Insulin degrading enzyme is a cellular receptor mediating varicella-zoster virus infection and cell-to-cell spread
about
Herpes simplex virus and varicella zoster virus, the house guests who never leaveZika Fetal Neuropathogenesis: Etiology of a Viral SyndromeDecoding protein networks during virus entry by quantitative proteomicsAnion Activation Site of Insulin-degrading EnzymeThe last enzyme of the de novo purine synthesis pathway 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase (ATIC) plays a central role in insulin signaling and the Golgi/endosomes protein networkThe insulin degrading enzyme binding domain of varicella-zoster virus (VZV) glycoprotein E is important for cell-to-cell spread and VZV infectivity, while a glycoprotein I binding domain is essential for infection.Functions of the unique N-terminal region of glycoprotein E in the pathogenesis of varicella-zoster virus infectionInsulin degrading enzyme induces a conformational change in varicella-zoster virus gE, and enhances virus infectivity and stabilityMyelin-associated glycoprotein mediates membrane fusion and entry of neurotropic herpesviruses.Equine major histocompatibility complex class I molecules act as entry receptors that bind to equine herpesvirus-1 glycoprotein DIntegrative functional genomics of hepatitis C virus infection identifies host dependencies in complete viral replication cycleCholesterol dependence of varicella-zoster virion entry into target cellsHerpes virus fusion and entry: a story with many characters.Infected peripheral blood mononuclear cells transmit latent varicella zoster virus infection to the guinea pig enteric nervous system.Varicella-zoster virus glycoprotein E is a critical determinant of virulence in the SCID mouse-human model of neuropathogenesisHuman sensory neurons derived from induced pluripotent stem cells support varicella-zoster virus infection.The irreversible binding of amyloid peptide substrates to insulin-degrading enzyme: a biological perspectivePathogenesis of varicelloviruses in primatesThe capacity of UL49.5 proteins to inhibit TAP is widely distributed among members of the genus Varicellovirus.Amyloid beta-degrading cryptidases: insulin degrading enzyme, presequence peptidase, and neprilysin.Deletion of the fission yeast homologue of human insulinase reveals a TORC1-dependent pathway mediating resistance to proteotoxic stress.Pathogen-inspired drug delivery to the central nervous system.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.Insulin-degrading enzyme sorting in exosomes: a secretory pathway for a key brain amyloid-beta degrading proteaseTHY-1 Cell Surface Antigen (CD90) Has an Important Role in the Initial Stage of Human Cytomegalovirus InfectionVaricella-zoster virus infects human embryonic stem cell-derived neurons and neurospheres but not pluripotent embryonic stem cells or early progenitors.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.Cellular and viral factors regulate the varicella-zoster virus gE promoter during viral replication.Rodent models of varicella-zoster virus neurotropism.The varicella-zoster virus genomeDeletion in open reading frame 49 of varicella-zoster virus reduces virus growth in human malignant melanoma cells but not in human embryonic fibroblastsVaricella-zoster virus glycoprotein M homolog is glycosylated, is expressed on the viral envelope, and functions in virus cell-to-cell spreadInsights into the role of immunosenescence during varicella zoster virus infection (shingles) in the aging cell modelDirectional spread of alphaherpesviruses in the nervous system.Varicella-zoster virus immediate-early 63 protein interacts with human antisilencing function 1 protein and alters its ability to bind histones h3.1 and h3.3.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.Global Mapping of O-Glycosylation of Varicella Zoster Virus, Human Cytomegalovirus, and Epstein-Barr Virus.Productive vs non-productive infection by cell-free varicella zoster virus of human neurons derived from embryonic stem cells is dependent upon infectious viral doseDetergent resistant membrane-associated IDE in brain tissue and cultured cells: Relevance to Abeta and insulin degradation.
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P2860
Insulin degrading enzyme is a cellular receptor mediating varicella-zoster virus infection and cell-to-cell spread
description
2006 nî lūn-bûn
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2006 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
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2006 թվականի հոտեմբերին 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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2006年論文
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2006年論文
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2006年論文
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2006年论文
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Insulin degrading enzyme is a ...... ection and cell-to-cell spread
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Insulin degrading enzyme is a ...... ection and cell-to-cell spread
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Insulin degrading enzyme is a ...... ection and cell-to-cell spread
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Jeffrey I Cohen
Qingxue Li
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10.1016/J.CELL.2006.08.046
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2006-10-20T00:00:00Z