Cholangiocyte expression of alpha2beta1-integrin confers susceptibility to rotavirus-induced experimental biliary atresia. - Wikidata - awgldk - TriplyDB

Cholangiocyte expression of alpha2beta1-integrin confers susceptibility to rotavirus-induced experimental biliary atresia.

Cholangiocyte expression of alpha2beta1-integrin confers susceptibility to rotavirus-induced experimental biliary atresia.

http://www.wikidata.org/entity/Q36807785

about

Cholestatic liver disease in children Pathogenesis of biliary atresia: defining biology to understand clinical phenotypes The integrin alpha2beta1 agonist, aggretin, promotes proliferation and migration of VSMC through NF-kB translocation and PDGF production Biliary atresia: will blocking inflammation tame the disease?Determinants of the specificity of rotavirus interactions with the alpha2beta1 integrin Integrative genomics identifies candidate microRNAs for pathogenesis of experimental biliary atresia.The rhesus rotavirus gene encoding VP4 is a major determinant in the pathogenesis of biliary atresia in newborn mice.Rhesus rotavirus VP4 sequence-specific activation of mononuclear cells is associated with cholangiopathy in murine biliary atresia.Rotavirus infection of human cholangiocytes parallels the murine model of biliary atresia Rotavirus replication in the cholangiocyte mediates the temporal dependence of murine biliary atresia.Aetiology of biliary atresia: what is actually known?Clues to the etiology of bile duct injury in biliary atresia Biliary atresia: Where do we stand now?Advances in biliary atresia: from patient care to research.Epithelial-mesenchymal interactions in biliary diseases Role of integrins in fibrosing liver diseases.Recent Advances in Etiology of Biliary Atresia.Dendritic cells regulate natural killer cell activation and epithelial injury in experimental biliary atresia.A Point Mutation in the Rhesus Rotavirus VP4 Protein Generated through a Rotavirus Reverse Genetics System Attenuates Biliary Atresia in the Murine Model.The SRL peptide of rhesus rotavirus VP4 protein governs cholangiocyte infection and the murine model of biliary atresia.Rhesus rotavirus VP6 regulates ERK-dependent calcium influx in cholangiocytes.The Sea Lamprey as an Etiological Model for Biliary Atresia.Regulatory T cells control the CD8 adaptive immune response at the time of ductal obstruction in experimental biliary atresia.Gene and Protein Expression Profiles in a Mouse Model of Collagen-Induced Arthritis.Combinatory effects of hepatic CD8+ and NK lymphocytes in bile duct injury from biliary atresia

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Cholangiocyte expression of alpha2beta1-integrin confers susceptibility to rotavirus-induced experimental biliary atresia.

http://www.wikidata.org/entity/Q36807785

description

2008 nî lūn-bûn

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2008年论文

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Cholangiocyte expression of al ...... experimental biliary atresia.

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Cholangiocyte expression of al ...... experimental biliary atresia.

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Cholangiocyte expression of al ...... experimental biliary atresia.

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AJPGI.00442.2007

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American Journal of Physiology - Gastrointestinal and Liver Physiology

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Cholangiocyte expression of al ...... experimental biliary atresia.

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P2093

Alex Bondoc

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Bryan Donnelly

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Greg Tiao

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Monica McNeal

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Mubeen Jafri

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Paul D Rennert

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Paul H Weinreb

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Richard Ward

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Steven Allen

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P2860

Integrins alpha2beta1 and alpha4beta1 can mediate SA11 rotavirus attachment and entry into cells.

Differential infection of polarized epithelial cell lines by sialic acid-dependent and sialic acid-independent rotavirus strains.

Molecular biology of rotavirus cell entry.

Liver transplantation. The pediatric challenge.

Activation of the platelet collagen receptor integrin alpha(2)beta(1): its mechanism and participation in the physiological functions of platelets.

VLA-2 (alpha2beta1) integrin promotes rotavirus entry into cells but is not necessary for rotavirus attachment.

Etiopathogenesis of biliary atresia.

Mechanisms of integrin-mediated virus attachment and internalization process.

The pathogenesis of biliary atresia: evidence for a virus-induced autoimmune disease.

Collagen-platelet interactions: recognition and signalling.

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