ArticleInternational journal of molecular sciences2017
Tubacin, an HDAC6 Selective Inhibitor, Reduces the Replication of the Japanese Encephalitis Virus via the Decrease of Viral RNA Synthesis.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- The evolution of heat shock protein 90 C-terminal inhibitors: From novobiocin to potential clinical candidates.Cell stress & chaperones · 2026Review
- Spatial transcriptomics uncovers vasculature-centered cellular interactions driving Japanese encephalitis progression in a mouse model.Nature communications · 2026Article
- Article
- Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- SARS-CoV-2 nucleocapsid protein promotes self-deacetylation by inducing HDAC6 to facilitate viral replication.Virology journal · 2024Article
- Dual molecule targeting HDAC6 leads to intratumoral CD4+ cytotoxic lymphocytes recruitment through MHC-II upregulation on lung cancer cells.Journal for immunotherapy of cancer · 2024Article
- Review
- Review
- Review
- Male histone deacetylase 6 (HDAC6) knockout mice have enhanced ventilatory responses to hypoxic challenge.Frontiers in physiology · 2023Article
- Histone deacetylase 6's function in viral infection, innate immunity, and disease: latest advances.Frontiers in immunology · 2023Review
- Antiviral drug research for Japanese encephalitis: an updated review.Pharmacological reports : PR · 2022Review
- Posttranslational modification and beyond: interplay between histone deacetylase 6 and heat-shock protein 90.Molecular medicine (Cambridge, Mass.) · 2021Review
- Improved HDAC Inhibition, Stronger Cytotoxic Effect and Higher Selectivity against Leukemias and Lymphomas of Novel, Tricyclic Vorinostat Analogues.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Application of multiple omics and network projection analyses to drug repositioning for pathogenic mosquito-borne viruses.Scientific reports · 2021Article
- Role of Host-Mediated Post-Translational Modifications (PTMs) in RNA Virus Pathogenesis.International journal of molecular sciences · 2020Review
- Host-Directed Antiviral Therapy.Clinical microbiology reviews · 2020Review
- Flavivirus Nonstructural Protein NS5 Dysregulates HSP90 to Broadly Inhibit JAK/STAT Signaling.Cells · 2020Article
- Article
- The Role of HDAC6 in TDP-43-Induced Neurotoxicity and UPS Impairment.Frontiers in cell and developmental biology · 2020Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Japanese encephalitis virus (JEV), a neurotropic flavivirus, annually causes over 30,000 Japanese Encephalitis (JE) cases in East and Southeast Asia. Histone deacetylases (HDACs) modulate lysine acetylation of histones and non-histone proteins, regulating many processes including inflammation and antiviral immune response. This study investigated antiviral activity of pan- and selective-HDAC inhibitors as host-targeting agents against JEV. Among HDAC inhibitors, selective HDAC6 inhibitors (tubastatin-A (TBSA) and tubacin) concentration-dependently inhibited JEV-induced cytopathic effect and apoptosis, as well as reduced virus yield in human cerebellar medulloblastoma cells. The 50% inhibitory concentration (IC50) values of virus yield was 0.26 μM for tubacin and 1.75 μM for TBSA, respectively. Tubacin (IC50 of 1.52 μM), but not TBSA, meaningfully blocked the production of intracellular infectious virus particles. In time-of-addition assays, the greatest potency of antiviral activity was observed in the mode of pre-treatment with tubacin (IC50 of 1.89 μM) compared to simultaneous (IC50 of 4.88 μM) and post-treatment (IC50 of 2.05 μM) modes. Interestingly, tubacin induced the hyperacetylation of a HDAC6 substrate Hsp90 and reduced the interaction of Hsp90 with JEV NS5 protein. Novobiocin, an Hsp90 inhibitor, diminished the NS5 protein amount and virus replication in JEV-infected cells. Meantime, tubacin suppressed the NS5 expression and antisense RNA genome synthesis in infected cells. Tubacin-induced Hsp90 hyperacetylation was suggested to influence the NS5 activity in JEV replication. Therefore, tubacin had a high potential of a host-targeting agent against JEV, exhibiting preventive and therapeutic activities against JEV infection.
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