Palmitoyl-transferase 3 promotes mitochondrial antiviral signaling protein degradation by modulating its ubiquitination
文献类型： 外文期刊
作者： Yi, Li 1 ; Song, Jiangwei 2 ; Zhang, Zheng 3 ; Li, Longping 1 ; Wu, Yongqing 4 ; Xue, Mengzhou 5 ; Zheng, Chunfu 6 ; Liu, Chenggang 4 ;
作者机构： 1.Yiyang Cent Hosp, Dept Clin Lab, Yiyang 413099, Hunan, Peoples R China
2.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing Key Lab Prevent & Control Infect Dis Lives, Beijing 100097, Peoples R China
3.Capital Med Univ, Beijing Tiantan Hosp, Dept Neurosurg, Beijing, Peoples R China
4.Shanwei Acad Agr Sci, Shanwei, Peoples R China
5.Zhengzhou Univ, Affiliated Hosp 2, Dept Cerebrovascular Dis, Zhengzhou 450001, Peoples R China
6.Univ Calgary, Dept Microbiol Immunol & Infect Dis, Calgary, AB, Canada
关键词： Protein acyltransferases; IFN-beta; MAVS; RIG-I; ZDHHC
期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：8.5； 五年影响因子：8.7 ）
ISSN： 0141-8130
年卷期： 2025 年 310 卷
页码：
收录情况： SCI
摘要： The innate antiviral immunity of humans serves as their first line of defence against viral and microbial illnesses. The retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) signaling pathway requires the mitochondrial antiviral signaling protein (MAVS) to function properly. ZDHHCs, a family of acyltransferases, regulate diverse biological processes via interactions with numerous mammalian proteins and viral proteins. However, the role of ZDHHCs in antiviral innate immunity against RNA viruses remains largely elusive. Here, we show that ZDHHC3 downregulates the RLR signaling pathway. Ectopic ZDHHC3 expression reduces RIG-IN- and SeV-mediated IFN-beta promoter activity, IRF3 nuclear transduction, and transcription of the IFN-beta and ISG genes. Furthermore, ectopic expression of ZDHHC3 decreases MAVS stability by promoting proteasomal degradation, which can be reversed by MG132 but not CQ. ZDHHC3 interacts with MAVS and promotes its breakdown by increasing K48-linked ubiquitination rather than K63-linked ubiquitination. ZDHHC3 deletion resulted in increased IFN-beta promoter activity and transcription of the IFN-beta and ISG genes. ZDHHC3 knockdown promotes subsequent antiviral signaling and reduces viral replication, indicating the role of ZDHHC3 in antiviral innate immunity. In addition, the catalytically inactive mutant ZDHHC3 C157S efficiently reversed the IFN-beta promoter activity produced by RIG-IN, which was consistent with the results of 2-BP treatment. Collectively, these data show that ZDHHC3 inhibits the RNA virus-triggered signaling cascade by targeting MAVS and provides new insights into the role of ZDHHC3 in antiviral innate immunity.
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