ICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.
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The molecular basis of herpes simplex virus latencyTransient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neuronsChanges to euchromatin on LAT and ICP4 following reactivation are more prevalent in an efficiently reactivating strain of HSV-1.Entry of herpes simplex virus type 1 (HSV-1) into the distal axons of trigeminal neurons favors the onset of nonproductive, silent infectionA5-positive primary sensory neurons are nonpermissive for productive infection with herpes simplex virus 1 in vitro.CTCF occupation of the herpes simplex virus 1 genome is disrupted at early times postreactivation in a transcription-dependent manner.C-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.DNA damage promotes herpes simplex virus-1 protein expression in a neuroblastoma cell line.Efficacy of Herpes Simplex Virus Vector Encoding the Human Preproenkephalin Gene for Treatment of Facial Pain in Mice.Efficient quiescent infection of normal human diploid fibroblasts with wild-type herpes simplex virus type 1.The zinc RING finger of bovine herpesvirus 1-encoded bICP0 protein is crucial for viral replication and virulence.Stress-induced cellular transcription factors expressed in trigeminal ganglionic neurons stimulate the herpes simplex virus 1 ICP0 promoterEvidence that the herpes simplex virus type 1 ICP0 protein does not initiate reactivation from latency in vivo.Virus reactivation: a panoramic view in human infectionsAnalysis of the functions of herpes simplex virus type 1 regulatory protein ICP0 that are critical for lytic infection and derepression of quiescent viral genomes.Replication of ICP0-null mutant herpes simplex virus type 1 is restricted by both PML and Sp100.VP16 serine 375 is a critical determinant of herpes simplex virus exit from latency in vivo.Relaxed repression of herpes simplex virus type 1 genomes in Murine trigeminal neuronsTrichostatin A and oncolytic HSV combination therapy shows enhanced antitumoral and antiangiogenic effects.Induction of cellular stress overcomes the requirement of herpes simplex virus type 1 for immediate-early protein ICP0 and reactivates expression from quiescent viral genomes.Reactivation of expression from quiescent herpes simplex virus type 1 genomes in the absence of immediate-early protein ICP0.
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P2860
ICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.
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2006 nî lūn-bûn
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2006 թվականի ապրիլին հրատարակված գիտական հոդված
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2006年の論文
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2006年論文
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2006年論文
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ICP0 is not required for effic ...... ently infected neuronal cells.
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ICP0 is not required for effic ...... ently infected neuronal cells.
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ICP0 is not required for effic ...... ently infected neuronal cells.
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ICP0 is not required for effic ...... ently infected neuronal cells.
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ICP0 is not required for effic ...... ently infected neuronal cells.
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ICP0 is not required for effic ...... ently infected neuronal cells.
@nl
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ICP0 is not required for effic ...... ently infected neuronal cells.
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ICP0 is not required for effic ...... ently infected neuronal cells.
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ICP0 is not required for effic ...... ently infected neuronal cells.
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ICP0 is not required for effic ...... ently infected neuronal cells.
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Craig S Miller
Robert J Danaher
Robert J Jacob
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10.1128/JVI.80.7.3360-3368.2006
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2006-04-01T00:00:00Z