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自我保护:E3泛素连接酶与T细胞耐受性概述

Preservation of self: an overview of E3 ubiquitin ligases and T cell tolerance.

作者信息

Schartner J M, Fathman C G, Seroogy C M

机构信息

University of Wisconsin, Department of Pediatrics, Division of Allergy/Immunology/Rheumatology, Madison, WI 53792, USA.

出版信息

Semin Immunol. 2007 Jun;19(3):188-96. doi: 10.1016/j.smim.2007.02.010. Epub 2007 Apr 2.

DOI:10.1016/j.smim.2007.02.010
PMID:17403607
Abstract

Until recently ubiquitination of a protein was thought to simply serve the mundane task of targeting a protein for proteasomal degradation. Accumulating evidence over the past decade has demonstrated the importance of ubiquitination in non-degradative functions including regulating cellular signaling, that highlight its role in human disease and thus potential development of novel therapeutics. Much has been written about ubiquitination in the immune system, in this review we will outline our current knowledge of ubiquitination with respect to T cell tolerance. Specifically, we will provide on overview of E3 ubiquitin ligases and their role in various states of CD4+ T cell tolerance: central and peripheral.

摘要

直到最近,人们还认为蛋白质的泛素化仅仅是为将蛋白质靶向蛋白酶体降解这一普通任务服务。过去十年间不断积累的证据表明,泛素化在包括调节细胞信号传导在内的非降解性功能中具有重要作用,这凸显了其在人类疾病中的作用以及新型疗法的潜在开发价值。关于免疫系统中的泛素化已有诸多论述,在本综述中,我们将概述目前关于T细胞耐受性方面泛素化的知识。具体而言,我们将综述E3泛素连接酶及其在CD4+ T细胞耐受性的各种状态(中枢性和外周性)中的作用。

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Protein multifunctionality: principles and mechanisms.蛋白质多功能性:原理与机制
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GRAIL: a unique mediator of CD4 T-lymphocyte unresponsiveness.GRAIL:一种独特的 CD4 T 淋巴细胞无应答的介导物。
FEBS J. 2011 Jan;278(1):47-58. doi: 10.1111/j.1742-4658.2010.07922.x. Epub 2010 Nov 16.
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Gene related to anergy in lymphocytes (GRAIL) expression in CD4+ T cells impairs actin cytoskeletal organization during T cell/antigen-presenting cell interactions.淋巴细胞无反应相关基因(GRAIL)在 CD4+T 细胞中的表达在 T 细胞/抗原呈递细胞相互作用过程中损害肌动蛋白细胞骨架的组织。
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Naive CD4 t cell proliferation is controlled by mammalian target of rapamycin regulation of GRAIL expression.初始CD4 T细胞增殖受雷帕霉素哺乳动物靶标对GRAIL表达的调控。
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Control of virus-specific CD8+ T-cell exhaustion and immune-mediated pathology by E3 ubiquitin ligase Cbl-b during chronic viral infection.慢性病毒感染期间E3泛素连接酶Cbl-b对病毒特异性CD8 + T细胞耗竭和免疫介导病理的控制
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