ArticleJournal of virology2008
Translocation and colocalization of ICP4 and ICP0 in cells infected with herpes simplex virus 1 mutants lacking glycoprotein E, glycoprotein I, or the virion host shutoff product of the UL41 gene.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Interactome and Ubiquitinome Analyses Identify Functional Targets of Herpes Simplex Virus 1 Infected Cell Protein 0.Frontiers in microbiology · 2022Article
- Diverse Populations of Extracellular Vesicles with Opposite Functions during Herpes Simplex Virus 1 Infection.Journal of virology · 2021Article
- Biogenesis of Extracellular Vesicles during Herpes Simplex Virus 1 Infection: Role of the CD63 Tetraspanin.Journal of virology · 2019Article
- Molecular characterization of the duck enteritis virus US10 protein.Virology journal · 2017Article
- Analysis of the early steps of herpes simplex virus 1 capsid tegumentation.Journal of virology · 2013Article
- Interwoven roles of cyclin D3 and cdk4 recruited by ICP0 and ICP4 in the expression of herpes simplex virus genes.Journal of virology · 2010Article
- Role of herpes simplex virus ICP0 in the transactivation of genes introduced by infection or transfection: a reappraisal.Journal of virology · 2010Article
- Cellular localization of the herpes simplex virus ICP0 protein dictates its ability to block IRF3-mediated innate immune responses.PloS one · 2010Article
- Article
- ICP0 enables and monitors the function of D cyclins in herpes simplex virus 1 infected cells.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Host responses to wild-type and attenuated herpes simplex virus infection in the absence of Stat1.Journal of virology · 2009Article
- Nuclear retention of ICP0 in cells exposed to HDAC inhibitor or transfected with DNA before infection with herpes simplex virus 1.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Comprehensive characterization of extracellular herpes simplex virus type 1 virions.Journal of virology · 2008Article
- Herpes simplex virus virion host shutoff attenuates establishment of the antiviral state.Journal of virology · 2008Article
- Enhanced pathogenesis of an attenuated herpes simplex virus for mice lacking Stat1.Journal of virology · 2008Article
- Expression of gamma interferon-dependent genes is blocked independently by virion host shutoff RNase and by US3 protein kinase.Journal of virology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In wild-type herpes simplex virus 1-infected cells, the major regulatory protein ICP4 resides in the nucleus whereas ICP0 becomes dynamically associated with proteasomes and late in infection is translocated and dispersed in the cytoplasm. Inhibition of proteasomal function results in retention or transport of ICP0 to the nucleus. We report that in cells infected with mutants lacking glycoprotein E (gE), glycoprotein I (gI), or the product of the U(L)41 gene, both ICP4 and ICP0 are translocated to the cytoplasm and coaggregate in small dense structures that, in the presence of proteasomal inhibitor MG132, also contain proteasomal components. Gold particle-conjugated antibody to ICP0 reacted in thin sections with dense protein aggregates in the cytoplasm of mutant virus-infected cells. Similar aggregates were present in the nuclei but not in the cytoplasm of wild-type virus-infected cells. Exposure of cells early in infection to MG132 does not result in retention of ICP0 as in wild-type virus-infected cells. The results suggest that the retention of ICP4 and ICP0 in the nucleus is a dynamic process that involves the function of other viral proteins that may include the Fc receptor formed by the gE/gI complex and is not merely the consequence of expression of a nuclear localization signal. It is noteworthy that in DeltaU(L)41-infected cells gE is retained in the trans-Golgi network and is not widely dispersed in cellular membranes.
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