Varicella-zoster virus glycoprotein gpI/gpIV receptor: expression, complex formation, and antigenicity within the vaccinia virus-T7 RNA polymerase transfection system.
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Varicella-Zoster Virus Infectious Cycle: ER Stress, Autophagic Flux, and Amphisome-Mediated TraffickingFunctions of the unique N-terminal region of glycoprotein E in the pathogenesis of varicella-zoster virus infectionVaricella-zoster virus Fc receptor component gI is phosphorylated on its endodomain by a cyclin-dependent kinaseThe herpes simplex virus gE-gI complex facilitates cell-to-cell spread and binds to components of cell junctionsCytoplasmic domain of herpes simplex virus gE causes accumulation in the trans-Golgi network, a site of virus envelopment and sorting of virions to cell junctions.Mutagenesis of varicella-zoster virus glycoprotein I (gI) identifies a cysteine residue critical for gE/gI heterodimer formation, gI structure, and virulence in skin cells.Essential functions of the unique N-terminal region of the varicella-zoster virus glycoprotein E ectodomain in viral replication and in the pathogenesis of skin infectionMultiple regulatory effects of varicella-zoster virus (VZV) gL on trafficking patterns and fusogenic properties of VZV gH.Varicella-zoster virus Fc receptor gE glycoprotein: serine/threonine and tyrosine phosphorylation of monomeric and dimeric formsVaricella-zoster virus glycoprotein I is essential for growth of virus in Vero cells.The amino terminus of varicella-zoster virus (VZV) glycoprotein E is required for binding to insulin-degrading enzyme, a VZV receptor.Aberrant infection and persistence of varicella-zoster virus in human dorsal root ganglia in vivo in the absence of glycoprotein I.Deletion of the first cysteine-rich region of the varicella-zoster virus glycoprotein E ectodomain abolishes the gE and gI interaction and differentially affects cell-cell spread and viral entry.Varicella-zoster virus glycoprotein I is essential for spread in dorsal root ganglia and facilitates axonal localization of structural virion components in neuronal cultures.The disulfide-bonded structure of feline herpesvirus glycoprotein I.Trafficking of varicella-zoster virus glycoprotein gI: T(338)-dependent retention in the trans-Golgi network, secretion, and mannose 6-phosphate-inhibitable uptake of the ectodomain.Varicella-zoster Virus gB and gE coexpression, but not gB or gE alone, leads to abundant fusion and syncytium formation equivalent to those from gH and gL coexpression.Responses of herpes simplex virus type 1-infected cells to the presence of extracellular antibodies: gE-dependent glycoprotein capping and enhancement in cell-to-cell spread.Promoter sequences of varicella-zoster virus glycoprotein I targeted by cellular transactivating factors Sp1 and USF determine virulence in skin and T cells in SCIDhu mice in vivo.Herpes simplex virus gE/gI expressed in epithelial cells interferes with cell-to-cell spread.A functional YNKI motif in the short cytoplasmic tail of varicella-zoster virus glycoprotein gH mediates clathrin-dependent and antibody-independent endocytosis.Glycoprotein I of varicella-zoster virus is required for viral replication in skin and T cells.An indirect double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) using baculovirus-expressed antigen for the detection of antibodies to glycoprotein E of pseudorabies virus and comparison of the method with blocking ELISAs.Biosynthesis of glycoproteins E and I of feline herpesvirus: gE-gI interaction is required for intracellular transport.Synthesis, processing, and oligomerization of bovine herpesvirus 1 gE and gI membrane proteins.Pseudorabies virus recombinants expressing functional virulence determinants gE and gI from bovine herpesvirus 1.1.The gE and gI homologs from two alphaherpesviruses have conserved and divergent neuroinvasive properties.Mutational analysis of the role of glycoprotein I in varicella-zoster virus replication and its effects on glycoprotein E conformation and trafficking.Structure-function analysis of the gE-gI complex of feline herpesvirus: mapping of gI domains required for gE-gI interaction, intracellular transport, and cell-to-cell spread.Unusual phosphorylation sequence in the gpIV (gI) component of the varicella-zoster virus gpI-gpIV glycoprotein complex (VZV gE-gI complex).Specific pseudorabies virus infection of the rat visual system requires both gI and gp63 glycoproteins.Identification of the phosphorylation sequence in the cytoplasmic tail of the varicella-zoster virus Fc receptor glycoprotein gpI.Regulation of varicella-zoster virus-induced cell-to-cell fusion by the endocytosis-competent glycoproteins gH and gE.A tyrosine-based motif and a casein kinase II phosphorylation site regulate the intracellular trafficking of the varicella-zoster virus glycoprotein I, a protein localized in the trans-Golgi network
P2860
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P2860
Varicella-zoster virus glycoprotein gpI/gpIV receptor: expression, complex formation, and antigenicity within the vaccinia virus-T7 RNA polymerase transfection system.
description
1993 nî lūn-bûn
@nan
1993年の論文
@ja
1993年論文
@yue
1993年論文
@zh-hant
1993年論文
@zh-hk
1993年論文
@zh-mo
1993年論文
@zh-tw
1993年论文
@wuu
1993年论文
@zh
1993年论文
@zh-cn
name
Varicella-zoster virus glycopr ...... olymerase transfection system.
@ast
Varicella-zoster virus glycopr ...... olymerase transfection system.
@en
type
label
Varicella-zoster virus glycopr ...... olymerase transfection system.
@ast
Varicella-zoster virus glycopr ...... olymerase transfection system.
@en
prefLabel
Varicella-zoster virus glycopr ...... olymerase transfection system.
@ast
Varicella-zoster virus glycopr ...... olymerase transfection system.
@en
P2093
P2860
P1433
P1476
Varicella-zoster virus glycopr ...... olymerase transfection system.
@en
P2093
P2860
P304
P407
P577
1993-01-01T00:00:00Z