ArticlePLoS pathogens2025
RNF149 modulates the type I IFN innate antiviral immune responses through degrading IRF3.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- TOR3A represses type I interferon production and limits viral clearance during respiratory syncytial virus infection.Emerging microbes & infections · 2026Article
- Encephalomyocarditis virus evades IFN-mediated antiviral response by RNF149 targeting JAK1 for ubiquitination and degradation.Virulence · 2026Article
- ZFP91 restricts RSV replication by driving K48-linked ubiquitination and proteasomal degradation of M2-1.Cellular and molecular life sciences : CMLS · 2026Article
- TRIM25 promotes antiviral innate immune response by stabilizing IRF7 and its nuclear translocation.mBio · 2026Article
- CRM1-dependent nuclear export of TRIM28 promotes MAVS K48-linked ubiquitination and suppresses RIG-I-mediated antiviral response.Frontiers in immunology · 2026Article
- ARCN1 suppresses innate immune responses against respiratory syncytial virus by promoting STUB1-mediated IKKε degradation.PLoS pathogens · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
E3 ubiquitin ligases are key molecules in regulating the innate immune responses against virus. They catalyze the activation or degradation of various signaling proteins involved in the innate immune responses. Herein, we found the regulatory role of RNF149 in the host's innate immune responses against viral infection. Virus infection induced the expression of RNF149. Overexpression of RNF149 was associated with reduced production of IFN-β and enhanced viral replication. Mechanically, RNF149 interacted with IRF3 and downregulated its protein level. As an E3 ubiquitin ligase, RNF149 promoted the K27-linked ubiquitination of IRF3 at K409 and K33-linked ubiquitination at K366 and K409, which promoted IRF3 degradation through the proteasome pathway. Our results revealed the regulatory mechanism of RNF149 during viral infection and provided new insights into host cells responding to viral infection. Downregulating the expression of RNF149 may help enhance the antiviral ability of host cells and inhibit viral replication, thus providing a new strategy for the treatment of viral infection.
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