ArticleJournal of virology2013
MDA5 localizes to stress granules, but this localization is not required for the induction of type I interferon.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 106 citations in OpenAlex.
- Differential assembly of RNP granules via activation of distinct dsRNA sensors by adenovirus mutants.PLoS pathogens · 2026Article
- Antagonism of stress granules key for SARS-CoV-2 infection and pathogenesis.bioRxiv : the preprint server for biology · 2026Article
- The assembly of stress granules during foot-and-mouth disease virus infection is uncoupled from activation of cellular intrinsic antiviral signalling.PLoS pathogens · 2026Article
- A Viral Protein Antagonist for Both AID and APOBEC3.Viruses · 2026Review
- Differential assembly of RNP granules via activation of distinct dsRNA sensors by adenovirus mutants.bioRxiv : the preprint server for biology · 2026Article
- The leader proteins of Theiler's virus and Boone cardiovirus use a combination of short linear motifs (SLiMs) to target RSK kinases to the nuclear pore complex.Journal of virology · 2025Article
- Condensation of human OAS proteins initiates diverse antiviral activities in response to West Nile virus.Genes & development · 2025Article
- Granular Insights on Innate and Intrinsic Immunity to Flaviviruses.Microorganisms · 2025Review
- TRBP modulates RLR signaling by inhibiting PKR-mediated antiviral stress granule formation.Scientific reports · 2025Article
- IFN alpha inducible protein 27 (IFI27) acts as a positive regulator of PACT-dependent PKR activation after RNA virus infections.PLoS pathogens · 2025Article
- Mitochondrial double-stranded RNA homeostasis depends on cell-cycle progression.Life science alliance · 2024Article
- Trafficking of mitochondrial double-stranded RNA from mitochondria to the cytosol.Life science alliance · 2024Article
- A closer look at mammalian antiviral condensates.Biochemical Society transactions · 2024Review
- Picornavirus security proteins promote the release of extracellular vesicle enclosed viruses via the modulation of host kinases.PLoS pathogens · 2024Article
- G3BP1-dependent condensation of translationally inactive viral RNAs antagonizes infection.Science advances · 2024Article
- Understanding the impact ofFrontiers in molecular biosciences · 2024Review
- Ribonucleoprotein Granules: Between Stress and Transposable Elements.Biomolecules · 2023Review
- Review
- Stress granules are shock absorbers that prevent excessive innate immune responses to dsRNA.Molecular cell · 2023Article
- Nucleic acid-protein condensates in innate immune signaling.The EMBO journal · 2023Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Virus infection can initiate a type I interferon (IFN-α/β) response via activation of the cytosolic RNA sensors retinoic acid-inducible gene-I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). Furthermore, it can activate kinases that phosphorylate eukaryotic translation initiation factor 2α (eIF2α), which leads to inhibition of (viral) protein translation and formation of stress granules (SG). Most viruses have evolved mechanisms to suppress these cellular responses. Here, we show that a mutant mengovirus expressing an inactive leader (L) protein, which we have previously shown to be unable to suppress IFN-α/β, triggered SG formation in a protein kinase R (PKR)-dependent manner. Furthermore, we show that infection of cells that are defective in SG formation yielded higher viral RNA levels, suggesting that SG formation acts as an antiviral defense mechanism. Since the induction of both IFN-α/β and SG is suppressed by mengovirus L, we set out to investigate a potential link between these pathways. We observed that MDA5, the intracellular RNA sensor that recognizes picornaviruses, localized to SG. However, activation of the MDA5 signaling pathway did not trigger and was not required for SG formation. Moreover, cells that were unable to form SG-by protein kinase R (PKR) depletion, using cells expressing a nonphosphorylatable eIF2α protein, or by drug treatment that inhibits SG formation-displayed a normal IFN-α/β response. Thus, although MDA5 localizes to SG, this localization seems to be dispensable for induction of the IFN-α/β pathway.
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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.