Ring finger protein 166 potentiates RNA virus-induced interferon-β production via enhancing the ubiquitination of TRAF3 and TRAF6

被引：33
|
作者：
Chen, Hai-Wei [1 ]
Yang, Yong-Kang [1 ]
Xu, Hao [1 ]
Yang, Wei-Wei [1 ]
Zhai, Zhong-He [1 ]
Chen, Dan-Ying [1 ]
机构：
[1] Peking Univ, Sch Life Sci, Key Lab Cell Proliferat & Differentiat, Minist Educ, Beijing 100871, Peoples R China
来源：
SCIENTIFIC REPORTS | 2015年 / 5卷
基金：
中国国家自然科学基金;
关键词：
CYCLIC GMP-AMP; INNATE IMMUNE-RESPONSES; NF-KAPPA-B; NEGATIVE REGULATOR; ADAPTER PROTEIN; IFN-BETA; LIGASE; 2ND-MESSENGER; PHOSPHORYLATION; IDENTIFICATION;
D O I：
10.1038/srep14770
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Host cells orchestrate the production of IFN-beta upon detecting invading viral pathogens. Here, we report that Ring finger protein 166 (RNF166) potentiates RNA virus-triggered IFN-beta production. Overexpression of RNF166 rather than its homologous proteins RNF114, RNF125, and RNF138, enhanced Sendai virus (SeV)-induced activation of the IFN-beta promoter. Knockdown of endogenous RNF166, but not other RNFs, inhibited the IFN-beta 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-beta production by enhancing the ubiquitination of TRAF3 and TRAF6.
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页数：10
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