ArticlePLoS pathogens2019
14-3-3 scaffold proteins mediate the inactivation of trim25 and inhibition of the type I interferon response by herpesvirus deconjugases.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Review
- Article
- The vaccinia virus protein, C16, promotes the ubiquitylation and relocalization of the antiviral E3 ubiquitin-ligase, TRIM25.Journal of virology · 2025Article
- E2-Ub-R74G strategy reveals E2-specific ubiquitin conjugation profiles in live cells.Nature chemical biology · 2025Article
- Review
- Potato virus Y viral protein 6K1 inhibits the interaction between defense proteins during virus infection.Plant physiology · 2024Article
- Cleavage of 14-3-3ε by the enteroviral 3C protease dampens RIG-I-mediated antiviral signaling.Journal of virology · 2023Article
- Viral evasion of the interferon response at a glance.Journal of cell science · 2023Review
- Exploiting RIG-I-like receptor pathway for cancer immunotherapy.Journal of hematology & oncology · 2023Review
- Barrier-to-autointegration factor 1 promotes gammaherpesvirus reactivation from latency.Nature communications · 2023Article
- Suppression of cGAS- and RIG-I-mediated innate immune signaling by Epstein-Barr virus deubiquitinase BPLF1.PLoS pathogens · 2023Article
- Autophagy as a dual-faced host response to viral infections.Frontiers in cellular and infection microbiology · 2023Review
- The oncogenic gamma herpesviruses Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) hijack retinoic acid-inducible gene I (RIG-I) facilitating both viral and tumour immune evasion.Tumour virus research · 2022Review
- Review
- Anemoside B4 inhibits enterovirus 71 propagation in mice through upregulating 14-3-3 expression and type I interferon responses.Acta pharmacologica Sinica · 2022Article
- Activation and Evasion of Innate Immunity by Gammaherpesviruses.Journal of molecular biology · 2022Review
- Article
- The Role of Deubiquitinases in Virus Replication and Host Innate Immune Response.Frontiers in microbiology · 2022Review
- Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host.Frontiers in microbiology · 2022Review
- The Epstein-Barr virus deubiquitinase BPLF1 targets SQSTM1/p62 to inhibit selective autophagy.Autophagy · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 14-3-3 molecular scaffolds promote type I interferon (IFN) responses by stabilizing the interaction of RIG-I with the TRIM25 ligase. Viruses have evolved unique strategies to halt this cellular response to support their replication and spread. Here, we report that the ubiquitin deconjugase (DUB) encoded in the N-terminus of the Epstein-Barr virus (EBV) large tegument protein BPLF1 harnesses 14-3-3 molecules to promote TRIM25 autoubiquitination and sequestration of the ligase into inactive protein aggregates. Catalytically inactive BPLF1 induced K48-linked autoubiquitination and degradation of TRIM25 while the ligase was mono- or di-ubiquitinated in the presence of the active viral enzyme and formed cytosolic aggregates decorated by the autophagy receptor p62/SQSTM1. Aggregate formation and the inhibition of IFN response were abolished by mutations of solvent exposed residues in helix-2 of BPLF1 that prevented binding to 14-3-3 while preserving both catalytic activity and binding to TRIM25. 14-3-3 interacted with the Coiled-Coil (CC) domain of TRIM25 in in vitro pulldown, while BPLF1 interacted with both the CC and B-box domains, suggesting that 14-3-3 positions BPLF1 at the ends of the CC dimer, close to known autoubiquitination sites. Our findings provide a molecular understanding of the mechanism by which a viral deubiquitinase inhibits the IFN response and emphasize the role of 14-3-3 proteins in modulating antiviral defenses.
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