Perturbation of cell cycle progression and cellular gene expression as a function of herpes simplex virus ICP0.
about
ICP0 dismantles microtubule networks in herpes simplex virus-infected cellsThe bovine herpesvirus 1 immediate-early protein (bICP0) associates with histone deacetylase 1 to activate transcription.Functional interaction between class II histone deacetylases and ICP0 of herpes simplex virus type 1Inactivating a cellular intrinsic immune defense mediated by Daxx is the mechanism through which the human cytomegalovirus pp71 protein stimulates viral immediate-early gene expressionBovine Herpes Virus 1 (BHV-1) and Herpes Simplex Virus Type 1 (HSV-1) Promote Survival of Latently Infected Sensory Neurons, in Part by Inhibiting ApoptosisChk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growthRole for A-type lamins in herpesviral DNA targeting and heterochromatin modulationICP0 induces the accumulation of colocalizing conjugated ubiquitin.Towards an understanding of the herpes simplex virus type 1 latency-reactivation cycleICP0 inhibits the decrease of HSV amplicon-mediated transgene expression.Comparison of the biological and biochemical activities of several members of the alphaherpesvirus ICP0 family of proteins.Chromatin assembly on herpes simplex virus genomes during lytic infection.E2F proteins are posttranslationally modified concomitantly with a reduction in nuclear binding activity in cells infected with herpes simplex virus 1.Reovirus-induced G(2)/M cell cycle arrest requires sigma1s and occurs in the absence of apoptosis.Efficient activation of viral genomes by levels of herpes simplex virus ICP0 insufficient to affect cellular gene expression or cell survival.Herpesvirus lytic replication and the cell cycle: arresting new developmentsICP0, 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.Epstein-Barr virus (EBV) Rta-mediated EBV and Kaposi's sarcoma-associated herpesvirus lytic reactivations in 293 cells.The coronavirus nucleocapsid is a multifunctional protein.The cyclin-dependent kinase inhibitor roscovitine inhibits the transactivating activity and alters the posttranslational modification of herpes simplex virus type 1 ICP0.Reovirus-induced alterations in gene expression related to cell cycle regulation.Histone deacetylase inhibitors induce reactivation of herpes simplex virus type 1 in a latency-associated transcript-independent manner in neuronal cellsThe Epstein-Barr virus immediate-early protein BZLF1 induces both a G(2) and a mitotic blockHIV-1 viral infectivity factor interacts with TP53 to induce G2 cell cycle arrest and positively regulate viral replication.HSV-1 genome subnuclear positioning and associations with host-cell PML-NBs and centromeres regulate LAT locus transcription during latency in neurons.CCAAT/enhancer binding protein alpha interacts with ZTA and mediates ZTA-induced p21(CIP-1) accumulation and G(1) cell cycle arrest during the Epstein-Barr virus lytic cycle.ICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.Cellular stress rather than stage of the cell cycle enhances the replication and plating efficiencies of herpes simplex virus type 1 ICP0- virusesICP0 and the US3 protein kinase of herpes simplex virus 1 independently block histone deacetylation to enable gene expression.Herpes simplex virus ICP0 promotes both histone removal and acetylation on viral DNA during lytic infection.Whole tumor antigen vaccines.Identification of herpesvirus proteins that contribute to G1/S arrest.Relationship of herpes simplex virus genome configuration to productive and persistent infections.Analysis of the cell cycle regulatory protein (E2F1) after infection of cultured cells with bovine herpesvirus 1 (BHV-1) or herpes simplex virus type 1 (HSV-1)Barrier to auto integration factor becomes dephosphorylated during HSV-1 Infection and Can Act as a host defense by impairing viral DNA replication and gene expressionActivation and evasion of innate antiviral immunity by herpes simplex virusHerpes simplex viral-vector design for efficient transduction of nonneuronal cells without cytotoxicity.Selective recruitment of nuclear factors to productively replicating herpes simplex virus genomes.Role of ICP0 in the strategy of conquest of the host cell by herpes simplex virus 1mRNA decay during herpes simplex virus (HSV) infections: mutations that affect translation of an mRNA influence the sites at which it is cleaved by the HSV virion host shutoff (Vhs) protein.
P2860
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P2860
Perturbation of cell cycle progression and cellular gene expression as a function of herpes simplex virus ICP0.
description
1999 nî lūn-bûn
@nan
1999 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Perturbation of cell cycle pro ...... of herpes simplex virus ICP0.
@ast
Perturbation of cell cycle pro ...... of herpes simplex virus ICP0.
@en
type
label
Perturbation of cell cycle pro ...... of herpes simplex virus ICP0.
@ast
Perturbation of cell cycle pro ...... of herpes simplex virus ICP0.
@en
prefLabel
Perturbation of cell cycle pro ...... of herpes simplex virus ICP0.
@ast
Perturbation of cell cycle pro ...... of herpes simplex virus ICP0.
@en
P2860
P1433
P1476
Perturbation of cell cycle pro ...... of herpes simplex virus ICP0.
@en
P2093
P2860
P304
P577
1999-10-01T00:00:00Z