Functions of Varicella-zoster virus ORF23 capsid protein in viral replication and the pathogenesis of skin infection. - Wikidata - wikimedia - TriplyDB

Functions of Varicella-zoster virus ORF23 capsid protein in viral replication and the pathogenesis of skin infection.

Functions of Varicella-zoster virus ORF23 capsid protein in viral replication and the pathogenesis of skin infection.

http://www.wikidata.org/entity/Q39953349

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A beta-herpesvirus with fluorescent capsids to study transport in living cells 3D reconstruction of VZV infected cell nuclei and PML nuclear cages by serial section array scanning electron microscopy and electron tomography Genome-wide mutagenesis reveals that ORF7 is a novel VZV skin-tropic factor Improper tagging of the non-essential small capsid protein VP26 impairs nuclear capsid egress of herpes simplex virus.The cytoplasmic domain of varicella-zoster virus glycoprotein H regulates syncytia formation and skin pathogenesis Anti-glycoprotein H antibody impairs the pathogenicity of varicella-zoster virus in skin xenografts in the SCID mouse model.Molecular mechanisms of varicella zoster virus pathogenesis.Entrapment of viral capsids in nuclear PML cages is an intrinsic antiviral host defense against varicella-zoster virus.A hydrophobic domain within the small capsid protein of Kaposi's sarcoma-associated herpesvirus is required for assembly.Disruption of PML nuclear bodies is mediated by ORF61 SUMO-interacting motifs and required for varicella-zoster virus pathogenesis in skin.Identification of a varicella-zoster virus replication inhibitor that blocks capsid assembly by interacting with the floor domain of the major capsid protein.Varicella-zoster virus glycoprotein E is a critical determinant of virulence in the SCID mouse-human model of neuropathogenesis Molecular characterization of varicella zoster virus in latently infected human ganglia: physical state and abundance of VZV DNA, Quantitation of viral transcripts and detection of VZV-specific proteins.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.Varicella-zoster virus (VZV) origin of DNA replication oriS influences origin-dependent DNA replication and flanking gene transcription.The varicella-zoster virus genome An Sp1/Sp3 site in the downstream region of varicella-zoster virus (VZV) oriS influences origin-dependent DNA replication and flanking gene transcription and is important for VZV replication in vitro and in human skin Mutational analysis of varicella-zoster virus (VZV) immediate early protein (IE62) subdomains and their importance in viral replication.Regulation of the varicella-zoster virus ORF3 promoter by cellular and viral factors Self-assembly of Epstein-Barr virus capsids.Regulation of the ORF61 promoter and ORF61 functions in varicella-zoster virus replication and pathogenesis Bacterial artificial chromosome derived simian varicella virus is pathogenic in vivo.Cellular transcription factor YY1 mediates the varicella-zoster virus (VZV) IE62 transcriptional activation.Insertion of reticuloendotheliosis virus long terminal repeat into a bacterial artificial chromosome clone of a very virulent Marek's disease virus alters its pathogenicity.Herpes Simplex Virus 1 Small Capsomere-Interacting Protein VP26 Regulates Nucleocapsid Maturation.ORF7 of Varicella-Zoster Virus Is Required for Viral Cytoplasmic Envelopment in Differentiated Neuronal Cells.Artificially inserting a reticuloendotheliosis virus long terminal repeat into a bacterial artificial chromosome clone of Marek's disease virus (MDV) alters expression of nearby MDV genes.The replication cycle of varicella-zoster virus: analysis of the kinetics of viral protein expression, genome synthesis, and virion assembly at the single-cell level.A Functional Carboxy-Terminal Fluorescent Protein Fusion to Pseudorabies Virus Small Capsid Protein VP26.

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Functions of Varicella-zoster virus ORF23 capsid protein in viral replication and the pathogenesis of skin infection.

http://www.wikidata.org/entity/Q39953349

description

2008 nî lūn-bûn

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2008年の論文

@ja

2008年学术文章

@wuu

2008年学术文章

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2008年学术文章

@zh-hans

2008年学术文章

@zh-my

2008年学术文章

@zh-sg

2008年學術文章

@yue

2008年學術文章

@zh

2008年學術文章

@zh-hant

name

Functions of Varicella-zoster ...... athogenesis of skin infection.

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Functions of Varicella-zoster ...... athogenesis of skin infection.

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type

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Functions of Varicella-zoster ...... athogenesis of skin infection.

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Functions of Varicella-zoster ...... athogenesis of skin infection.

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prefLabel

Functions of Varicella-zoster ...... athogenesis of skin infection.

@en

Functions of Varicella-zoster ...... athogenesis of skin infection.

@nl

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Journal of Virology

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Functions of Varicella-zoster ...... athogenesis of skin infection.

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P2093

Ann M Arvin

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Jaya Rajamani

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Leigh Zerboni

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Marvin Sommer

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Vaishali Chaudhuri

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P2860

Evidence for controlled incorporation of herpes simplex virus type 1 UL26 protease into capsids

Assembly of the herpes simplex virus capsid: preformed triplexes bind to the nascent capsid.

Finding a needle in a haystack: detection of a small protein (the 12-kDa VP26) in a large complex (the 200-MDa capsid of herpes simplex virus).

Distinct monoclonal antibodies separately label the hexons or the pentons of herpes simplex virus capsid.

Structure of the herpes simplex virus capsid. Molecular composition of the pentons and the triplexes.

Incorporation of the green fluorescent protein into the herpes simplex virus type 1 capsid.

Mutational analysis of the repeated open reading frames, ORFs 63 and 70 and ORFs 64 and 69, of varicella-zoster virus.

Structural analysis of the capsid polypeptides of herpes simplex virus types 1 and 2.

Construction of varicella-zoster virus recombinants from parent Oka cosmids and demonstration that ORF65 protein is dispensable for infection of human skin and T cells in the SCID-hu mouse model

Tropism of varicella-zoster virus for human CD4+ and CD8+ T lymphocytes and epidermal cells in SCID-hu mice.

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10231-10246

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10.1128/JVI.01890-07

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20

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82

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18684828

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