Ras-GAP binding and phosphorylation by herpes simplex virus type 2 RR1 PK (ICP10) and activation of the Ras/MEK/MAPK mitogenic pathway are required for timely onset of virus growth.
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Pedilanthus tithymaloides Inhibits HSV Infection by Modulating NF-κB SignalingLocalization of ERK/MAP kinase is regulated by the alphaherpesvirus tegument protein Us2Distinct effects of knocking down MEK1 and MEK2 on replication of herpes simplex virus type 2.Human papillomavirus type 6b virus-like particles are able to activate the Ras-MAP kinase pathway and induce cell proliferation.Biological approaches to therapy of pancreatic cancer.Quantitative proteomic analyses of influenza virus-infected cultured human lung cells.Visna virus-induced activation of MAPK is required for virus replication and correlates with virus-induced neuropathologyA short polypeptide from the herpes simplex virus type 2 ICP10 gene can induce antigen aggregation and autophagosomal degradation for enhanced immune presentation.Targeting apoptosis in neurological disease using the herpes simplex virus.Role of Fas/FasL in regulation of inflammation in vaginal tissue during HSV-2 infection.Identity of zinc finger nucleases with specificity to herpes simplex virus type II genomic DNA: novel HSV-2 vaccine/therapy precursorsPerformance and use of a ribonucleotide reductase herpes simplex virus type-specific serological assay.Oncolytic virotherapy for pancreatic cancer.Oncolytic virotherapy for ovarian cancer.The HSV-2 protein ICP10PK prevents neuronal apoptosis and loss of function in an in vivo model of neurodegeneration associated with glutamate excitotoxicity.H11/HspB8 and Its Herpes Simplex Virus Type 2 Homologue ICP10PK Share Functions That Regulate Cell Life/Death Decisions and Human DiseaseVaricella-zoster virus ORF12 protein activates the phosphatidylinositol 3-kinase/Akt pathway to regulate cell cycle progression.The herpes simplex virus type 2 gene ICP10PK protects from apoptosis caused by nerve growth factor deprivation through inhibition of caspase-3 activation and XIAP up-regulation.The growth compromised HSV-2 mutant DeltaRR prevents kainic acid-induced apoptosis and loss of function in organotypic hippocampal culturesMulti-targeted neuroprotection by the HSV-2 gene ICP10PK includes robust bystander activity through PI3-K/Akt and/or MEK/ERK-dependent neuronal release of vascular endothelial growth factor and fractalkine.Calpain-dependent clearance of the autophagy protein p62/SQSTM1 is a contributor to ΔPK oncolytic activity in melanoma.ΔPK oncolytic activity includes modulation of the tumour cell milieu.The oncolytic virus ΔPK has multimodal anti-tumor activity.The herpes simplex virus type 2 R1 protein kinase (ICP10 PK) blocks apoptosis in hippocampal neurons, involving activation of the MEK/MAPK survival pathway.The herpes simplex virus type 2 R1 protein kinase (ICP10 PK) functions as a dominant regulator of apoptosis in hippocampal neurons involving activation of the ERK survival pathway and upregulation of the antiapoptotic protein Bag-1.Effect of p38 mitogen-activated protein kinase on the replication of encephalomyocarditis virusThe HSV-2 mutant DeltaPK induces melanoma oncolysis through nonredundant death programs and associated with autophagy and pyroptosis proteins.Pseudorabies virus US3 protein kinase mediates actin stress fiber breakdown.Inhibition of Epstein-Barr virus (EBV) reactivation by short interfering RNAs targeting p38 mitogen-activated protein kinase or c-myc in EBV-positive epithelial cells.DeltaRR vaccination protects from KA-induced seizures and neuronal loss through ICP10PK-mediated modulation of the neuronal-microglial axis.Intranasal administration of the growth-compromised HSV-2 vector DeltaRR prevents kainate-induced seizures and neuronal loss in rats and mice.ICP10PK inhibits calpain-dependent release of apoptosis-inducing factor and programmed cell death in response to the toxin MPP+.Comparison of infectivity and spread between HSV-1 and HSV-2 based oncolytic viruses on tumor cells with different receptor expression profiles.Programmed cell death: the battlefield between the host and alpha-herpesviruses and a potential avenue for cancer treatmentHerpes simplex virus type 2 infection triggers AP-1 transcription activity through TLR4 signaling in genital epithelial cells
P2860
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P2860
Ras-GAP binding and phosphorylation by herpes simplex virus type 2 RR1 PK (ICP10) and activation of the Ras/MEK/MAPK mitogenic pathway are required for timely onset of virus growth.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
@zh
2000年论文
@zh-cn
name
Ras-GAP binding and phosphoryl ...... timely onset of virus growth.
@en
Ras-GAP binding and phosphorylation by herpes simplex virus type 2 RR1 PK
@nl
type
label
Ras-GAP binding and phosphoryl ...... timely onset of virus growth.
@en
Ras-GAP binding and phosphorylation by herpes simplex virus type 2 RR1 PK
@nl
prefLabel
Ras-GAP binding and phosphoryl ...... timely onset of virus growth.
@en
Ras-GAP binding and phosphorylation by herpes simplex virus type 2 RR1 PK
@nl
P2093
P2860
P1433
P1476
Ras-GAP binding and phosphoryl ...... timely onset of virus growth.
@en
P2093
P2860
P304
10417-10429
P356
10.1128/JVI.74.22.10417-10429.2000
P407
P577
2000-11-01T00:00:00Z