ZNF205 positively regulates RLR antiviral signaling by targeting RIG-I  

作　　者：Ni Zhong Chen Wang Guangxiu Weng Ting Ling Liangguo Xu 

机构地区：[1]College of Life Science,Jiangxi Normal University,Nanchang 330022,China

出　　处：《Acta Biochimica et Biophysica Sinica》2023年第10期1582-1591,共10页生物化学与生物物理学报（英文版）

基　　金：supported by the grants from the National Natural Science Foundation of China(Nos.81971502 and 82060298).

摘　　要：Retinoic acid-inducible gene I(RIG-I)is a cytosolic viral RNA receptor.Upon viral infection,the protein recognizes and then recruits adapter protein mitochondrial antiviral signaling(MAVS)protein,initiating the production of interferons and proinflammatory cytokines to establish an antiviral state.In the present study,we identify zinc finger protein 205(ZNF205)which associates with RIG-I and promotes the Sendai virus(SeV)-induced antiviral innate immune response.Overexpression of ZNF205 facilitates interferon-beta(IFN-β)introduction,whereas ZNF205 deficiency restricts its introduction.Mechanistically,the C-terminal zinc finger domain of ZNF205 interacts with the Nterminal tandem caspase recruitment domains(CARDs)of RIG-I;this interaction markedly promotes K63 ubiquitinlinked polyubiquitination of RIG-I,which is crucial for RIG-I activation.Thus,our results demonstrate that ZNF205 is a positive regulator of the RIG-I-mediated innate antiviral immune signaling pathway.

关 键 词：ZNF205 RIG-I UBIQUITINATION RLR signaling 

分 类 号：R51[医药卫生—内科学]