RNF19a inhibits antiviral immune response to RNA viruses through degradation of TBK1.
In: Molecular Immunology, Jg. 143 (2022-03-01), S. 1-6
Online
academicJournal
Zugriff:
• The expression of RNF19a is increased in macrophages upon virus infection. • RNF19a selectively inhibits type I interferon production upon RNA virus infection. • RNF19a inhibits the RIG-I signaling upon RNA virus infection. • RNF19a promotes the degradation of TBK1 through K48-linked ubiquitination. 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-α/β) and of NF-κB 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. [ABSTRACT FROM AUTHOR]
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RNF19a inhibits antiviral immune response to RNA viruses through degradation of TBK1.
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Autor/in / Beteiligte Person: | Yang, Yingyun ; Cao, Xinyuan ; Huang, Lisong ; Yang, Aiming |
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Zeitschrift: | Molecular Immunology, Jg. 143 (2022-03-01), S. 1-6 |
Veröffentlichung: | 2022 |
Medientyp: | academicJournal |
ISSN: | 0161-5890 (print) |
DOI: | 10.1016/j.molimm.2021.12.021 |
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