TRIM41 is required to innate antiviral response by polyubiquitinating BCL10 and recruiting NEMO
作者机构：Center for Systems MedicineDepartment of ImmunologyInstitute of Basic Medical SciencesPeking Union Medical CollegeChinese Academy of Medical SciencesBeijing 100005China Suzhou Institute of Systems MedicineSuzhou 215123 JiangsuChina National Key Laboratory of Medical Immunology&Institute of ImmunologySecond Military Medical UniversityShanghai 200433China Institute of ImmunologyZhejiang University School of MedicineHangzhou 310058China College of Life ScienceNankai UniversityTianjin 300071China
出 版 物：《Signal Transduction and Targeted Therapy》 (信号转导与靶向治疗（英文）)
年 卷 期：2021年第6卷第3期
页 面：1057-1068页
核心收录：
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学]
基 金：supported by grants from the National Natural Science Foundation of China(31770937,31970848,82001677,31970892,81788101,31570914,and 81222039) National Key R&D Program of China(2018YFA0507401) the"Shuguang Program"of the Shanghai Education Development Foundation and the Shanghai Municipal Education Commission(15SG32) the Program of Shanghai Subject Chief Scientist(18XD1405200)
摘 要：Sensing of pathogenic nucleic acids by pattern recognition receptors(PRR)not only initiates anti-microbe defense but causes inflammatory and autoimmune diseases.E3 ubiquitin ligase(s)critical in innate response need to be further *** we report that the tripartite motif-containing E3 ubiquitin ligase TRIM41 is required to innate antiviral response through facilitating pathogenic nucleic acids-triggered signaling ***41 deficiency impairs the production of inflammatory cytokines and type I interferons in macrophages after transfection with nucleic acid-mimics and infection with both DNA and RNA *** vivo,TRIM41 deficiency leads to impaired innate response against ***,TRIM41 directly interacts with BCL10(B cell lymphoma 10),a core component of CARD proteins-BCL10—MALT1(CBM)complex,and modifies the Lys63-linked polyubiquitylation of BCL10,which,in turn,hubs NEMO for activation of NF-kB and TANK-binding kinase 1(TBK1)—interferon regulatory factor 3(IRF3)*** study suggests that TRIM41 is the potential universal E3 ubiquitin ligase responsible for Lys63 linkage of BCL10 during innate antiviral response,adding new insight into the molecular mechanism for the control of innate antiviral response.
维普期刊数据库