ArticleProceedings of the National Academy of Sciences of the United States of America2010
Circadian CLOCK histone acetyl transferase localizes at ND10 nuclear bodies and enables herpes simplex virus gene expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 88 citations in OpenAlex.
- Timing of immune checkpoint inhibitors infusion and prognosis in recurrent/metastatic nasopharyngeal carcinoma: a single-center, retrospective study.Cancer immunology, immunotherapy : CII · 2026Article
- Chronobiology of neurotropic viruses: rhythmic viral entry and arrhythmic host clocks.Cell discovery · 2026Article
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- HSV-1 virions and related particles: biogenesis and implications in the infection.Journal of virology · 2025Review
- Time to start taking time seriously: how to investigate unexpected biological rhythms within infectious disease research.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Alterations in Circadian Rhythms, Sleep, and Physical Activity in COVID-19: Mechanisms, Interventions, and Lessons for the Future.Molecular neurobiology · 2024Review
- Crosstalk between circadian clocks and pathogen niche.PLoS pathogens · 2024Review
- Chikungunya Virus, Metabolism, and Circadian Rhythmicity Interplay in Phagocytic Cells.Metabolites · 2023Review
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- A CRISPR-based rapid DNA repositioning strategy and the early intranuclear life of HSV-1.eLife · 2023Article
- SARS-CoV-2 Harnesses Host Translational Shutoff and Autophagy To Optimize Virus Yields: the Role of the Envelope (E) Protein.Microbiology spectrum · 2023Article
- When the clock ticks wrong with COVID-19.Clinical and translational medicine · 2022Review
- The role of circadian clock pathways in viral replication.Seminars in immunopathology · 2022Review
- Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy.Antiviral research · 2021Review
- The Circadian Clock and Viral Infections.Journal of biological rhythms · 2021Review
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- Circadian control of interferon-sensitive gene expression in murine skin.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- For Whom the Clock Ticks: Clinical Chronobiology for Infectious Diseases.Frontiers in immunology · 2020Review
- The ICP0 Protein of Herpes Simplex Virus 1 (HSV-1) Downregulates Major Autophagy Adaptor Proteins Sequestosome 1 and Optineurin during the Early Stages of HSV-1 Infection.Journal of virology · 2019Article
- Discovery of Small-Molecule Inhibitors Targeting the E3 Ubiquitin Ligase Activity of the Herpes Simplex Virus 1 ICP0 Protein Using anJournal of virology · 2019Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Expression of herpes simplex virus genes at the initiation of replication involves two steps that take place at ND10 nuclear bodies. These are suppression of cellular repressors that attempt to silence viral DNA and remodeling of the viral chromatin to make it accessible for transcription. In earlier studies we reported on the mechanism by which viral proteins ICP0 and U(S)3 protein kinase modify and disrupt the HDAC1/CoREST/REST/LSD1 repressor complex. The remodeling step requires in addition acetylation of histones bound to DNA. In an attempt to identify the enzyme, we took note of the observation that ICP0 physically and functionally interacts with Bmal1, a partner of the CLOCK histone acetyl transferase, and key members of the bHLH-PAS family of transcriptional factors. The Bmal11 and CLOCK heterodimer is best known as a regulator of the circadian oscillation in the mammalian CLOCK system. In this article we report the following: (i) in infected cells both Bmal1 and CLOCK localize at ND10 bodies; (ii) wild-type virus stabilizes the CLOCK protein; (iii) overexpression of CLOCK partially compensates for the absence of ICP0 and enables higher yields in cells infected with a ΔICP0 mutant and this activity is not expressed by CLOCK mutants lacking histone acetyl transferase activity; and (iv) depletion of CLOCK in cells infected with wild-type virus results in significant decrease in the expression of all viral proteins tested. We conclude that ICP0 interacts with Bmal1 and by extension with CLOCK histone acetyl transferase to remodel viral chromatin.
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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.