine-rich repeat containing gene family.NLR，即富含亮氨酸重复序列的核苷酸结合结构域基因家族。
Curr Opin Immunol. 2008 Feb;20(1):3-9. doi: 10.1016/j.coi.2008.01.003. Epub 2008 Feb 15.
6
Mitogen-activated protein kinase ERK1/2 regulates the class II transactivator.丝裂原活化蛋白激酶ERK1/2调节II类反式激活因子。
J Biol Chem. 2008 Apr 4;283(14):9031-9. doi: 10.1074/jbc.M706487200. Epub 2008 Feb 1.
7
The age of crosstalk: phosphorylation, ubiquitination, and beyond.串扰的时代：磷酸化、泛素化及其他。
Mol Cell. 2007 Dec 14;28(5):730-8. doi: 10.1016/j.molcel.2007.11.019.
8
CIITA mediates interferon-gamma repression of collagen transcription through phosphorylation-dependent interactions with co-repressor molecules.CIITA通过与共抑制分子的磷酸化依赖性相互作用介导干扰素-γ对胶原蛋白转录的抑制。
J Biol Chem. 2008 Jan 18;283(3):1243-1256. doi: 10.1074/jbc.M707180200. Epub 2007 Nov 8.
9
Crippling p53 activities via knock-in mutations in mouse models.通过在小鼠模型中敲入突变来削弱p53活性。
Oncogene. 2007 Apr 2;26(15):2177-84. doi: 10.1038/sj.onc.1210278.
10
Minocycline down-regulates MHC II expression in microglia and macrophages through inhibition of IRF-1 and protein kinase C (PKC)alpha/betaII.米诺环素通过抑制干扰素调节因子-1（IRF-1）和蛋白激酶C（PKC）α/βII来下调小胶质细胞和巨噬细胞中主要组织相容性复合体II（MHC II）的表达。
J Biol Chem. 2007 May 18;282(20):15208-16. doi: 10.1074/jbc.M611907200. Epub 2007 Mar 29.

通过翻译后修饰调节II类反式激活因子的活性：探索可能性

Regulating the activity of class II transactivator by posttranslational modifications: exploring the possibilities.

作者信息

Wu Xiaoyan, Kong Xiaocen, Luchsinger Larry, Smith Barbara D, Xu Yong

机构信息

Atherosclerosis Research Center, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing, Jiangsu 210029, China.

出版信息

Mol Cell Biol. 2009 Nov;29(21):5639-44. doi: 10.1128/MCB.00661-09. Epub 2009 Aug 31.

DOI:10.1128/MCB.00661-09
PMID:19720744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2772741/
Abstract

First identified as the master regulator of major histocompatibility complex II transcription, class II transactivator (CIITA) has since been implicated in a host of pathologies by modulating the transcription of multiple different genes. How CIITA caters to cell- and tissue-specific transcriptional needs is hotly debated and investigated. One of the possible mechanisms underlying spatiotemporal control of CIITA transcriptional activity is the posttranslational modification (PTM) machinery that refines certain amino acid residues of CIITA and hence alters its activity in response to specific cellular and environmental cues. This review discusses our current understanding of the PTM map of CIITA, how these modifications fine-tune its activity, and how the study of this area may lead to potential therapeutic strategies.

摘要

II类反式激活因子（CIITA）最初被鉴定为主要组织相容性复合体II转录的主调节因子，此后通过调节多个不同基因的转录参与了一系列病理过程。CIITA如何满足细胞和组织特异性转录需求是一个备受争议和研究的热点。CIITA转录活性时空控制的潜在机制之一是翻译后修饰（PTM）机制，该机制对CIITA的某些氨基酸残基进行修饰，从而根据特定的细胞和环境信号改变其活性。本文综述了我们目前对CIITA的PTM图谱的理解，这些修饰如何微调其活性，以及该领域的研究如何可能带来潜在的治疗策略。