RNF19a inhibits antiviral immune response to RNA viruses through degradation of TBK1

Yang, Yingyun; Cao, Xinyuan; Huang, Lisong; Yang, Aiming

doi:10.1016/j.molimm.2021.12.021

Cited by 5 publications

(4 citation statements)

References 30 publications

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“…For instance, RNF122 promoted RIG-I degradation via K48-linked ubiquitination to inhibit host immunity against virus infection [12]. RNF19a catalyzed K48-linked ubiquitination to degrade RIG-I, and finally attenuated RIG-I-mediated immune responses [27]. Here, we found that RNF34 functions as a negative regulator of RLRs-mediated signaling pathway to facilitate NNV replication via targeting TBK1 and IRF3.…”

Section: Discussionmentioning

confidence: 83%

“…TBK1 and IRF3 are important adaptors of the RLRs-mediated signaling pathway, therefore, both are tightly regulated by a variety of mechanisms such as ubiquitination, phosphorylation, prevention of active TBK1 complexes formation, and blocking of the IRF3 translocation from cytoplasm into the nucleus [27]. Recently, emerging evidence has shown the regulation of TBK1-IRF3 activity via the ubiquitin system.…”

Section: Discussionmentioning

confidence: 99%

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Ring-finger protein 34 facilitates nervous necrosis virus evading antiviral innate immunity by targeting TBK1 and IRF3 for ubiquitination and degradation

Zhang

Chen

Yao

et al. 2022

Preprint

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Ubiquitination enables a tight control on host immune responses, and could be hijacked by viruses for their survival. Here, we found fish pathogen nervous necrosis virus (NNV) recruited an E3 ubiquitin ligase ring finger protein 34 (RNF34) to inhibit RLRs-mediated interferons (IFN) response via ubiquitinating TBK1 and IRF3. RNF34 was found greatly enhanced NNV replication and prevented IFN production. Mechanically, RNF34 targeted TBK1 and IRF3 of different fish species for K27 and K48-linked ubiquitination degradation, which in turn diminishing TBK1-induced translocation of IRF3 from cytoplasm to nucleus. Furthermore, NNV capsid protein (CP) directly bind with different fishes RNF34, and CP-induced TBK1 and IRF3 degradation and IFN suppression depended on RNF34. Our findings demonstrated a novel mechanism by which NNV CP evaded host innate immunity via RNF34, and provided a potential drug target for the control of NNV infection.

show abstract

Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Ring-finger protein 34 facilitates nervous necrosis virus evading antiviral innate immunity by targeting TBK1 and IRF3 for ubiquitination and degradation

Zhang

Chen

Yao

et al. 2022

Preprint

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“…40 RNF19a suppresses the production of type I IFN by degrading TBK1. 41 Therefore, the difference in TBK1 expression caused by wt-ASFV or ASFVΔ9L infection may result in the difference of wt-ASFV or ASFVΔ9L in type IFN I production. Obviously, TBK1 degradation is usually mediated the ubiquitin-proteasome pathway or autophagylysosome pathway.…”

Section: Discussionmentioning

confidence: 99%

“…RAF‐interacting protein (TRIP) degrades TBK1 by directly binding to and promoting K48‐linked polyubiquitination of TBK1 40 . RNF19a suppresses the production of type I IFN by degrading TBK1 41 . Therefore, the difference in TBK1 expression caused by wt ‐ASFV or ASFVΔ9L infection may result in the difference of wt ‐ASFV or ASFVΔ9L in type IFN I production.…”

Section: Discussionmentioning

confidence: 99%

Deletion of MGF‐110‐9L gene from African swine fever virus weakens autophagic degradation of TBK1 as a mechanism for enhancing type I interferon production

Ren

Zhu

et al. 2023

The FASEB Journal

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African swine fever (ASF) caused by African swine fever virus (ASFV) is a devastating disease for the global pig industry and economic benefit. The limited knowledge on the pathogenesis and infection mechanisms of ASF restricts progress toward vaccine development and ASF control. Previously, we illustrated that deletion of the MGF-110-9L gene from highly virulent ASFV CN/GS/2018 strains (ASFV∆9L) results in attenuated virulence in swine, but the underlying mechanism remains unclear. In this study, we found that the difference in virulence between wild-type ASFV (wt-ASFV) and ASFV∆9L strains was mainly caused by the difference in TANK Binding Kinase 1 (TBK1) reduction. TBK1 reduction was further identified to be mediated by the autophagy pathway and this degradative process requires the up-regulation of a positive autophagy regulation molecule-Phosphatidylinositol-4-Phosphate 3-Kinase Catalytic Subunit Type 2 Beta (PIK3C2B). Moreover, TBK1 over-expression was confirmed to inhibit ASFV replication in vitro. In summary, these results indicate that wt-ASFV counteracts type I interferon (IFN) production by degrading TBK1, while ASFVΔ9L enhanced type I IFN production by weakening TBK1 reduction, clarifying the mechanism that ASFVΔ9L present the attenuated virulence in vitro.

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UBL7 enhances antiviral innate immunity by promoting Lys27-linked polyubiquitination of MAVS

Jiang¹,

Li²,

Xu³

et al. 2023

Cell Reports

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RNF19a inhibits antiviral immune response to RNA viruses through degradation of TBK1

Cited by 5 publications

References 30 publications

Ring-finger protein 34 facilitates nervous necrosis virus evading antiviral innate immunity by targeting TBK1 and IRF3 for ubiquitination and degradation

Ring-finger protein 34 facilitates nervous necrosis virus evading antiviral innate immunity by targeting TBK1 and IRF3 for ubiquitination and degradation

Deletion of MGF‐110‐9L gene from African swine fever virus weakens autophagic degradation of TBK1 as a mechanism for enhancing type I interferon production

UBL7 enhances antiviral innate immunity by promoting Lys27-linked polyubiquitination of MAVS

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