ArticleiScience2025
MAVS phosphorylation acts as a cellular stress sensor that modulates antiviral immunity.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Review
- Dietary berberine supplementation regulates production performance, antioxidant capacity, and immunity of Wenchang chicken (Gallus gallus domestics).Poultry science · 2026Article
- Methyltransferase SETD7 as a Regulator of STING-Dependent Cytokine Response in Lung Cancer Cells.International journal of molecular sciences · 2026Article
- Metabolic-Epigenetic Crosstalk in Takayasu Arteritis: The ANK2-MAVS-IL-8 Axis as a Novel Therapeutic Paradigm.International journal of molecular sciences · 2026Review
- Post-translational control of MAVS signaling: linking mitochondrial antiviral immunity to metabolic and cellular stress contexts.Frontiers in physiology · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon viral infection, cytosolic RIG-I-like receptors recognize viral RNA and activate innate immune responses through the mitochondrial antiviral-signaling protein (MAVS), leading to type I interferon (IFN) production and apoptosis. Cellular stress influences immune activation, but its impact on MAVS signaling remains largely unclear. Here, we show that MAVS undergoes phosphorylation via p38 MAPK signaling, activated by the stress-activated MAPKKK ASK1. This modification enhances MAVS interaction with TRAF, a key downstream adaptor, thereby promoting type I IFN induction. Oxidative and endoplasmic reticulum stress significantly amplified type I IFN expression upon viral infection, but this effect was attenuated in cells expressing MAVS mutants lacking phosphorylation sites. These findings suggest MAVS phosphorylation as a key mechanism integrating cellular stress signals into antiviral immunity. By linking the MAPK pathway to MAVS-dependent IFN expression, we propose MAVS phosphorylation as a cellular stress sensor that modulates antiviral immunity in a context-dependent manner.
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Registered trials
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