Ring finger protein 166 potentiates RNA virus-induced interferon-β production via enhancing the ubiquitination of TRAF3 and TRAF6.
Ring finger protein 166 potentiates RNA virus-induced interferon-β production via enhancing the ubiquitination of TRAF3 and TRAF6.
复制标题
环指蛋白 166 通过增强 TRAF3 和 TRAF6 的泛素化来增强 RNA 病毒诱导的干扰素 β 的产生
DOI：
10.1038/srep14770
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发表时间：
2015-10-12
影响因子：
4.6
通讯作者：
Chen DY
中科院分区：
文献类型：
--
作者：
Chen HW;Yang YK;Xu H;Yang WW;Zhai ZH;Chen DY
宿主细胞在检测到入侵的病毒病原体后协调IFN-β的产生。在这里，我们报道无名指蛋白166 （RNF166）增强了RNA病毒触发的IFN-β的产生。过表达RNF166而不是其同源蛋白RNF114、RNF125和RNF138，增强了仙台病毒（SeV）诱导的IFN-β启动子的激活。内源性RNF166的敲除抑制了SeV和脑心肌炎病毒诱导的IFN-β的产生，而其他RNF166的敲除不抑制。RNF166与TRAF3和TRAF6相互作用。当内源性RNF166而非RNF114/138被敲除时，sev诱导的TRAF3和TRAF6泛素化被抑制。这些发现表明，RNF166通过增强TRAF3和TRAF6的泛素化，正调控RNA病毒引发的IFN-β的产生。
Host cells orchestrate the production of IFN-β upon detecting invading viral pathogens. Here, we report that Ring finger protein 166 (RNF166) potentiates RNA virus-triggered IFN-β production. Overexpression of RNF166 rather than its homologous proteins RNF114, RNF125, and RNF138, enhanced Sendai virus (SeV)-induced activation of the IFN-β promoter. Knockdown of endogenous RNF166, but not other RNFs, inhibited the IFN-β production induced by SeV and encephalomyocarditis virus. RNF166 interacted with TRAF3 and TRAF6. SeV-induced ubiquitination of TRAF3 and TRAF6 was suppressed when endogenous RNF166 rather than RNF114/138 was knocked down. These findings suggest that RNF166 positively regulates RNA virus-triggered IFN-β production by enhancing the ubiquitination of TRAF3 and TRAF6.