RNF19a inhibits antiviral immune response to RNA viruses through degradation of TBK1.
TANK-binding kinase 1 (TBK1) plays a pivotal role in antiviral innate immunity. TBK1 mediates the activation of interferon regulatory factor (IRF) 3, leading to the induction of type I IFNs (IFN-?/?) and of NF-?B signal transduction following viral infections. TBK1 must be tightly regulated to effectively control viral infections and ... maintain immune homeostasis. Here, we found that E3 ubiquitin ligase RNF19a mediated K48-linked ubiquitination and proteasomal degradation of TBK1. Specifically, the silence of RNF19a enhanced the production of type I interferons and suppressed RNA viral replication. Our results uncover that RNF19a acts as a negative mediator in the RIG-I signaling pathway to attenuate antiviral immune responses and suggest RNF19a as a potential therapy target in clinical infectious and inflammatory diseases.
Mesh Terms:
Animals, Antiviral Agents, Herpesvirus 1, Human, Immunity, Interferon Type I, Lysine, Macrophages, Peritoneal, Male, Mice, Inbred C57BL, Protein Serine-Threonine Kinases, Proteolysis, RNA Viruses, Ubiquitin-Protein Ligases, Ubiquitination, Vesiculovirus
Animals, Antiviral Agents, Herpesvirus 1, Human, Immunity, Interferon Type I, Lysine, Macrophages, Peritoneal, Male, Mice, Inbred C57BL, Protein Serine-Threonine Kinases, Proteolysis, RNA Viruses, Ubiquitin-Protein Ligases, Ubiquitination, Vesiculovirus
Mol Immunol
Date: Dec. 01, 2021
PubMed ID: 34990937
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