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.
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ICP0 dismantles microtubule networks in herpes simplex virus-infected cellsICP0 antagonizes ICP4-dependent silencing of the herpes simplex virus ICP0 geneExplant-induced reactivation of herpes simplex virus occurs in neurons expressing nuclear cdk2 and cdk4Targeted DNA mutagenesis for the cure of chronic viral infectionsBaculovirus-mediated promoter assay and transcriptional analysis of white spot syndrome virus orf427 gene.Functional inaccessibility of quiescent herpes simplex virus genomesThe 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 responsesImmune Escape via a Transient Gene Expression Program Enables Productive Replication of a Latent Pathogen.The herpes simplex virus-1 transactivator infected cell protein-4 drives VEGF-A dependent neovascularization.Role of chromatin during herpesvirus infections.Role of nuclear factor Y in stress-induced activation of the herpes simplex virus type 1 ICP0 promoterInterferon alpha induces establishment of alphaherpesvirus latency in sensory neurons in vitro.Changes to euchromatin on LAT and ICP4 following reactivation are more prevalent in an efficiently reactivating strain of HSV-1.Effects of simian virus 40 large and small tumor antigens on mammalian target of rapamycin signaling: small tumor antigen mediates hypophosphorylation of eIF4E-binding protein 1 late in infection.Green fluorescent protein is a quantitative reporter of gene expression in individual eukaryotic cells.Current knowledge of MicroRNAs and noncoding RNAs in virus-infected cells.Herpes simplex virus type 1 origins of DNA replication play no role in the regulation of flanking promoters.Alpha/Beta interferon and gamma interferon synergize to inhibit the replication of herpes simplex virus type 1.Experimental human cytomegalovirus latency in CD14+ monocytes.ICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAsICP0 antagonizes Stat 1-dependent repression of herpes simplex virus: implications for the regulation of viral latency.Herpes simplex virus type 1 latently infected neurons differentially express latency-associated and ICP0 transcripts.Herpes simplex virus 2 (HSV-2) infected cell proteins are among the most dominant antigens of a live-attenuated HSV-2 vaccine.CK2 inhibitors increase the sensitivity of HSV-1 to interferon-β.A system for creating stable cell lines that express a gene of interest from a bidirectional and regulatable herpes simplex virus type 1 promoter.Role of ICP0 in the strategy of conquest of the host cell by herpes simplex virus 1The number of alphaherpesvirus particles infecting axons and the axonal protein repertoire determines the outcome of neuronal infectionDevelopment of a novel cell-based assay to monitor the transactivation activity of the HSV-1 protein ICP0.Antibodies Are Required for Complete Vaccine-Induced Protection against Herpes Simplex Virus 2.Attenuation of the adaptive immune response in rhesus macaques infected with simian varicella virus lacking open reading frame 61.DNA damage promotes herpes simplex virus-1 protein expression in a neuroblastoma cell line.Viral E3 ubiquitin ligase-mediated degradation of a cellular E3: viral mimicry of a cellular phosphorylation mark targets the RNF8 FHA domain.Efficient quiescent infection of normal human diploid fibroblasts with wild-type herpes simplex virus type 1.Herpes simplex virus type 1 ICP0 phosphorylation mutants impair the E3 ubiquitin ligase activity of ICP0 in a cell type-dependent manner.Glutamine deprivation causes enhanced plating efficiency of a herpes simplex virus type 1 ICP0-null mutant.The zinc RING finger of bovine herpesvirus 1-encoded bICP0 protein is crucial for viral replication and virulence.Differential functions of interferon-upregulated Sp100 isoforms: herpes simplex virus type 1 promoter-based immediate-early gene suppression and PML protection from ICP0-mediated degradation
P2860
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P2860
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.
description
2001 nî lūn-bûn
@nan
2001 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
ICP0, ICP4, or VP16 expressed ...... ted trigeminal ganglion cells.
@ast
ICP0, ICP4, or VP16 expressed ...... ted trigeminal ganglion cells.
@en
type
label
ICP0, ICP4, or VP16 expressed ...... ted trigeminal ganglion cells.
@ast
ICP0, ICP4, or VP16 expressed ...... ted trigeminal ganglion cells.
@en
prefLabel
ICP0, ICP4, or VP16 expressed ...... ted trigeminal ganglion cells.
@ast
ICP0, ICP4, or VP16 expressed ...... ted trigeminal ganglion cells.
@en
P2093
P2860
P1433
P1476
ICP0, ICP4, or VP16 expressed ...... ted trigeminal ganglion cells.
@en
P2093
D J Davido
P A Schaffer
W P Halford
P2860
P304
P356
10.1128/JVI.75.13.6143-6153.2001
P577
2001-07-01T00:00:00Z