ArticleProceedings of the National Academy of Sciences of the United States of America2006
ICP0 and the US3 protein kinase of herpes simplex virus 1 independently block histone deacetylation to enable gene expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. 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, 123 citations in OpenAlex.
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
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- Impaired endocytosis and accumulation in early endosomal compartments defines herpes simplex virus-mediated disruption of the nonclassical MHC class I-related molecule MR1.The Journal of biological chemistry · 2024Article
- The therapeutic implications of all-in-one AAV-delivered epigenome-editing platform in neurodegenerative disorders.Nature communications · 2024Article
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- Regulation of alphaherpesvirus protein via post-translational phosphorylation.Veterinary research · 2022Review
- A DeacetylaseViruses · 2022Article
- Two lymphoid cell lines potently silence unintegrated HIV-1 DNAs.Retrovirology · 2022Article
- CHAF1A/B mediate silencing of unintegrated HIV-1 DNAs early in infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Therapeutic modulation of gene expression in the disease state: Treatment strategies and approaches for the development of next-generation of the epigenetic drugs.Frontiers in bioengineering and biotechnology · 2022Review
- Regulation of Krüppel-Like Factor 15 Expression by Herpes Simplex Virus Type 1 or Bovine Herpesvirus 1 Productive Infection.Viruses · 2021Article
- Marek's disease virus US3 protein kinase phosphorylates chicken HDAC 1 and 2 and regulates viral replication and pathogenesis.PLoS pathogens · 2021Article
- Host Innate Immune Response and Viral Immune Evasion During Alphaherpesvirus Infection.Current issues in molecular biology · 2021Review
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- An Unbiased Approach to Mapping the Signaling Network of the Pseudorabies Virus US3 Protein.Pathogens (Basel, Switzerland) · 2020Article
- Roles of the Different Isoforms of the Pseudorabies Virus Protein Kinase pUS3 in Nuclear Egress.Journal of virology · 2020Article
- Chromatin dynamics and the transcriptional competence of HSV-1 genomes during lytic infections.PLoS pathogens · 2019Article
- Bclaf1 critically regulates the type I interferon response and is degraded by alphaherpesvirus US3.PLoS pathogens · 2019Article
- HSV-1 tegument protein and the development of its genome editing technology.Virology journal · 2016Review
- Characterization of a Herpes Simplex Virus 1 (HSV-1) Chimera in Which the Us3 Protein Kinase Gene Is Replaced with the HSV-2 Us3 Gene.Journal of virology · 2016Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
SK-N-SH cells exposed to low ratios of ICP0-null (DeltaICP0) mutants of herpes simplex virus per cell express the viral alpha proteins, but the progression to beta and gamma gene expression does not ensue. In these restrictive cells, post-alpha gene expression can be induced after exposure of the infected cells to sodium butyrate, an indication that VP16 brought into cells by the virus and the alpha gene products made after infection cannot block the silencing of viral post-alpha genes by histone deacetylases (HDACs). This observation is consistent with evidence reported earlier that ICP0 dissociates HDAC1/2 from the CoREST/REST complex. In permissive U2OS cells, replication is independent of the ratio of DeltaICP0 mutant per cell. To determine whether other viral genes are involved in blocking HDACs, we used a surrogate system consisting of baculoviruses carrying viral or cellular genes driven by CMV immediate-early promoter. Expression of these genes requires blocking of histone deacetylation. We report that (i) cotransduced U(S)3 or U(S)3.5 protein kinase substitutes for sodium butyrate in enabling the expression of a reporter gene in restrictive cells and enhancing it in permissive cells; (ii) HDAC1 is phosphorylated concomitant with the expression of reporter genes; and (iii) the amounts and appearance of HDAC1 are altered in transduced cells expressing U(S)3 protein kinase in the absence of other viral proteins. We conclude that the U(S)3 protein kinase blocks histone deacetylation by a mechanism distinct from that of ICP0 and that debilitated histone deacetylation contributes to the permissiveness of U2OS cells for DeltaICP0 mutants.
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