ArticleJournal of virology2025
Restriction of influenza A virus replication by host DCAF7-CRL4B axis.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Ubiquitin-Dependent Regulation of Influenza A Virus Polymerase and vRNP Function: Mechanisms and Therapeutic Opportunities.Microorganisms · 2026Review
- N-terminal acetylation controls multiple functional aspects of the influenza A virus ribonuclease PA-X.Journal of virology · 2026Article
- N-terminal acetylation controls multiple functional aspects of the influenza A virus ribonuclease PA-X.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The balance between cellular defense and viral escape determines the fate of influenza A virus (IAV) infection. Viral polymerase activity is critical for the replication and propagation of IAV. The antiviral strategies of host cells against IAV infection have not been fully elucidated. Here, we identified DCAF7 as an antiviral factor for IAV, which inhibits the replication of H1N1 and H3N2. Mechanistically, DCAF7 weakens the viral heterotrimer polymerase activity and restricts IAV replication and transcription. DCAF7 as a substrate recognition receptor forms a complete CRL4B IMPORTANCE: Until now, the key host factors that affect IAV polymerase have not been fully elucidated. In this study, we identified host DCAF7 as a novel restriction factor for IAV replication. Importantly, DCAF7 acts as a substrate recognition receptor to recruit CRL4B E3 ligase to mediate the degradation of PA through the ubiquitin-proteasome pathway. Further exploration demonstrated that a specific cullin-RING E3 ligase inhibitor MLN4924 promotes IAV replication
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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.