Utilization of sialic acid as a coreceptor is required for reovirus-induced biliary disease - Wikidata - wikimedia - TriplyDB

Utilization of sialic acid as a coreceptor is required for reovirus-induced biliary disease

Utilization of sialic acid as a coreceptor is required for reovirus-induced biliary disease

http://www.wikidata.org/entity/Q35095524

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Potential for Improving Potency and Specificity of Reovirus Oncolysis with Next-Generation Reovirus Variants Leukocyte-derived IFN-α/β and epithelial IFN-λ constitute a compartmentalized mucosal defense system that restricts enteric virus infections Diminished reovirus capsid stability alters disease pathogenesis and littermate transmission The GM2 Glycan Serves as a Functional Coreceptor for Serotype 1 Reovirus Bid regulates the pathogenesis of neurotropic reovirus.Enterovirus 70 binds to different glycoconjugates containing alpha2,3-linked sialic acid on different cell lines.Cancer screening by systemic administration of a gene delivery vector encoding tumor-selective secretable biomarker expression Organ-specific roles for transcription factor NF-kappaB in reovirus-induced apoptosis and disease.Rotavirus viremia and extraintestinal viral infection in the neonatal rat model.The pathogenesis of biliary atresia: evidence for a virus-induced autoimmune disease.Differential distribution of the JC virus receptor-type sialic acid in normal human tissues.Glycan engagement dictates hydrocephalus induction by serotype 1 reovirus.Reovirus receptors and pathogenesis.Mechanisms of reovirus bloodstream dissemination.Prediction of GCRV virus-host protein interactome based on structural motif-domain interactions.Comparison of three neurotropic viruses reveals differences in viral dissemination to the central nervous system From touchdown to transcription: the reovirus cell entry pathway The sweet spot: defining virus-sialic acid interactions.Directional release of reovirus from the apical surface of polarized endothelial cells Reovirus activates a caspase-independent cell death pathway.Aetiology of biliary atresia: what is actually known?Clues to the etiology of bile duct injury in biliary atresia Recent Advances in Etiology of Biliary Atresia.Utilization of sialylated glycans as coreceptors enhances the neurovirulence of serotype 3 reovirus.Junctional adhesion molecule a serves as a receptor for prototype and field-isolate strains of mammalian reovirus.The reovirus sigma1s protein is a determinant of hematogenous but not neural virus dissemination in mice.Nonstructural protein σ1s mediates reovirus-induced cell cycle arrest and apoptosis.Intestinal microbiota promote enteric virus replication and systemic pathogenesis.Optimum length and flexibility of reovirus attachment protein σ1 are required for efficient viral infection.Genetic and pharmacologic alteration of cathepsin expression influences reovirus pathogenesis.Ganglioside-linked terminal sialic acid moieties on murine macrophages function as attachment receptors for murine noroviruses.Theiler's murine encephalomyelitis virus attachment to the gastrointestinal tract is associated with sialic acid binding A new group B adenovirus receptor is expressed at high levels on human stem and tumor cells.Virus persistence in an animal model of multiple sclerosis requires virion attachment to sialic acid coreceptors Nonstructural protein sigma1s is a determinant of reovirus virulence and influences the kinetics and severity of apoptosis induction in the heart and central nervous system.Viral gene expression potentiates reovirus-induced necrosis.Obstruction of extrahepatic bile ducts by lymphocytes is regulated by IFN-gamma in experimental biliary atresia.The bulky and the sweet: How neutralizing antibodies and glycan receptors compete for virus binding.Junctional adhesion molecule-A is required for hematogenous dissemination of reovirus Interferon regulatory factor 3 attenuates reovirus myocarditis and contributes to viral clearance.

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P2860

Utilization of sialic acid as a coreceptor is required for reovirus-induced biliary disease

http://www.wikidata.org/entity/Q35095524

description

2003 nî lūn-bûn

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2003 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2003 թվականի հունիսին հրատարակված գիտական հոդված

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2003年の論文

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2003年論文

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2003年論文

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Journal of Clinical Investigation

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Utilization of sialic acid as ...... ovirus-induced biliary disease

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P2093

Bryan E Youree

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Daniel H Ebert

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Erik S Barton

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J Craig Forrest

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J Denise Wetzel

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Jodi L Connolly

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Kay Washington

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Terence S Dermody

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Tibor Valyi-Nagy

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P2860

Junctional adhesion molecule, a novel member of the immunoglobulin superfamily that distributes at intercellular junctions and modulates monocyte transmigration

Antibody protects against lethal infection with the neurally spreading reovirus type 3 (Dearing)

Human junction adhesion molecule regulates tight junction resealing in epithelia

Junction adhesion molecule is a receptor for reovirus

Glycophorin is the reovirus receptor on human erythrocytes

Reovirus binding to cell surface sialic acid potentiates virus-induced apoptosis

Identification of carbohydrate-binding domains in the attachment proteins of type 1 and type 3 reoviruses

Viral receptors on isolated murine and human ependymal cells.

Biliary atresia: an update on our understanding of the disorder.

Molecular basis of reovirus virulence: role of the S1 gene.

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1823-1833

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10.1172/JCI16303

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12

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111

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2003-06-01T00:00:00Z

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10702735

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12813018

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161418

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