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

被引：36

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.

引用

页数：10

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