ArticleNature communications2024
Oxygen enhances antiviral innate immunity through maintenance of EGLN1-catalyzed proline hydroxylation of IRF3.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- TANK potentiates antiviral innate immunity by recruiting deubiquitinase USP46 to activate IKKε.PLoS pathogens · 2026Article
- PHD1-dependent hydroxylation of RepoMan (CDCA2) on P604 modulates the control of mitotic progression.eLife · 2026Article
- Article
- HCMV infection depends on EGLN1-mediated mitochondrial activation to increase dNTP pools for viral DNA replication.Cell reports · 2026Article
- Manipulating Unisexual-Sexual Reproduction Transition to Engineer Genome-Reconstructed Polyploids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MYLIP attenuates hypoxia tolerance by inducing K27-linked polyubiquitination and subsequent proteasomal degradation of HIF-α.Communications biology · 2025Article
- Direct lysine dimethylation of IRF3 by the methyltransferase SMYD3 attenuates antiviral innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ZebrafishJournal of virology · 2024Article
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxygen is essential for aerobic organisms, but little is known about its role in antiviral immunity. Here, we report that during responses to viral infection, hypoxic conditions repress antiviral-responsive genes independently of HIF signaling. EGLN1 is identified as a key mediator of the oxygen enhancement of antiviral innate immune responses. Under sufficient oxygen conditions, EGLN1 retains its prolyl hydroxylase activity to catalyze the hydroxylation of IRF3 at proline 10. This modification enhances IRF3 phosphorylation, dimerization and nuclear translocation, leading to subsequent IRF3 activation. Furthermore, mice and zebrafish with Egln1 deletion, treatment with the EGLN inhibitor FG4592, or mice carrying an Irf3 P10A mutation are more susceptible to viral infections. These findings not only reveal a direct link between oxygen and antiviral responses, but also provide insight into the mechanisms by which oxygen regulates innate immunity.
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