Truncation of the C-terminal acidic transcriptional activation domain of herpes simplex virus VP16 produces a phenotype similar to that of the in1814 linker insertion mutation.
about
Herpes simplex virus transactivator VP16 discriminates between HCF-1 and a novel family member, HCF-2.An activation domain in the C-terminal subunit of HCF-1 is important for transactivation by VP16 and LZIP.Functional inaccessibility of quiescent herpes simplex virus genomesTransient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neuronsDe novo synthesis of VP16 coordinates the exit from HSV latency in vivo.Herpes simplex virus VP16, but not ICP0, is required to reduce histone occupancy and enhance histone acetylation on viral genomes in U2OS osteosarcoma cells.Analysis of HCF, the cellular cofactor of VP16, in herpes simplex virus-infected cells.Herpes simplex virus ICP0 mutants are hypersensitive to interferonEvidence that herpes simplex virus VP16 is required for viral egress downstream of the initial envelopment event.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 ICP0Entry of herpes simplex virus type 1 (HSV-1) into the distal axons of trigeminal neurons favors the onset of nonproductive, silent infectionVaricella-zoster virus open reading frame 10 is a virulence determinant in skin cells but not in T cells in vivoICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.A single amino acid substitution in herpes simplex virus type 1 VP16 inhibits binding to the virion host shutoff protein and is incompatible with virus growth.Phosphorylation of the VP16 transcriptional activator protein during herpes simplex virus infection and mutational analysis of putative phosphorylation sites.Varicella-Zoster virus IE63, a major viral latency protein, is required to inhibit the alpha interferon-induced antiviral responseC-terminal trans-activation sub-region of VP16 is uniquely required for forskolin-induced herpes simplex virus type 1 reactivation from quiescently infected-PC12 cells but not for replication in neuronally differentiated-PC12 cells.Herpes simplex virus 1-encoded tegument protein VP16 abrogates the production of beta interferon (IFN) by inhibiting NF-κB activation and blocking IFN regulatory factor 3 to recruit its coactivator CBP.Histone Deacetylase Inhibitors Reduce the Number of Herpes Simplex Virus-1 Genomes Initiating Expression in Individual Cells.A targeted RNA interference screen reveals novel epigenetic factors that regulate herpesviral gene expression.Equine herpesvirus 1 gene 12 can substitute for vmw65 in the growth of herpes simplex virus (HSV) type 1, allowing the generation of optimized cell lines for the propagation of HSV vectors with multiple immediate-early gene defects.Hexamethylene bisacetamide leads to reduced helper virus-free HSV-1 amplicon expression titers via suppression of ICP0.The pseudorabies virus VP22 homologue (UL49) is dispensable for virus growth in vitro and has no effect on virulence and neuronal spread in rodents.Cell fusion-induced activation of interferon-stimulated genes is not required for restriction of a herpes simplex virus VP16/ICP0 mutant in heterokarya formed between permissive and restrictive cells.The UL14 tegument protein of herpes simplex virus type 1 is required for efficient nuclear transport of the alpha transinducing factor VP16 and viral capsids.The alpha-TIF (VP16) homologue (ETIF) of equine herpesvirus 1 is essential for secondary envelopment and virus egress.Herpes simplex virus type 1 immediate-early gene expression is required for the induction of apoptosis in human epithelial HEp-2 cellsCompartmentalization of VP16 in cells infected with recombinant herpes simplex virus expressing VP16-green fluorescent protein fusion proteins.De Novo Herpes Simplex Virus VP16 Expression Gates a Dynamic Programmatic Transition and Sets the Latent/Lytic Balance during Acute Infection in Trigeminal Ganglia.VP16 serine 375 is a critical determinant of herpes simplex virus exit from latency in vivo.Multiple immediate-early gene-deficient herpes simplex virus vectors allowing efficient gene delivery to neurons in culture and widespread gene delivery to the central nervous system in vivo.Reactivation of expression from quiescent herpes simplex virus type 1 genomes in the absence of immediate-early protein ICP0.The herpes simplex virus type 1 glycoprotein D (gD) cytoplasmic terminus and full-length gE are not essential and do not function in a redundant manner for cytoplasmic virion envelopment and egress.
P2860
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P2860
Truncation of the C-terminal acidic transcriptional activation domain of herpes simplex virus VP16 produces a phenotype similar to that of the in1814 linker insertion mutation.
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
Truncation of the C-terminal a ...... 814 linker insertion mutation.
@ast
Truncation of the C-terminal a ...... 814 linker insertion mutation.
@en
type
label
Truncation of the C-terminal a ...... 814 linker insertion mutation.
@ast
Truncation of the C-terminal a ...... 814 linker insertion mutation.
@en
prefLabel
Truncation of the C-terminal a ...... 814 linker insertion mutation.
@ast
Truncation of the C-terminal a ...... 814 linker insertion mutation.
@en
P2860
P1433
P1476
Truncation of the C-terminal a ...... 814 linker insertion mutation.
@en
P2093
P2860
P304
P407
P577
1997-08-01T00:00:00Z