ArticleProceedings of the National Academy of Sciences of the United States of America2004
Herpes simplex virus infections are arrested in Oct-1-deficient cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Bovine Transcription Factor POU Class 2 Homeobox 1 (POU2F1/Oct1) Protein Promotes BoHV-1 Replication in MDBK Cells.Viruses · 2024Article
- Sp1 facilitates continued HSV-1 gene expression in the absence of key viral transactivators.mBio · 2024Article
- Neuronal miR-9 promotes HSV-1 epigenetic silencing and latency by repressing Oct-1 and Onecut family genes.Nature communications · 2024Article
- CRISPR activation as a platform to identify interferon stimulated genes with anti-viral function.Innate immunity · 2024Article
- GARP and EARP are required for efficient BoHV-1 replication as identified by a genome wide CRISPR knockout screen.PLoS pathogens · 2023Article
- HSV-1 selectively packs the transcription factor Oct-1 into EVs to facilitate its infection.Frontiers in microbiology · 2023Article
- Neuronal miR-138 Represses HSV-2 Lytic Infection by Regulating Viral and Host Genes with Mechanistic Differences from HSV-1.Journal of virology · 2022Article
- How an increase in the copy number of HSV-1 during latency can cause Alzheimer's disease: the viral and cellular dynamics according to the microcompetition model.Journal of neurovirology · 2021Article
- Regulation of host and virus genes by neuronal miR-138 favours herpes simplex virus 1 latency.Nature microbiology · 2021Article
- Novel transcription regulatory sequences and factors of the immune evasion protein ICP47 (US12) of herpes simplex viruses.Virology journal · 2020Article
- Identification of Putative UL54 (ICP27) Transcription Regulatory Sequences Binding to Oct-1, v-Myb, Pax-6 and Hairy in Herpes Simplex Viruses.Journal of Cancer · 2019Article
- Herpes Simplex Virus Establishment, Maintenance, and Reactivation: In Vitro Modeling of Latency.Pathogens (Basel, Switzerland) · 2017Review
- De Novo Herpes Simplex Virus VP16 Expression Gates a Dynamic Programmatic Transition and Sets the Latent/Lytic Balance during Acute Infection in Trigeminal Ganglia.PLoS pathogens · 2016Article
- Comparative Genomics of Herpesviridae Family to Look for Potential Signatures of Human Infecting Strains.International journal of genomics · 2016Article
- A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation.The Journal of general virology · 2015Review
- Octamer-binding transcription factors: genomics and functions.Frontiers in bioscience (Landmark edition) · 2013Review
- The dynamics of HCF-1 modulation of herpes simplex virus chromatin during initiation of infection.Viruses · 2013Review
- A locked nucleic acid clamp-mediated PCR assay for detection of a p53 codon 249 hotspot mutation in urine.The Journal of molecular diagnostics : JMD · 2011Article
- Tegument protein control of latent herpesvirus establishment and animation.Herpesviridae · 2011Article
- Involvement of p63 in the herpes simplex virus-1-induced demise of corneal cells.Journal of biomedical science · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Expression of the herpes simplex virus (HSV) immediate early (IE) genes is regulated by a multiprotein complex that is assembled on the TAATGARAT enhancer core element. The complex contains the cellular POU domain protein Oct-1, the viral transactivator VP16, and the cellular cofactor host cell factor 1. The current model suggests that the assembly depends on recognition of the core element by Oct-1. Here, HSV infection of Oct-1-deficient mouse embryonic fibroblast cells demonstrates that Oct-1 is critical for IE gene expression at low multiplicities of infection (moi). However, the protein is not essential for IE gene expression at high moi, indicating that VP16-mediated transcriptional induction through other IE regulatory elements is also important. This induction depends, at least in part, on the GA-binding protein binding elements that are present in each IE enhancer domain. Surprisingly, whereas the viral IE genes are expressed after high moi infection of Oct-1-deficient cells, the assembly of viral replication factories is severely impaired, revealing a second critical role for Oct-1 in HSV replication. The results have implications for both the HSV lytic and latency-reactivation cycles.
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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.