Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
about
Leucine zipper domain is required for Kaposi sarcoma-associated herpesvirus (KSHV) K-bZIP protein to interact with histone deacetylase and is important for KSHV replicationHerpes simplex virus VP16, but not ICP0, is required to reduce histone occupancy and enhance histone acetylation on viral genomes in U2OS osteosarcoma cells.Transcription of the herpes simplex virus 1 genome during productive and quiescent infection of neuronal and nonneuronal cells.Novel roles of cytoplasmic ICP0: proteasome-independent functions of the RING finger are required to block interferon-stimulated gene production but not to promote viral replication.A neuron-specific host microRNA targets herpes simplex virus-1 ICP0 expression and promotes latency.Nuclear interferon-inducible protein 16 promotes silencing of herpesviral and transfected DNA.Herpes simplex virus 1 ICP0 phosphorylation site mutants are attenuated for viral replication and impaired for explant-induced reactivation.Proteomic analysis of the herpes simplex virus 1 virion protein 16 transactivator protein in infected cellsDiversity and evolution of chromatin proteins encoded by DNA viruses.An Essential Viral Transcription Activator Modulates Chromatin DynamicsA Herpesviral Lytic Protein Regulates the Structure of Latent Viral Chromatin.Two overlapping regions within the N-terminal half of the herpes simplex virus 1 E3 ubiquitin ligase ICP0 facilitate the degradation and dissociation of PML and dissociation of Sp100 from ND10.In vitro Inactivation of Latent HSV by Targeted Mutagenesis Using an HSV-specific Homing EndonucleaseChromatin dynamics during lytic infection with herpes simplex virus 1.Requirement of the N-terminal activation domain of herpes simplex virus ICP4 for viral gene expression.Activities of ICP0 involved in the reversal of silencing of quiescent herpes simplex virus 1.Transcriptional regulation by HSV-1 induced HTRP via acetylation system.Deletion of the Virion Host Shut-off Gene Enhances Neuronal-Selective Transgene Expression from an HSV Vector Lacking Functional IE Genes.Reversal of heterochromatic silencing of quiescent herpes simplex virus type 1 by ICP0.Herpes simplex virus 1 DNA is in unstable nucleosomes throughout the lytic infection cycle, and the instability of the nucleosomes is independent of DNA replication.During lytic infections, herpes simplex virus type 1 DNA is in complexes with the properties of unstable nucleosomes.Cellular Antisilencing Elements Support Transgene Expression from Herpes Simplex Virus Vectors in the Absence of Immediate Early Gene ExpressionPromyelocytic leukemia (PML) nuclear bodies (NBs) induce latent/quiescent HSV-1 genomes chromatinization through a PML NB/Histone H3.3/H3.3 Chaperone Axis
P2860
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P2860
Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
description
2009 nî lūn-bûn
@nan
2009年の論文
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2009年学术文章
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2009年学术文章
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2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
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2009年學術文章
@zh-hant
name
Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
@en
Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
@nl
type
label
Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
@en
Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
@nl
prefLabel
Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
@en
Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
@nl
P2860
P356
P1433
P1476
Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.
@en
P2093
Michael W Ferenczy
Neal A DeLuca
P2860
P304
P356
10.1128/JVI.00785-09
P407
P577
2009-06-17T00:00:00Z