Phenotype of a herpes simplex virus type 1 mutant that fails to express immediate-early regulatory protein ICP0.
about
ICP0 dismantles microtubule networks in herpes simplex virus-infected cellsICP0 antagonizes ICP4-dependent silencing of the herpes simplex virus ICP0 genePML contributes to a cellular mechanism of repression of herpes simplex virus type 1 infection that is inactivated by ICP0Formation of nuclear foci of the herpes simplex virus type 1 regulatory protein ICP4 at early times of infection: localization, dynamics, recruitment of ICP27, and evidence for the de novo induction of ND10-like complexesHerpes simplex virus type 1 mediates fusion through a hemifusion intermediate by sequential activity of glycoproteins D, H, L, and BFunctional inaccessibility of quiescent herpes simplex virus genomesHerpes simplex virus type 1 latency and reactivation: an updateThe molecular basis of herpes simplex virus latencyThe potential link between PML NBs and ICP0 in regulating lytic and latent infection of HSV-1Dynamic Response of IFI16 and Promyelocytic Leukemia Nuclear Body Components to Herpes Simplex Virus 1 InfectionA viral E3 ligase targets RNF8 and RNF168 to control histone ubiquitination and DNA damage responsesA RING finger ubiquitin ligase is protected from autocatalyzed ubiquitination and degradation by binding to ubiquitin-specific protease USP7A viral ubiquitin ligase has substrate preferential SUMO targeted ubiquitin ligase activity that counteracts intrinsic antiviral defenceCrystal Structure of USP7 Ubiquitin-like Domains with an ICP0 Peptide Reveals a Novel Mechanism Used by Viral and Cellular Proteins to Target USP7ND10 components relocate to sites associated with herpes simplex virus type 1 nucleoprotein complexes during virus infection.Visualization by live-cell microscopy of disruption of ND10 during herpes simplex virus type 1 infection.Herpes simplex virus VP16, but not ICP0, is required to reduce histone occupancy and enhance histone acetylation on viral genomes in U2OS osteosarcoma cells.Elimination of ie1 significantly attenuates murine cytomegalovirus virulence but does not alter replicative capacity in cell cultureDeletion of the herpes simplex virus VP22-encoding gene (UL49) alters the expression, localization, and virion incorporation of ICP0.Gamma interferon can block herpes simplex virus type 1 reactivation from latency, even in the presence of late gene expressionThe intrinsic antiviral defense to incoming HSV-1 genomes includes specific DNA repair proteins and is counteracted by the viral protein ICP0.Disruption of HDAC/CoREST/REST repressor by dnREST reduces genome silencing and increases virulence of herpes simplex virusNuclear IFI16 induction of IRF-3 signaling during herpesviral infection and degradation of IFI16 by the viral ICP0 proteinNuclear interferon-inducible protein 16 promotes silencing of herpesviral and transfected DNA.HSV-1 genome subnuclear positioning and associations with host-cell PML-NBs and centromeres regulate LAT locus transcription during latency in neurons.Functional reorganization of promyelocytic leukemia nuclear bodies during BK virus infection.Cellular stress rather than stage of the cell cycle enhances the replication and plating efficiencies of herpes simplex virus type 1 ICP0- virusesICP0 and the US3 protein kinase of herpes simplex virus 1 independently block histone deacetylation to enable gene expression.Herpes simplex virus ICP0 promotes both histone removal and acetylation on viral DNA during lytic infection.Upregulation of mouse genes in HSV-1 latent TG after butyrate treatment implicates the multiple roles of the LAT-ICP0 locus.ICP22 is required for wild-type composition and infectivity of herpes simplex virus type 1 virions.Herpes simplex virus immediate-early protein ICP0 is targeted by SIAH-1 for proteasomal degradation.Identification of nuclear and nucleolar localization signals of pseudorabies virus (PRV) early protein UL54 reveals that its nuclear targeting is required for efficient production of PRV.L Particles Transmit Viral Proteins from Herpes Simplex Virus 1-Infected Mature Dendritic Cells to Uninfected Bystander Cells, Inducing CD83 DownmodulationGene Expression Correlates with the Number of Herpes Viral Genomes Initiating Infection in Single Cells.Interactions between DNA viruses, ND10 and the DNA damage response.Characterization of mre11 loss following HSV-1 infection.The control of viral infection by tripartite motif proteins and cyclophilin A.HSV-1 amplicon vectors: a promising and versatile tool for gene delivery.Herpes simplex virus downregulates secretory leukocyte protease inhibitor: a novel immune evasion mechanism
P2860
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P2860
Phenotype of a herpes simplex virus type 1 mutant that fails to express immediate-early regulatory protein ICP0.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
2004年论文
@zh
2004年论文
@zh-cn
name
Phenotype of a herpes simplex ...... early regulatory protein ICP0.
@en
type
label
Phenotype of a herpes simplex ...... early regulatory protein ICP0.
@en
prefLabel
Phenotype of a herpes simplex ...... early regulatory protein ICP0.
@en
P2860
P1433
P1476
Phenotype of a herpes simplex ...... early regulatory protein ICP0.
@en
P2093
Roger D Everett
P2860
P304
P356
10.1128/JVI.78.4.1763-1774.2004
P407
P577
2004-02-01T00:00:00Z