TRIM52 inhibits Japanese Encephalitis Virus replication by degrading the viral NS2A
TRIM52 inhibits Japanese Encephalitis Virus replication by degrading the viral NS2A
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DOI：
10.1038/srep33698
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Qian P
中科院分区：
文献类型：
--
作者：
Fan W;Wu M;Qian S;Zhou Y;Chen H;Li X;Qian P
The members of tripartite-motif containing (TRIM) protein participate in various cellular processes and play an important role in host antiviral function. TRIM proteins exert their antiviral activity either directly by degrading viral proteins through their E3 ligase activity, or indirectly by promoting host innate immunity. This study demonstrated for the first time that TRIM52 is a novel antiviral TRIM protein against Japanese encephalitis virus (JEV) infection. Overexpression of TRIM52 restricted JEV replication in BHK-21 and 293T cells. In addition, JEV nonstructural protein 2A (NS2A) is a protein that interacts with TRIM52. Their interaction degraded NS2A in a proteasome-dependent manner via the E3 ligase activity of TRIM52. Thus, TRIM52 is a novel antiviral TRIM protein, and it exerted antiviral activity against JEV infection by targeting and degrading viral NS2A
