期刊
PROTEIN & CELL
卷 11, 期 12, 页码 894-914出版社
SPRINGER
DOI: 10.1007/s13238-020-00734-6
关键词
influenza A virus; PB2; TRIM35; TRAF3; ubiquitination; antiviral immunity
类别
资金
- National Key Research and Development Program of China [2016YFD0500205]
- National Natural Science Foundation of China (NSFC) [31521005, 31672582, 31422054, 31472215]
- Natural Science Foundation of Heilongjiang Province [JQ2019C005]
- Central Public-Interest Scientific Institution Basal Research Fund [Y2017JC35]
Tripartite motif (TRIM) family proteins are important effectors of innate immunity against viral infections. Here we identified TRIM35 as a regulator of TRAF3 activation. Deficiency in or inhibition of TRIM35 suppressed the production of type I interferon (IFN) in response to viral infection.Trim35-deficient mice were more susceptible to influenza A virus (IAV) infection than were wild-type mice. TRIM35 promoted the RIG-I-mediated signaling by catalyzing Lys63-linked polyubiquitination of TRAF3 and the subsequent formation of a signaling complex with VISA and TBK1. IAV PB2 polymerase countered the innate antiviral immune response by impeding the Lys63-linked polyubiquitination and activation of TRAF3. TRIM35 mediated Lys48-linked polyubiquitination and proteasomal degradation of IAV PB2, thereby antagonizing its suppression of TRAF3 activation. Ourin vitroandin vivofindings thus reveal novel roles of TRIM35, through catalyzing Lys63- or Lys48-linked polyubiquitination, in RIG-I antiviral immunity and mechanism of defense against IAV infection.
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