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http://purl.uniprot.org/citations/16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16195373http://www.w3.org/2000/01/rdf-schema#comment"Endothelial cell (EC) barrier dysfunction results in increased vascular permeability observed in inflammation, tumor angiogenesis, and atherosclerosis. The platelet-derived phospholipid sphingosine-1-phosphate (S1P) decreases EC permeability in vitro and in vivo and thus has obvious therapeutic potential. We examined S1P-mediated human pulmonary artery EC signaling and barrier regulation in caveolin-enriched microdomains (CEM). Immunoblotting from S1P-treated EC revealed S1P-mediated rapid recruitment (1 microM, 5 min) to CEMs of the S1P receptors S1P1 and S1P3, p110 PI3 kinase alpha and beta catalytic subunits, the Rac1 GEF, Tiam1, and alpha-actinin isoforms 1 and 4. Immunoprecipitated p110 PI3 kinase catalytic subunits from S1P-treated EC exhibited PIP3 production in CEMs. Immunoprecipitation of S1P receptors from CEM fractions revealed complexes containing Tiam1 and S1P1. PI3 kinase inhibition (LY294002) attenuated S1P-induced Tiam1 association with S1P1, Tiam1/Rac1 activation, alpha-actinin-1/4 recruitment, and EC barrier enhancement. Silencing of either S1P1 or Tiam1 expression resulted in the loss of S1P-mediated Rac1 activation and alpha-actinin-1/4 recruitment to CEM. Finally, silencing S1P1, Tiam1, or both alpha-actinin isoforms 1/4 inhibits S1P-induced cortical F-actin rearrangement and S1P-mediated barrier enhancement. Taken together, these results suggest that S1P-induced recruitment of S1P1 to CEM fractions promotes PI3 kinase-mediated Tiam1/Rac1 activation required for alpha-actinin-1/4-regulated cortical actin rearrangement and EC barrier enhancement."xsd:string
http://purl.uniprot.org/citations/16195373http://purl.org/dc/terms/identifier"doi:10.1096/fj.05-3928com"xsd:string
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/author"Chiang E.T."xsd:string
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/author"Dudek S.M."xsd:string
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/author"Singleton P.A."xsd:string
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/author"Garcia J.G."xsd:string
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/name"FASEB J"xsd:string
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/pages"1646-1656"xsd:string
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/title"Regulation of sphingosine 1-phosphate-induced endothelial cytoskeletal rearrangement and barrier enhancement by S1P1 receptor, PI3 kinase, Tiam1/Rac1, and alpha-actinin."xsd:string
http://purl.uniprot.org/citations/16195373http://purl.uniprot.org/core/volume"19"xsd:string
http://purl.uniprot.org/citations/16195373http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16195373
http://purl.uniprot.org/citations/16195373http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16195373
http://purl.uniprot.org/uniprot/#_A0A024R694-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_A1L0V1-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_A0A8V8TN84-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_B4DFY0-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_A0A2X0TW27-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_B3KUX9-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_B4DRP5-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_B4DLH9-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_B7Z565-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_Q13009-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373
http://purl.uniprot.org/uniprot/#_Q86TX4-mappedCitation-16195373http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16195373