The herpes simplex virus immediate-early protein ICP0 affects transcription from the viral genome and infected-cell survival in the absence of ICP4 and ICP27
about
Functional inaccessibility of quiescent herpes simplex virus genomesThe Role of microRNAs in the Pathogenesis of Herpesvirus InfectionHerpes simplex virus VP16, but not ICP0, is required to reduce histone occupancy and enhance histone acetylation on viral genomes in U2OS osteosarcoma cells.Herpes simplex virus type 1 vector-mediated expression of nerve growth factor protects dorsal root ganglion neurons from peroxide toxicityThe herpes simplex virus type 1 regulatory protein ICP27 is required for the prevention of apoptosis in infected human cells.Towards an understanding of the herpes simplex virus type 1 latency-reactivation cycleEngineered HSV vector achieves safe long-term transgene expression in the central nervous system.ATR and ATRIP are recruited to herpes simplex virus type 1 replication compartments even though ATR signaling is disabled.ICP0 inhibits the decrease of HSV amplicon-mediated transgene expression.Comparison of the biological and biochemical activities of several members of the alphaherpesvirus ICP0 family of proteins.Transcription of the herpes simplex virus 1 genome during productive and quiescent infection of neuronal and nonneuronal cells.Persistence and expression of the herpes simplex virus genome in the absence of immediate-early proteins.The disruption of ND10 during herpes simplex virus infection correlates with the Vmw110- and proteasome-dependent loss of several PML isoformsLong-term transgene expression in mice infected with a herpes simplex virus type 1 mutant severely impaired for immediate-early gene expression.Pseudotyping of glycoprotein D-deficient herpes simplex virus type 1 with vesicular stomatitis virus glycoprotein G enables mutant virus attachment and entry.Optimized 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 ICP0ICP0 is required for efficient reactivation of herpes simplex virus type 1 from neuronal latency.Efficient activation of viral genomes by levels of herpes simplex virus ICP0 insufficient to affect cellular gene expression or cell survival.The U(S)3 protein kinase blocks apoptosis induced by the d120 mutant of herpes simplex virus 1 at a premitochondrial stage.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.Herpes simplex virus vector-mediated gene delivery of glutamic acid decarboxylase reduces detrusor overactivity in spinal cord-injured ratsHSV-1-based vectors for gene therapy of neurological diseases and brain tumors: part I. HSV-1 structure, replication and pathogenesis.HSV-1-based vectors for gene therapy of neurological diseases and brain tumors: part II. Vector systems and applicationsThe cyclin-dependent kinase inhibitor roscovitine inhibits the transactivating activity and alters the posttranslational modification of herpes simplex virus type 1 ICP0.Phosphorylation of transcription factor Sp1 during herpes simplex virus type 1 infectionEfficient herpes simplex virus 1 replication requires cellular ATR pathway proteinsInhibition of HSV-1 Replication by Gene Editing StrategyhTERT extends the life of human fibroblasts without compromising type I interferon signaling.Cellular stress rather than stage of the cell cycle enhances the replication and plating efficiencies of herpes simplex virus type 1 ICP0- virusesHerpes simplex virus type 1 single strand DNA binding protein and helicase/primase complex disable cellular ATR signaling.Herpes simplex virus type 1 and bovine herpesvirus 1 latency.Whole tumor antigen vaccines.Early induction of autophagy in human fibroblasts after infection with human cytomegalovirus or herpes simplex virus 1Relationship of herpes simplex virus genome configuration to productive and persistent infections.CK2 inhibitors increase the sensitivity of HSV-1 to interferon-β.Herpes simplex viral-vector design for efficient transduction of nonneuronal cells without cytotoxicity.DNA mismatch repair proteins are required for efficient herpes simplex virus 1 replicationHerpes simplex virus 1 ICP0 phosphorylation site mutants are attenuated for viral replication and impaired for explant-induced reactivation.
P2860
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P2860
The herpes simplex virus immediate-early protein ICP0 affects transcription from the viral genome and infected-cell survival in the absence of ICP4 and ICP27
description
1997 nî lūn-bûn
@nan
1997年の論文
@ja
1997年論文
@yue
1997年論文
@zh-hant
1997年論文
@zh-hk
1997年論文
@zh-mo
1997年論文
@zh-tw
1997年论文
@wuu
1997年论文
@zh
1997年论文
@zh-cn
name
The herpes simplex virus immed ...... the absence of ICP4 and ICP27
@ast
The herpes simplex virus immed ...... the absence of ICP4 and ICP27
@en
type
label
The herpes simplex virus immed ...... the absence of ICP4 and ICP27
@ast
The herpes simplex virus immed ...... the absence of ICP4 and ICP27
@en
prefLabel
The herpes simplex virus immed ...... the absence of ICP4 and ICP27
@ast
The herpes simplex virus immed ...... the absence of ICP4 and ICP27
@en
P2093
P2860
P1433
P1476
The herpes simplex virus immed ...... the absence of ICP4 and ICP27
@en
P2093
P2860
P304
P407
P577
1997-06-01T00:00:00Z