TRIM25 in the Regulation of the Antiviral Innate Immunity.
TRIM25 in the Regulation of the Antiviral Innate Immunity.
复制标题
DOI：
10.3389/fimmu.2017.01187
复制
发表时间：
2017
影响因子：
7.3
通讯作者：
Martínez I
中科院分区：
文献类型：
--
作者：
Martín-Vicente M;Medrano LM;Resino S;García-Sastre A;Martínez I
TRIM 25是一种E3泛素连接酶，参与各种细胞过程，包括调节针对病毒的先天免疫应答。TRIM 25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重要步骤，并且已经被充分记录。然而，近年来，TRIM 25在早期先天免疫中的其他作用正在出现，包括RIG-I的负调节，黑色素瘤分化相关蛋白5-线粒体抗病毒信号传导蛋白-TRAF 6抗病毒轴的激活以及p53水平和活性的调节。此外，TRIM 25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。
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.