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本文引用的文献

1
Regulation of IkappaB kinase-related kinases and antiviral responses by tumor suppressor CYLD.肿瘤抑制因子CYLD对IkappaB激酶相关激酶及抗病毒反应的调控
J Biol Chem. 2008 Jul 4;283(27):18621-6. doi: 10.1074/jbc.M801451200. Epub 2008 May 8.
2
Deubiquitinating enzyme CYLD negatively regulates RANK signaling and osteoclastogenesis in mice.去泛素化酶CYLD对小鼠中的RANK信号传导和破骨细胞生成起负向调节作用。
J Clin Invest. 2008 May;118(5):1858-66. doi: 10.1172/JCI34257.
3
The ubiquitin-editing enzyme A20 restricts nucleotide-binding oligomerization domain containing 2-triggered signals.泛素编辑酶A20可限制含核苷酸结合寡聚化结构域2引发的信号。
Immunity. 2008 Mar;28(3):381-90. doi: 10.1016/j.immuni.2008.02.002.
4
The structure of the CYLD USP domain explains its specificity for Lys63-linked polyubiquitin and reveals a B box module.CYLD泛素特异性蛋白酶结构域的结构解释了其对赖氨酸63连接的多聚泛素的特异性,并揭示了一个B盒模块。
Mol Cell. 2008 Feb 29;29(4):451-64. doi: 10.1016/j.molcel.2007.12.018.
5
Homeostatic MyD88-dependent signals cause lethal inflamMation in the absence of A20.在缺乏A20的情况下,稳态的依赖MyD88的信号会导致致命性炎症。
J Exp Med. 2008 Feb 18;205(2):451-64. doi: 10.1084/jem.20071108. Epub 2008 Feb 11.
6
The E3 ligase Itch negatively regulates inflammatory signaling pathways by controlling the function of the ubiquitin-editing enzyme A20.E3 泛素连接酶 Itch 通过控制泛素编辑酶 A20 的功能对炎症信号通路进行负调控。
Nat Immunol. 2008 Mar;9(3):254-62. doi: 10.1038/ni1563. Epub 2008 Feb 3.
7
Inflammatory cardiac valvulitis in TAX1BP1-deficient mice through selective NF-kappaB activation.TAX1BP1缺陷小鼠中通过选择性激活核因子κB导致的炎症性心脏瓣膜炎。
EMBO J. 2008 Feb 20;27(4):629-41. doi: 10.1038/emboj.2008.5. Epub 2008 Jan 31.
8
T cell antigen receptor stimulation induces MALT1 paracaspase-mediated cleavage of the NF-kappaB inhibitor A20.T细胞抗原受体刺激诱导MALT1半胱天冬酶样蛋白酶介导的核因子κB抑制剂A20的裂解。
Nat Immunol. 2008 Mar;9(3):263-71. doi: 10.1038/ni1561. Epub 2008 Jan 27.
9
The tumor suppressor CYLD regulates microtubule dynamics and plays a role in cell migration.肿瘤抑制因子CYLD调节微管动力学,并在细胞迁移中发挥作用。
J Biol Chem. 2008 Apr 4;283(14):8802-9. doi: 10.1074/jbc.M708470200. Epub 2008 Jan 24.
10
Ubiquitin binding mediates the NF-kappaB inhibitory potential of ABIN proteins.泛素结合介导ABIN蛋白对核因子κB的抑制潜能。
Oncogene. 2008 Jun 12;27(26):3739-45. doi: 10.1038/sj.onc.1211042. Epub 2008 Jan 21.

去泛素化与免疫反应的调节

Deubiquitylation and regulation of the immune response.

作者信息

Sun Shao-Cong

机构信息

Department of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, BOX 902, Houston, Texas 77030, USA.

出版信息

Nat Rev Immunol. 2008 Jul;8(7):501-11. doi: 10.1038/nri2337.

DOI:10.1038/nri2337
PMID:18535581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5763493/
Abstract

Ubiquitylation is a fundamental mechanism of signal transduction that regulates immune responses and many other biological processes. Similar to phosphorylation, ubiquitylation is a reversible process that is counter-regulated by ubiquitylating enzymes and deubiquitylating enzymes (DUBs). Despite the identification of a large number of DUBs, our knowledge of the function and activities of this family of enzymes is just starting to accumulate. As described in this Review, recent studies of several DUBs, in particular CYLD and A20, show that deubiquitylation has an important role in the regulation of both innate and adaptive immune responses.

摘要

泛素化是一种信号转导的基本机制,可调节免疫反应和许多其他生物学过程。与磷酸化类似,泛素化是一个可逆过程,由泛素化酶和去泛素化酶(DUBs)进行反向调节。尽管已经鉴定出大量的DUBs,但我们对该酶家族的功能和活性的了解才刚刚开始积累。正如本综述中所描述的,最近对几种DUBs的研究,特别是CYLD和A20,表明去泛素化在先天免疫和适应性免疫反应的调节中都起着重要作用。