ArticleCellular microbiology2011
Influenza A virus-induced early activation of ERK and PI3K mediates V-ATPase-dependent intracellular pH change required for fusion.
Article in Cellular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 117 citations in OpenAlex.
- Host nucleolin-targeting unique peptide drugs as potent broad-spectrum anti-influenza therapies.PNAS nexus · 2026Article
- MEK Inhibitors and Toll-like Receptor Signaling: Implications for Infection and Inflammation.International journal of molecular sciences · 2026Review
- A reversible broad-spectrum antiviral targets the human V-ATPase VResearch square · 2026Article
- Article
- Sorting Nexin 10 Mediates Endosomal Acidification and Autophagy to Promote Influenza A Virus Infection.Viruses · 2026Article
- Advancing influenza virus treatment:Materials today. Bio · 2025Article
- Metabolic Reprogramming in Respiratory Viral Infections: A Focus on SARS-CoV-2, Influenza, and Respiratory Syncytial Virus.Biomolecules · 2025Review
- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
- Monoclonal nanobodies alter the activity and assembly of the yeast vacuolar HbioRxiv : the preprint server for biology · 2025Article
- Intersection of inflammation and viral replication: the central role of MAPK signaling in viral respiratory infections.Frontiers in microbiology · 2025Review
- Human V-ATPase function is positively and negatively regulated by TLDc proteins.Structure (London, England : 1993) · 2024Article
- Repurposing Anticancer Drugs Targeting the MAPK/ERK Signaling Pathway for the Treatment of Respiratory Virus Infections.International journal of molecular sciences · 2024Review
- Reduced vacuolar ATPase protects mice from Friend virus infection - an unintended but instructive effect in Hif-2afl mice.Journal of cell science · 2024Article
- Molecular mechanism of Oxr1p mediated disassembly of yeast V-ATPase.EMBO reports · 2024Article
- Unveiling the role of host kinases at different steps of influenza A virus life cycle.Journal of virology · 2024Review
- The Roles of Endocytosis and Autophagy at the Cellular Level During Influenza Virus Infection: A Mini-Review.Infection and drug resistance · 2024Review
- Tender love and disassembly: How a TLDc domain protein breaks the V-ATPase.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- Article
- MEK inhibitors as novel host-targeted antivirals with a dual-benefit mode of action against hyperinflammatory respiratory viral diseases.Current opinion in virology · 2023Review
- β-arrestins and G protein-coupled receptor kinases in viral entry: A graphical review.Cellular signalling · 2023Review
19 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The vacuolar (H+)-ATPases (V-ATPases) facilitate the release of influenza A virus (IAV) genome into the cytoplasm by acidifying the endosomal interior. The regulation of V-ATPases by signalling pathways has been demonstrated in various model systems. However, little is known about signalling-regulated V-ATPase activation during IAV infection. Here we show that V-ATPase activity is elevated during infection of cell monolayers with IAV, as measured by intracellular pH change, via a mechanism mediated by extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI3K). Inhibition of IAV-induced early activation of these kinases reduced V-ATPase activity and the acidification of intracellular compartments in infected cells. IAV-activated ERK and PI3K appear to interact directly, and they colocalize with the E subunit of V-ATPase V1 domain. Further, siRNAs targeting the E2 subunit isoform significantly reduced virus titres. Interestingly, suppression of PI3K early activation, but not that of ERK or V-ATPase, negatively affected virus internalization, suggesting the involvement of the pathway in earlier, V-ATPase-independent infection-promoting events. Cell treatment with a V-ATPase-specific inhibitor impaired the nuclear localization of incoming viral ribonucleoproteins, inhibiting replication/transcription of viral RNAs. These findings highlight the importance of IAV-induced ERK and PI3K early activation as signalling mediators in V-ATPase-stimulated endosomal acidification required for fusion.
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Registered trials
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