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Nuclear TRIM25 Specifically Targets Influenza Virus Ribonucleoproteins to Block the Onset of RNA Chain Elongation.
Cell Host & Microbe ( IF 30.3 ) Pub Date : 2017-11-05 , DOI: 10.1016/j.chom.2017.10.003
Nicholas R Meyerson 1 , Ligang Zhou 2 , Yusong R Guo 3 , Chen Zhao 2 , Yizhi J Tao 3 , Robert M Krug 2 , Sara L Sawyer 1
Affiliation  

TRIM25 is an E3 ubiquitin ligase that activates RIG-I to promote the antiviral interferon response. The NS1 protein from all strains of influenza A virus binds TRIM25, although not all virus strains block the interferon response, suggesting alternative mechanisms for TRIM25 action. Here we present a nuclear role for TRIM25 in specifically restricting influenza A virus replication. TRIM25 inhibits viral RNA synthesis through a direct mechanism that is independent of its ubiquitin ligase activity and the interferon pathway. This activity can be inhibited by the viral NS1 protein. TRIM25 inhibition of viral RNA synthesis results from its binding to viral ribonucleoproteins (vRNPs), the structures containing individual viral RNA segments, the viral polymerase, and multiple viral nucleoproteins. TRIM25 binding does not inhibit initiation of capped-RNA-primed viral mRNA synthesis by the viral polymerase. Rather, the onset of RNA chain elongation is inhibited because TRIM25 prohibits the movement of RNA into the polymerase complex.

中文翻译:

核TRIM25专门针对流感病毒核糖核蛋白,以阻止RNA链延长的发作。

TRIM25是一种E3泛素连接酶,可激活RIG-1以促进抗病毒干扰素应答。尽管并非所有病毒株都能阻断干扰素应答,但来自所有甲型流感病毒株的NS1蛋白都结合了TRIM25,提示了TRIM25作用的替代机制。在这里,我们介绍了TRIM25在特定限制甲型流感病毒复制中的核心作用。TRIM25通过直接机制抑制病毒RNA合成,而该机制与其泛素连接酶活性和干扰素途径无关。这种活性可以被病毒NS1蛋白抑制。TRIM25对病毒RNA合成的抑制作用是由于它与病毒核糖核蛋白(vRNPs),包含单个病毒RNA片段的结构,病毒聚合酶和多种病毒核蛋白结合而成。TRIM25结合不会抑制病毒聚合酶引发带帽RNA引发的病毒mRNA合成的启动。而是,由于TRIM25禁止RNA进入聚合酶复合物,因此抑制了RNA链延长的发生。
更新日期:2017-11-05
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