ArticleFrontiers in immunology2020
Interaction With 14-3-3 Correlates With Inactivation of the RIG-I Signalosome by Herpesvirus Ubiquitin Deconjugases.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- m5C RNA methylation is dysregulated by oncogenic herpesviruses via c-Myc signaling to counteract host antiviral factors.Nucleic acids research · 2026Article
- Differential regulation of translational stress responses by herpesvirus ubiquitin deconjugases.The FEBS journal · 2026Article
- Remodeling of the ribosomal quality control and integrated stress response by viral ubiquitin deconjugases.Nature communications · 2023Article
- Label-free proteomics analysis on the envelope of budded viruses of Bombyx mori nucleopolyhedrovirus harboring differential localized GP64.Virus genes · 2023Article
- 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
- Unraveling the links between neurodegeneration and Epstein-Barr virus-mediated cell cycle dysregulation.Current research in neurobiology · 2022Review
- Virus-Induced Tumorigenesis and IFN System.Biology · 2021Review
- Viral Induced Protein Aggregation: A Mechanism of Immune Evasion.International journal of molecular sciences · 2021Review
- Inhibition of selective autophagy by members of the herpesvirus ubiquitin-deconjugase family.The Biochemical journal · 2021Article
- The role of 14-3-3 proteins in cell signalling pathways and virus infection.Journal of cellular and molecular medicine · 2021Review
- Proximity Biotin Labeling Reveals Kaposi's Sarcoma-Associated Herpesvirus Interferon Regulatory Factor Networks.Journal of virology · 2021Article
- Article
- TRIMming Type I Interferon-Mediated Innate Immune Response in Antiviral and Antitumor Defense.Viruses · 2021Review
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hijacking of cellular function through expression of proteins that interfere with the activity of cellular enzymes and regulatory complexes is a common strategy used by viruses to remodel the cell environment in favor of their own replication and spread. Here we report that the ubiquitin deconjugases encoded in the N-terminal domain of the large tegument proteins of Epstein-Barr virus (EBV), Kaposi Sarcoma herpesvirus (KSHV) and human cytomegalovirus (HCMV), but not herpes simplex virus-1 (HSV-1), target an early step of the IFN signaling cascade that involves the formation of a trimolecular complex with the ubiquitin ligase TRIM25 and the 14-3-3 molecular scaffold. Different from other homologs, the HSV-1 encoded enzyme fails to interact with 14-3-3, which correlates with failure to promote the autoubiquitination and sequestration of TRIM25 in cytoplasmic aggregates, and inability to block the activation and nuclear translocation of the IRF3 transcription factor. These findings highlight a key role for 14-3-3 molecular scaffolds in the regulation of innate immune response to herpesvirus infections and points to a possible target for the development of a new type of antivirals with applications in a broad spectrum of human diseases.
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