G3BP1 inhibits RNA virus replication by positively regulating RIG-I-mediated cellular antiviral response

被引：74

作者：

Yang, Wenping ^{[1
,2
]}

Ru, Yi ^{[1
,2
]}

Ren, Jingjing ^{[1
,2
]}

Bai, Juncui ^{[1
,2
]}

Wei, Junshu ^{[1
,2
]}

Fu, Shaozu ^{[1
,2
]}

Liu, Xiangtao ^{[1
,2
]}

Li, Dan ^{[1
,2
]}

Zheng, Haixue ^{[1
,2
]}

机构：

[1] Chinese Acad Agr Sci, Lanzhou Vet Res Inst, State Key Lab Vet Etiol Biol, Lanzhou 730046, Gansu, Peoples R China

[2] Chinese Acad Agr Sci, Lanzhou Vet Res Inst, OIE Natl Foot & Mouth Dis Reference Lab, Lanzhou 730046, Gansu, Peoples R China

来源：

CELL DEATH & DISEASE | 2019年 / 10卷 / 12期

基金：

中国国家自然科学基金;

关键词：

UBIQUITIN LIGASE; NEGATIVE REGULATION; INNATE IMMUNITY; RECOGNITION; PROTEIN; MDA5; DEPHOSPHORYLATION; RECEPTORS; HELICASES; SENSORS;

D O I：

10.1038/s41419-019-2178-9

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Retinoic acid-inducible gene I (RIG-I) is a pattern recognition receptor and is involved in the innate immune response against RNA viruses infection. Here, we demonstrate that the Ras-GTPase-activating protein SH3-domain-binding protein 1 (G3BP1) serves as a positive regulator of the RIG-I-mediated signaling pathway. G3BP1-deficient cells inhibited RNA virus-triggered induction of downstream antiviral genes. Furthermore, we found that G3BP1 inhibited the replication of Sendai virus and vesicular stomatitis virus, indicating a positive regulation of G3BP1 to cellular antiviral responses. Mechanistically, G3BP1 formed a complex with RNF125 and RIG-I, leading to decreased RNF125 via its auto-ubiquitination; thus, promoting expression of RIG-I. Overall, the results suggest a novel mechanism for G3BP1 in the positive regulation of antiviral signaling mediated by RIG-I.

引用

页数：15

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