ArticleFrontiers in immunology2026
CRM1-dependent nuclear export of TRIM28 promotes MAVS K48-linked ubiquitination and suppresses RIG-I-mediated antiviral response.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Ubiquitination is a pivotal post-translational mechanism regulating antiviral innate immunity. TRIM28, a member of the transcription intermediary factor 1 (TIF1) subfamily of the TRIM protein family, has been implicated in the modulation of retinoic acid-inducible gene I (RIG-I) signaling. However, the molecular basis and Methods: TRIM28 overexpression and knockdown systems were used to evaluate type I interferon (IFN) responses and RNA virus replication Results: TRIM28 knockdown enhanced type I IFN responses and inhibited RNA virus replication Conclusion: TRIM28 functions as a negative regulator of RIG-I-mediated antiviral signaling by promoting K48-linked ubiquitination of MAVS. These findings define the TRIM28-MAVS axis as a regulatory checkpoint in innate antiviral immunity and suggest its potential as a target for antiviral intervention.
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