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TRIM25在抗病毒天然免疫调节中的作用

TRIM25 in the Regulation of the Antiviral Innate Immunity.

作者信息

Martín-Vicente María, Medrano Luz M, Resino Salvador, García-Sastre Adolfo, Martínez Isidoro

机构信息

Unidad de Infección Viral e Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain.

Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, United States.

出版信息

Front Immunol. 2017 Sep 22;8:1187. doi: 10.3389/fimmu.2017.01187. eCollection 2017.

DOI:10.3389/fimmu.2017.01187
PMID:29018447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5614919/
Abstract

TRIM25 is an E3 ubiquitin ligase enzyme that is involved in various cellular processes, including regulation of the innate immune response against viruses. TRIM25-mediated ubiquitination of the cytosolic pattern recognition receptor RIG-I is an essential step for initiation of the intracellular antiviral response and has been thoroughly documented. In recent years, however, additional roles of TRIM25 in early innate immunity are emerging, including negative regulation of RIG-I, activation of the melanoma differentiation-associated protein 5-mitochondrial antiviral signaling protein-TRAF6 antiviral axis and modulation of p53 levels and activity. In addition, the ability of TRIM25 to bind RNA may uncover new mechanisms by which this molecule regulates intracellular signaling and/or RNA virus replication.

摘要

TRIM25是一种E3泛素连接酶,参与多种细胞过程,包括对病毒的先天性免疫反应的调节。TRIM25介导的胞质模式识别受体RIG-I的泛素化是启动细胞内抗病毒反应的关键步骤,并且已经有充分的文献记载。然而,近年来,TRIM25在早期先天性免疫中的其他作用正在显现,包括对RIG-I的负调节、黑色素瘤分化相关蛋白5-线粒体抗病毒信号蛋白-TRAF6抗病毒轴的激活以及对p53水平和活性的调节。此外,TRIM25结合RNA的能力可能揭示该分子调节细胞内信号传导和/或RNA病毒复制的新机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/686c/5614919/08b7a9e34d37/fimmu-08-01187-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/686c/5614919/f844314ec965/fimmu-08-01187-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/686c/5614919/42e2ccf209ed/fimmu-08-01187-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/686c/5614919/08b7a9e34d37/fimmu-08-01187-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/686c/5614919/f844314ec965/fimmu-08-01187-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/686c/5614919/42e2ccf209ed/fimmu-08-01187-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/686c/5614919/08b7a9e34d37/fimmu-08-01187-g003.jpg

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The Severe Acute Respiratory Syndrome Coronavirus Nucleocapsid Inhibits Type I Interferon Production by Interfering with TRIM25-Mediated RIG-I Ubiquitination.
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