ArticleJournal of immunology (Baltimore, Md. : 1950)2015
WDR82 Negatively Regulates Cellular Antiviral Response by Mediating TRAF3 Polyubiquitination in Multiple Cell Lines.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Tracking single-cell evolution using clock-like chromatin accessibility loci.Nature biotechnology · 2025Article
- The Roles of TRAF3 in Immune Responses.Disease markers · 2023Review
- Population genomics of an icefish reveals mechanisms of glacier-driven adaptive radiation in Antarctic notothenioids.BMC biology · 2022Article
- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
- Histone demethylase LSD1 promotes RIG-I poly-ubiquitination and anti-viral gene expression.PLoS pathogens · 2021Article
- Inhibition of Antiviral Innate Immunity bymSystems · 2021Article
- TRIM35 mediates protection against influenza infection by activating TRAF3 and degrading viral PB2.Protein & cell · 2020Article
- Bioinformatics Analysis of Gene Expression Profiles for Risk Prediction in Patients with Septic Shock.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Upon Infection, Cellular WD Repeat-Containing Protein 5 (WDR5) Localizes to Cytoplasmic Inclusion Bodies and Enhances Measles Virus Replication.Journal of virology · 2018Article
- Host Interaction Analysis of PA-N155 and PA-N182 in Chicken Cells Reveals an Essential Role of UBA52 for Replication of H5N1 Avian Influenza Virus.Frontiers in microbiology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon virus infection, retinoic acid-inducible gene I-like receptors in host cells recognize viral RNA and activate type I IFN expression. Previously, we identified WD repeat domain (WDR) 5 as one positive regulator for pathway activation. In this study, we report that WDR82, a homolog protein of WDR5, acts opposite to WDR5 and inhibits the activation of the retinoic acid-inducible gene I signaling pathway. WDR82 overexpression inhibits virus-triggered pathway activation, whereas its knockdown enhances induced IFN-β expression. WDR82 is localized on the mitochondria, and its first N-terminal WD40 domain is critical for localization. WDR82 interacts with TNFR-associated factor (TRAF) 3, and its overexpression promotes K48-linked, but not K63-linked, polyubiquitination on TRAF3. Furthermore, WDR82 knockdown inhibits viral replication in the cell, whereas its overexpression has the opposite effect. Interestingly, WDR82 regulates Sendai virus-induced IFNB1 expression in a cell type-specific manner. Taken together, our findings demonstrate that WDR82 is a negative regulator of virus-triggered type I IFNs pathway through mediating TRAF3 polyubiquitination status and stability on mitochondria.
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