Deletion of the herpes simplex virus VP22-encoding gene (UL49) alters the expression, localization, and virion incorporation of ICP0.
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ICP0 dismantles microtubule networks in herpes simplex virus-infected cellsHerpes simplex virus type 1 immediate-early protein ICP27 is required for efficient incorporation of ICP0 and ICP4 into virionsTegument Assembly and Secondary Envelopment of AlphaherpesvirusesSpatial and Temporal Resolution of Global Protein Synthesis during HSV Infection Using Bioorthogonal Precursors and Click ChemistryHerpes simplex virus tegument ICP0 is capsid associated, and its E3 ubiquitin ligase domain is important for incorporation into virions.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.Characterization of VP22 in herpes simplex virus-infected cells.A virulent bioluminescent and fluorescent dual-reporter Marek's disease virus unveils an alternative spreading pathway in addition to cell-to-cell contact.Characterization of a UL49-null mutant: VP22 of herpes simplex virus type 1 facilitates viral spread in cultured cells and the mouse corneaHerpes simplex virus glycoproteins gB and gD function in a redundant fashion to promote secondary envelopmentA pre-immediate-early role for tegument ICP0 in the proteasome-dependent entry of herpes simplex virusHerpes simplex virus immediate-early protein ICP0 is targeted by SIAH-1 for proteasomal degradation.Cell cycle modulation by Marek's disease virus: the tegument protein VP22 triggers S-phase arrest and DNA damage in proliferating cells.Direct and specific binding of the UL16 tegument protein of herpes simplex virus to the cytoplasmic tail of glycoprotein E.Cytoplasmic residues of herpes simplex virus glycoprotein gE required for secondary envelopment and binding of tegument proteins VP22 and UL11 to gE and gDFluorescently tagged pUL47 of Marek's disease virus reveals differential tissue expression of the tegument protein in vivoHerpes simplex virus 1 VP22 regulates translocation of multiple viral and cellular proteins and promotes neurovirulence.Singapore Grouper Iridovirus ORF75R is a Scaffold Protein Essential for Viral AssemblyReplication-competent herpes simplex virus 1 isolates selected from cells transfected with a bacterial artificial chromosome DNA lacking only the UL49 gene vary with respect to the defect in the UL41 gene encoding host shutoff RNase.Marek's disease virus expresses multiple UL44 (gC) variants through mRNA splicing that are all required for efficient horizontal transmission.VP22 core domain from Herpes simplex virus 1 reveals a surprising structural conservation in both the Alpha- and Gammaherpesvirinae subfamiliesVirion incorporation of the herpes simplex virus type 1 tegument protein VP22 is facilitated by trans-Golgi network localization and is independent of interaction with glycoprotein E.ESCDL-1, a new cell line derived from chicken embryonic stem cells, supports efficient replication of Mardiviruses.Translocation and colocalization of ICP4 and ICP0 in cells infected with herpes simplex virus 1 mutants lacking glycoprotein E, glycoprotein I, or the virion host shutoff product of the UL41 gene.ORF9p phosphorylation by ORF47p is crucial for the formation and egress of varicella-zoster virus viral particles.VP22 of herpes simplex virus 1 promotes protein synthesis at late times in infection and accumulation of a subset of viral mRNAs at early times in infection.Mode of virus rescue determines the acquisition of VHS mutations in VP22-negative herpes simplex virus 1.Epidermal growth factor receptor-PI3K signaling controls cofilin activity to facilitate herpes simplex virus 1 entry into neuronal cells.Elucidation of the block to herpes simplex virus egress in the absence of tegument protein UL16 reveals a novel interaction with VP22.Role of tegument proteins in herpesvirus assembly and egress.Herpesviruses remodel host membranes for virus egress.Insights into the function of tegument proteins from the varicella zoster virus.Functions of the ORF9-to-ORF12 gene cluster in varicella-zoster virus replication and in the pathogenesis of skin infectionHerpes Simplex Virus 1 Enters Human Keratinocytes by a Nectin-1-Dependent, Rapid Plasma Membrane Fusion Pathway That Functions at Low Temperature.Quantitative Evaluation of Protein Heterogeneity within Herpes Simplex Virus 1 Particles.Nonmuscle myosin heavy chain IIb mediates herpes simplex virus 1 entryDiffering effects of herpes simplex virus 1 and pseudorabies virus infections on centrosomal function.ORF11 protein interacts with the ORF9 essential tegument protein in varicella-zoster virus infectionAnalysis of the early steps of herpes simplex virus 1 capsid tegumentation.Hexamethylene bisacetamide leads to reduced helper virus-free HSV-1 amplicon expression titers via suppression of ICP0.
P2860
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P2860
Deletion of the herpes simplex virus VP22-encoding gene (UL49) alters the expression, localization, and virion incorporation of ICP0.
description
2005 nî lūn-bûn
@nan
2005 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
Deletion of the herpes simplex ...... virion incorporation of ICP0.
@ast
Deletion of the herpes simplex ...... virion incorporation of ICP0.
@en
type
label
Deletion of the herpes simplex ...... virion incorporation of ICP0.
@ast
Deletion of the herpes simplex ...... virion incorporation of ICP0.
@en
prefLabel
Deletion of the herpes simplex ...... virion incorporation of ICP0.
@ast
Deletion of the herpes simplex ...... virion incorporation of ICP0.
@en
P2093
P2860
P1433
P1476
Deletion of the herpes simplex ...... virion incorporation of ICP0.
@en
P2093
Alison Whiteley
Emmanuelle Bernard
Gillian Elliott
Wali Hafezi
P2860
P304
P356
10.1128/JVI.79.15.9735-9745.2005
P577
2005-08-01T00:00:00Z