Herpes simplex virus type 1 ICP0 regulates expression of immediate-early, early, and late genes in productively infected cells.
about
Functional interaction between class II histone deacetylases and ICP0 of herpes simplex virus type 1Association of herpes simplex virus type 1 ICP8 and ICP27 proteins with cellular RNA polymerase II holoenzymeFormation 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 complexesVaricella-zoster virus open reading frame 61 protein is functionally homologous to herpes simplex virus type 1 ICP0Varicella-zoster virus (VZV) open reading frame 61 protein transactivates VZV gene promoters and enhances the infectivity of VZV DNAHerpes 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 genomesThe role of the CoREST/REST repressor complex in herpes simplex virus 1 productive infection and in latencyThe molecular basis of herpes simplex virus latencyThe potential link between PML NBs and ICP0 in regulating lytic and latent infection of HSV-1A viral E3 ligase targets RNF8 and RNF168 to control histone ubiquitination and DNA damage responsesHSV-1 ICP0: paving the way for viral replicationChk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growthCharacterization of an antisense transcript spanning the UL81-82 locus of human cytomegalovirus.Role of chromatin during herpesvirus infections.Cellular localization of the herpes simplex virus ICP0 protein dictates its ability to block IRF3-mediated innate immune responsesHerpes simplex virus tegument ICP0 is capsid associated, and its E3 ubiquitin ligase domain is important for incorporation into virions.Herpes simplex virus VP16, but not ICP0, is required to reduce histone occupancy and enhance histone acetylation on viral genomes in U2OS osteosarcoma cells.Regulated expression of a Sindbis virus replicon by herpesvirus promoters.Changes to euchromatin on LAT and ICP4 following reactivation are more prevalent in an efficiently reactivating strain of HSV-1.Persistence and expression of the herpes simplex virus genome in the absence of immediate-early proteins.Purification and characterization of a cellular protein that binds to the downstream activation sequence of the strict late UL38 promoter of herpes simplex virus type 1Optimized viral dose and transient immunosuppression enable herpes simplex virus ICP0-null mutants To establish wild-type levels of latency in vivo.Perturbation of cell cycle progression and cellular gene expression as a function of herpes simplex virus ICP0.Truncation of the C-terminal acidic transcriptional activation domain of herpes simplex virus VP16 renders expression of the immediate-early genes almost entirely dependent on ICP0Open reading frame S/L of varicella-zoster virus encodes a cytoplasmic protein expressed in infected cellsICP0 is required for efficient reactivation of herpes simplex virus type 1 from neuronal latency.ICP0, ICP4, or VP16 expressed from adenovirus vectors induces reactivation of latent herpes simplex virus type 1 in primary cultures of latently infected trigeminal ganglion cells.HSV-1 ICP0: An E3 Ubiquitin Ligase That Counteracts Host Intrinsic and Innate ImmunityAntagonistic determinants controlling replicative and latent states of human cytomegalovirus infectionGamma interferon can block herpes simplex virus type 1 reactivation from latency, even in the presence of late gene expressionMultimerization of ICP0, a herpes simplex virus immediate-early protein.The intrinsic antiviral defense to incoming HSV-1 genomes includes specific DNA repair proteins and is counteracted by the viral protein ICP0.A neuron-specific host microRNA targets herpes simplex virus-1 ICP0 expression and promotes latency.Interwoven roles of cyclin D3 and cdk4 recruited by ICP0 and ICP4 in the expression of herpes simplex virus genesThe cyclin-dependent kinase inhibitor roscovitine inhibits the transactivating activity and alters the posttranslational modification of herpes simplex virus type 1 ICP0.Neither LAT nor open reading frame P mutations increase expression of spliced or intron-containing ICP0 transcripts in mouse ganglia latently infected with herpes simplex virusThe neuronal host cell factor-binding protein Zhangfei inhibits herpes simplex virus replication.cGAS-mediated stabilization of IFI16 promotes innate signaling during herpes simplex virus infection.The CoREST/REST repressor is both necessary and inimical for expression of herpes simplex virus genes.
P2860
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P2860
Herpes simplex virus type 1 ICP0 regulates expression of immediate-early, early, and late genes in productively infected cells.
description
1992 nî lūn-bûn
@nan
1992年の論文
@ja
1992年論文
@yue
1992年論文
@zh-hant
1992年論文
@zh-hk
1992年論文
@zh-mo
1992年論文
@zh-tw
1992年论文
@wuu
1992年论文
@zh
1992年论文
@zh-cn
name
Herpes simplex virus type 1 IC ...... n productively infected cells.
@en
type
label
Herpes simplex virus type 1 IC ...... n productively infected cells.
@en
prefLabel
Herpes simplex virus type 1 IC ...... n productively infected cells.
@en
P2860
P1433
P1476
Herpes simplex virus type 1 IC ...... n productively infected cells.
@en
P2093
P2860
P304
P407
P577
1992-05-01T00:00:00Z