ArticlePLoS pathogens2020
Phosphorylation controls RNA binding and transcription by the influenza virus polymerase.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Evolutionary Rate Variation at Predicted PTM Sites Reveals Localized Host-Associated Patterns in Influenza A Virus.Genome biology and evolution · 2026Article
- Epidemiological and Genomic Characterization of H5 Subtype Avian Influenza Viruses in Jining City, 2024-2025.Pathogens (Basel, Switzerland) · 2026Article
- The roles of post-translational modifications in the pathogenesis of RNA viruses: allies or adversaries?Frontiers in microbiology · 2026Review
- Host Protein Kinase C⍺: The novel Mitogen Activated Protein Kinase (MAPK) specific scaffold regulating nuclear export of influenza virus ribonucleoprotein complexes.PLoS pathogens · 2025Article
- The pathogenicity and multi-organ proteomic profiles of Mpox virus infection in SIVmac239-infected rhesus macaques.Nature communications · 2025Article
- IFIT3 RNA-binding activity promotes influenza A virus infection and translation efficiency.Journal of virology · 2025Article
- ANP32 proteins from ticks and vertebrates are key host factors for replication of Bourbon virus across species.Journal of virology · 2025Article
- Protein-S-nitrosylation of human cytomegalovirus pp65 reduces its ability to undermine cGAS.Journal of virology · 2025Article
- IFIT3 RNA-binding activity promotes influenza A virus infection and translation efficiency.bioRxiv : the preprint server for biology · 2025Article
- Influenza virus antagonizes self sensing by RIG-I to enhance viral replication.bioRxiv : the preprint server for biology · 2025Article
- Mutagenesis studies suggest a mechanism for influenza polymerase stalling during polyadenylation.Nucleic acids research · 2025Article
- Targeting Non-Eosinophilic Immunological Pathways in COPD and AECOPD: Current Insights and Therapeutic Strategies.International journal of chronic obstructive pulmonary disease · 2025Review
- CK1 and PP1 regulate Rift Valley fever virus genome replication through L protein phosphorylation.Antiviral research · 2024Article
- Phosphorylation of PB2 at serine 181 restricts viral replication and virulence of the highly pathogenic H5N1 avian influenza virus in mice.Virologica Sinica · 2024Article
- Unveiling the role of host kinases at different steps of influenza A virus life cycle.Journal of virology · 2024Review
- Article
- Pathogen-driven CRISPR screens identify TREX1 as a regulator of DNA self-sensing during influenza virus infection.Cell host & microbe · 2023Article
- p38MAPK- and GSK3-Mediated Phosphorylation of Snakehead Vesiculovirus Phosphoprotein at Threonine 160 Facilitates Viral Replication.Journal of virology · 2023Article
- Phosphorylation of the PA subunit of influenza polymerase at Y393 prevents binding of the 5'-termini of RNA and polymerase function.Scientific reports · 2023Article
- The ubiquitination landscape of the influenza A virus polymerase.Nature communications · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The influenza virus polymerase transcribes and replicates the viral genome. The proper timing and balance of polymerase activity is important for successful replication. Genome replication is controlled in part by phosphorylation of NP that regulates assembly of the replication machinery. However, it remains unclear whether phosphorylation directly regulated polymerase activity. Here we identified polymerase phosphosites that control its function. Mutating phosphosites in the catalytic subunit PB1 altered polymerase activity and virus replication. Biochemical analyses revealed phosphorylation events that disrupted global polymerase function by blocking the NTP entry channel or preventing RNA binding. We also identified a regulatory site that split polymerase function by specifically suppressing transcription. These experiments show that host kinases phospho-regulate viral RNA synthesis directly by modulating polymerase activity and indirectly by controlling assembly of replication machinery. Further, they suggest polymerase phosphorylation may bias replication versus transcription at discrete times or locations during the infectious cycle.
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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.