ArticleCell reports2019
Vaccinia Virus Ankyrin-Repeat/F-Box Protein Targets Interferon-Induced IFITs for Proteasomal Degradation.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Poxvirus A52 protein subverts autophagy flux by blocking autophagosome-lysosome fusion to promote viral replication.PLoS pathogens · 2026Article
- Decoding cross-talk between Mpox and HIV: insights from transcriptomics and network-based analyses.Virology journal · 2025Article
- Poxvirus Host-Range Determinants: SAMD9/9L and Beyond.Annual review of virology · 2025Review
- The vaccinia virus protein, C16, promotes the ubiquitylation and relocalization of the antiviral E3 ubiquitin-ligase, TRIM25.Journal of virology · 2025Article
- A poxvirus ankyrin protein LSDV012 inhibits IFIT1 in a host-species-specific manner by compromising its RNA binding ability.PLoS pathogens · 2025Article
- Multi-omics characterization of the monkeypox virus infection.Nature communications · 2024Article
- A new MVA ancestor-derived oncolytic vaccinia virus induces immunogenic tumor cell death and robust antitumor immune responses.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Quantitative proteomics defines mechanisms of antiviral defence and cell death during modified vaccinia Ankara infection.Nature communications · 2023Article
- Article
- Poxviral ANKR/F-box Proteins: Substrate Adapters for Ubiquitylation and More.Pathogens (Basel, Switzerland) · 2022Review
- Poxvirus Interactions with the Host Ubiquitin System.Pathogens (Basel, Switzerland) · 2021Review
- Progress on Poxvirus E3 Ubiquitin Ligases and Adaptor Proteins.Frontiers in immunology · 2021Review
- Structure-Based Deep Mining Reveals First-Time Annotations for 46 Percent of the Dark Annotation Space of the 9,671-Member Superproteome of the Nucleocytoplasmic Large DNA Viruses.Journal of virology · 2020Article
- Review
- Vaccinia Virus as a Master of Host Shutoff Induction: Targeting Processes of the Central Dogma and Beyond.Pathogens (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
IFITs are interferon-induced proteins that can bind 5'-triphosphate or ribose-unmethylated capped ends of mRNA to inhibit translation. Although some viruses avoid IFITs by synthesizing RNAs with eukaryotic-like caps, no viral proteins were known to antagonize IFITs. We show that the N- and C-terminal portions of C9, a protein required for vaccinia virus to resist the human type I interferon-induced state, bind IFITs and ubiquitin regulatory complexes, respectively. Together, the two C9 domains target IFITs for proteasomal degradation, thereby providing interferon resistance similar to that also achieved by knockout of IFITs. Furthermore, ectopic expression of C9 rescues the interferon sensitivity of a vaccinia virus mutant with an inactivated cap 1-specific ribose-methyltransferase that is otherwise unable to express early proteins. In contrast, the C9-deletion mutant expresses early proteins but is blocked by IFITs at the subsequent genome uncoating/replication step. Thus, poxviruses use mRNA cap methylation and proteosomal degradation to defeat multiple antiviral activities of IFITs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.