ArticleJournal of virology2019
HDAC6 Restricts Influenza A Virus by Deacetylation of the RNA Polymerase PA Subunit.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Glycolytic enzyme PGK1 restricts viral replication via a glycolysis-independent mechanism.Science China. Life sciences · 2026Article
- Evolutionary Rate Variation at Predicted PTM Sites Reveals Localized Host-Associated Patterns in Influenza A Virus.Genome biology and evolution · 2026Article
- Acetylation-mediated regulation of ALV viral proteins: Implications for retroviral inhibition.PLoS pathogens · 2026Article
- The Avian Influenza Virus PA Protein Recruits Host RPS27A to Support Viral Replication.Viruses · 2026Article
- Proteomics-Based Trapping to Study Substrates of Histone Deacetylase 6 Catalytic Domain 1.Biochemistry · 2025Article
- Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Restriction of influenza A virus replication by host DCAF7-CRL4B axis.Journal of virology · 2025Article
- CRTC3 restricts SARS-CoV-2 replication and is antagonized by CREB.Virologica Sinica · 2025Article
- PROteolysis TArgeting Chimeras (PROTACs) and beyond: targeted degradation as a new path to fight microbial pathogens.FEMS microbiology reviews · 2025Review
- Article
- PA and PA-X: two key proteins from segment 3 of the influenza viruses.Frontiers in cellular and infection microbiology · 2025Review
- The Role of HDAC6 in Glioblastoma Multiforme: A New Avenue to Therapeutic Interventions?Biomedicines · 2024Review
- SARS-CoV-2 nucleocapsid protein promotes self-deacetylation by inducing HDAC6 to facilitate viral replication.Virology journal · 2024Article
- Triggering Degradation of Host Cellular Proteins for Robust Propagation of Influenza Viruses.International journal of molecular sciences · 2024Review
- Phosphorylation of PB2 at serine 181 restricts viral replication and virulence of the highly pathogenic H5N1 avian influenza virus in mice.Virologica Sinica · 2024Article
- Influenza Virus Host Restriction Factors: The ISGs and Non-ISGs.Pathogens (Basel, Switzerland) · 2024Review
- Review
- 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
- Histone deacetylase 6's function in viral infection, innate immunity, and disease: latest advances.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The life cycle of influenza A virus (IAV) is modulated by various cellular host factors. Although previous studies indicated that IAV infection is controlled by HDAC6, the deacetylase involved in the regulation of PA remained unknown. Here, we demonstrate that HDAC6 acts as a negative regulator of IAV infection by destabilizing PA. HDAC6 binds to and deacetylates PA, thereby promoting the proteasomal degradation of PA. Based on mass spectrometric analysis, Lys(664) of PA can be deacetylated by HDAC6, and the residue is crucial for PA protein stability. The deacetylase activity of HDAC6 is required for anti-IAV activity, because IAV infection was enhanced due to elevated IAV RNA polymerase activity upon HDAC6 depletion and an HDAC6 deacetylase dead mutant (HDAC6-DM; H216A, H611A). Finally, we also demonstrate that overexpression of HDAC6 suppresses IAV RNA polymerase activity, but HDAC6-DM does not. Taken together, our findings provide initial evidence that HDAC6 plays a negative role in IAV RNA polymerase activity by deacetylating PA and thus restricts IAV RNA transcription and replication.
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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.