ArticleNature communications2025
Prefoldin complex promotes interferon-stimulated gene expression and is inhibited by rotavirus VP3.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
The trial behind it
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Who cites it
6 citing papers in PubMed.
- Signal peptidase complex mediates rotavirus VP7 processing and virion assembly.PLoS pathogens · 2026Article
- Research Progress and Applications of the Rotavirus Reverse Genetics System.Animals : an open access journal from MDPI · 2026Review
- Article
- Review
- Plasma PFDN2 suppresses head and neck squamous cell carcinoma progression by restricting CD64 on monocyte-driven inflammatory microenvironments.Frontiers in immunology · 2026Article
- Signal peptidase complex mediates rotavirus VP7 processing and virion assembly.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Timely induction of interferons and interferon-stimulated genes (ISGs) is critical for successful host defense against viral infections. VP3 encoded by rotavirus is implicated in interferon antagonism. However, the precise mechanisms remain incompletely understood. By conducting tandem-affinity purification coupled with high-resolution mass spectrometry, we identify the prefoldin complex as the top cellular binding partner of VP3. Rotavirus infection is significantly enhanced in prefoldin subunit knockout cells. Using proteome-wide label-free quantification, we find that prefoldin assists in folding ubiquitin-like-modifier-activating-enzyme-3 (UBA3), both of which positively regulate ISG expression. Through direct and competitive binding, VP3 interferes with the chaperone activity of prefoldin, leading to unstable UBA3, reduces IRF9, and suppresses ISG transcription. Our findings report a novel function of a prefoldin-UBA3-IRF9-ISG axis in antiviral immunity and uncover new aspects of virus-host interactions that could be exploited for broad-spectrum antiviral therapeutic development.
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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 OpenQuestion graph.