ArticleProceedings of the National Academy of Sciences of the United States of America2009
ICP0 enables and monitors the function of D cyclins in herpes simplex virus 1 infected cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. 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, 25 citations in OpenAlex.
- The Host Cell Factor Phosphatase-2A Subunit PR130 Restricts Replication of Herpes Simplex Virus Type-1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- HSV-1 virions and related particles: biogenesis and implications in the infection.Journal of virology · 2025Review
- In Vitro Effect of 9,9'-Norharmane Dimer against Herpes Simplex Viruses.International journal of molecular sciences · 2024Article
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 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
- Human DNA Virus Exploitation of the MAPK-ERK Cascade.International journal of molecular sciences · 2019Review
- Discovery of Small-Molecule Inhibitors Targeting the E3 Ubiquitin Ligase Activity of the Herpes Simplex Virus 1 ICP0 Protein Using anJournal of virology · 2019Article
- Article
- The ERK-1 function is required for HSV-1-mediated G1/S progression in HEP-2 cells and contributes to virus growth.Scientific reports · 2017Article
- 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
- Infected cell protein 0 functional domains and their coordination in herpes simplex virus replication.World journal of virology · 2016Review
- Cellular Transcriptional Coactivator RanBP10 and Herpes Simplex Virus 1 ICP0 Interact and Synergistically Promote Viral Gene Expression and Replication.Journal of virology · 2016Article
- Combining HDAC inhibitors with oncolytic virotherapy for cancer therapy.Oncolytic virotherapy · 2015Review
- Novel roles of cytoplasmic ICP0: proteasome-independent functions of the RING finger are required to block interferon-stimulated gene production but not to promote viral replication.Journal of virology · 2014Article
- hTERT extends the life of human fibroblasts without compromising type I interferon signaling.PloS one · 2013Article
- Overexpression of the ubiquitin-specific protease 7 resulting from transfection or mutations in the ICP0 binding site accelerates rather than depresses herpes simplex virus 1 gene expression.Journal of virology · 2012Article
- The checkpoints of viral gene expression in productive and latent infection: the role of the HDAC/CoREST/LSD1/REST repressor complex.Journal of virology · 2011Review
- Virus reactivation: a panoramic view in human infections.Future virology · 2011Article
- Circadian CLOCK histone acetyl transferase localizes at ND10 nuclear bodies and enables herpes simplex virus gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The herpes simplex virus 1 ICP0 is a regulatory protein. Early in infection ICP0 localizes in ND10 bodies and performs two functions: As an E3 ligase in conjunction with E2 UbcH5a conjugating enzyme, it degrades the ND10 components PML and SP100. Concurrently, it suppresses the silencing of viral DNA by dispersing the HDAC1/CoREST/REST/LSD1 repressor complex. Subsequently, ICP0 is exported to the cytoplasm. In cells treated with HDAC inhibitors or transfected with irrelevant DNA, the export is delayed in a DNA dose-dependent fashion. Here, we follow up an observation that ICP0 binds cyclin D3 and that ICP0 mutants unable to bind cyclin D3 are not exported. Moreover, in infected cells cdk4 is activated, but cdk2 is not. We report that (i) cyclin D1, D2, or D3 colocalize with ND10 bodies and ICP0 early in infection and ultimately become incorporated into viral replication compartments, (ii) each of the D cyclins partially rescues DeltaICP0 mutants, and (iii) inhibition of cdk4 by inhibitor I sequesters ICP0 in the nucleus. A key finding is that overexpression of cyclin D3 enables the transport of ICP0 to the cytoplasm. We conclude that (i) ICP0 facilitates the recruitment of cyclin D3 to the sites of viral DNA synthesis, (ii) until its functions are completed, ICP0 is retained in the nucleus, and (iii) a common signal that results in the export of ICP0 to the cytoplasm is the accumulation of a viral DNA-synthesis-dependent late protein.
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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.