Herpes simplex virus gene expression in neurons: viral DNA synthesis is a critical regulatory event in the branch point between the lytic and latent pathways.
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Roscovitine, a specific inhibitor of cellular cyclin-dependent kinases, inhibits herpes simplex virus DNA synthesis in the presence of viral early proteinsPlaque2.0-A High-Throughput Analysis Framework to Score Virus-Cell Transmission and Clonal Cell ExpansionTransient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neuronsA dominant-negative herpesvirus protein inhibits intranuclear targeting of viral proteins: effects on DNA replication and late gene expression.Transcription of the herpes simplex virus 1 genome during productive and quiescent infection of neuronal and nonneuronal cells.The polyserine tract of herpes simplex virus ICP4 is required for normal viral gene expression and growth in murine trigeminal gangliaPhosphorylation of the herpes simplex virus type 1 origin binding protein.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.Regulation of herpes simplex virus type 1 thymidine kinase gene expression by thyroid hormone receptor in cultured neuronal cells.Site-directed mutagenesis of large DNA palindromes: construction and in vitro characterization of herpes simplex virus type 1 mutants containing point mutations that eliminate the oriL or oriS initiation functionIntrinsic innate immunity fails to control herpes simplex virus and vesicular stomatitis virus replication in sensory neurons and fibroblasts.An intertypic herpes simplex virus helicase-primase complex associated with a defect in neurovirulence has reduced primase activity.Herpes simplex virus DNA synthesis is not a decisive regulatory event in the initiation of lytic viral protein expression in neurons in vivo during primary infection or reactivation from latency.Point mutations in herpes simplex virus type 1 oriL, but not in oriS, reduce pathogenesis during acute infection of mice and impair reactivation from latency.Histone deacetylase inhibitors induce reactivation of herpes simplex virus type 1 in a latency-associated transcript-independent manner in neuronal cellsHerpes simplex virus type 1 origins of DNA replication play no role in the regulation of flanking promoters.ICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.Effects of thyroid hormone on HSV-1 gene regulation: implications in the control of viral latency and reactivation.HSV-1 gene expression from reactivated ganglia is disordered and concurrent with suppression of latency-associated transcript and miRNAsCellular transcription factors induced in trigeminal ganglia during dexamethasone-induced reactivation from latency stimulate bovine herpesvirus 1 productive infection and certain viral promoters.Gene expression during reactivation of herpes simplex virus type 1 from latency in the peripheral nervous system is different from that during lytic infection of tissue culturesC-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.Targeting the JMJD2 histone demethylases to epigenetically control herpesvirus infection and reactivation from latencyBovine herpesvirus 1 regulatory proteins bICP0 and VP16 are readily detected in trigeminal ganglionic neurons expressing the glucocorticoid receptor during the early stages of reactivation from latency.Stress-induced cellular transcription factors expressed in trigeminal ganglionic neurons stimulate the herpes simplex virus 1 ICP0 promoterA Novel Thyroid Hormone Mediated Regulation of HSV-1 Gene Expression and Replication is Specific to Neuronal Cells and Associated with Disruption of Chromatin Condensation.Thyroid hormone-dependent epigenetic suppression of herpes simplex virus-1 gene expression and viral replication in differentiated neuroendocrine cells.Herpes simplex virus type 1 ICP0 protein does not accumulate in the nucleus of primary neurons in cultureAccumulation of viral transcripts and DNA during establishment of latency by herpes simplex virus.Thyroid hormone controls the gene expression of HSV-1 LAT and ICP0 in neuronal cells.Herpes simplex virus 1 immediate-early and early gene expression during reactivation from latency under conditions that prevent infectious virus production.Relaxed repression of herpes simplex virus type 1 genomes in Murine trigeminal neuronsHuman cytomegalovirus early protein pUL21a promotes efficient viral DNA synthesis and the late accumulation of immediate-early transcripts.Reversing thyroid-hormone-mediated repression of a HSV-1 promoter via computationally guided mutagenesis.
P2860
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P2860
Herpes simplex virus gene expression in neurons: viral DNA synthesis is a critical regulatory event in the branch point between the lytic and latent pathways.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年学术文章
@wuu
1996年学术文章
@zh-cn
1996年学术文章
@zh-hans
1996年学术文章
@zh-my
1996年学术文章
@zh-sg
1996年學術文章
@yue
1996年學術文章
@zh
1996年學術文章
@zh-hant
name
Herpes simplex virus gene expr ...... the lytic and latent pathways.
@ast
Herpes simplex virus gene expr ...... the lytic and latent pathways.
@en
type
label
Herpes simplex virus gene expr ...... the lytic and latent pathways.
@ast
Herpes simplex virus gene expr ...... the lytic and latent pathways.
@en
prefLabel
Herpes simplex virus gene expr ...... the lytic and latent pathways.
@ast
Herpes simplex virus gene expr ...... the lytic and latent pathways.
@en
P2093
P2860
P1433
P1476
Herpes simplex virus gene expr ...... the lytic and latent pathways
@en
P2093
E M Johnson
P F Nichol
P2860
P304
P407
P577
1996-08-01T00:00:00Z