ArticleVirology journal2007
Repressor element-1 silencing transcription factor/neuronal restrictive silencer factor (REST/NRSF) can regulate HSV-1 immediate-early transcription via histone modification.
Article in Virology journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- REST Is Restless in Neuronal and Non-Neuronal Virus Infections: An In Silico Analysis-Based Perspective.Viruses · 2025Review
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- Establishing a Herpesvirus Quiescent Infection in Differentiated Human Dorsal Root Ganglion Neuronal Cell Line Mediated by Micro-RNA Overexpression.Pathogens (Basel, Switzerland) · 2022Article
- Single AAV-Mediated CRISPR-SaCas9 Inhibits HSV-1 Replication by Editing ICP4 in Trigeminal Ganglion Neurons.Molecular therapy. Methods & clinical development · 2020Article
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- Serine/Arginine-rich Splicing Factor 2 Modulates Herpes Simplex Virus Type 1 Replication via Regulating Viral Gene Transcriptional Activity and Pre-mRNA Splicing.The Journal of biological chemistry · 2016Article
- Overexpression of thyroid hormone receptor β1 altered thyroid hormone-mediated regulation of herpes simplex virus-1 replication in differentiated cells.Journal of neurovirology · 2016Article
- KDM1 class flavin-dependent protein lysine demethylases.Biopolymers · 2015Review
- Molecular characterization of Brazilian equid herpesvirus type 1 strains based on neuropathogenicity markers.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2015Article
- Combining HDAC inhibitors with oncolytic virotherapy for cancer therapy.Oncolytic virotherapy · 2015Review
- Review
- A Novel Thyroid Hormone Mediated Regulation of HSV-1 Gene Expression and Replication is Specific to Neuronal Cells and Associated with Disruption of Chromatin Condensation.SOJ pharmacy & pharmaceutical sciences · 2014Article
- Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.PLoS pathogens · 2012Article
- The roles of viruses in brain tumor initiation and oncomodulation.Journal of neuro-oncology · 2011Review
- A5-positive primary sensory neurons are nonpermissive for productive infection with herpes simplex virus 1 in vitro.Journal of virology · 2011Article
- Zmynd15 encodes a histone deacetylase-dependent transcriptional repressor essential for spermiogenesis and male fertility.The Journal of biological chemistry · 2010Article
- Thyroid hormone controls the gene expression of HSV-1 LAT and ICP0 in neuronal cells.Cell research · 2010Article
- Regulation of herpes simplex virus type 1 thymidine kinase gene expression by thyroid hormone receptor in cultured neuronal cells.Journal of neurovirology · 2010Article
- Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.Journal of virology · 2009Article
- Chromatin organization and virus gene expression.Journal of cellular physiology · 2008Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDuring primary infection of its human host, Herpes Simplex Virus Type-1 (HSV-1) establishes latency in neurons where the viral genome is maintained in a circular form associated with nucleosomes in a chromatin configration. During latency, most viral genes are silenced, although the molecular mechanisms responsible for this are unclear. We hypothesized that neuronal factors repress HSV-1 gene expression during latency. A search of the HSV-1 DNA sequence for potential regulatory elements identified a Repressor Element-1/Neuronal Restrictive Silencer Element (RE-1/NRSE) located between HSV-1 genes ICP22 and ICP4. We predicted that the Repressor Element Silencing Transcription Factor/Neuronal Restrictive Silencer Factor (REST/NRSF) regulates expression of ICP22 and ICP4.
resultsTransient cotransfection indicated that REST/NRSF inhibited the activity of both promoters. In contrast, cotransfection of a mutant form of REST/NRSF encoding only the DNA-binding domain of the protein resulted in less inhibition. Stably transformed cell lines containing episomal reporter plasmids with a chromatin structure showed that REST/NRSF specifically inhibited the ICP4 promoter, but not the ICP22 promoter. REST/NRSF inhibition of the ICP4 promoter was reversed by histone deacetylase (HDAC) inhibitor Trichostatin A (TSA). Additionally, chromatin immuno-precipitation (ChIP) assays indicated that the corepressor CoREST was recruited to the proximity of ICP4 promoter and that acetylation of histone H4 was reduced in the presence of REST/NRSF.
conclusionSince the ICP4 protein is a key transactivator of HSV-1 lytic cycle genes, these results suggest that REST/NRSF may have an important role in the establishment and/or maintenance of HSV-1 gene silencing during latency by targeting ICP4 expression.
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