2002
Src Kinase Mediates Phosphatidylinositol 3-Kinase/Akt-dependent Rapid Endothelial Nitric-oxide Synthase Activation by Estrogen*
Haynes MP, Li L, Sinha D, Russell KS, Hisamoto K, Baron R, Collinge M, Sessa WC, Bender JR. Src Kinase Mediates Phosphatidylinositol 3-Kinase/Akt-dependent Rapid Endothelial Nitric-oxide Synthase Activation by Estrogen*. Journal Of Biological Chemistry 2002, 278: 2118-2123. PMID: 12431978, DOI: 10.1074/jbc.m210828200.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsBlotting, WesternCell LineCells, CulturedElectrophoresis, Polyacrylamide GelEndoplasmic ReticulumEndothelium, VascularEnzyme ActivationEnzyme InhibitorsEstrogensHumansMiceMutationNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesPhosphorylationPrecipitin TestsProtein BindingProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptors, EstrogenSignal TransductionSrc-Family KinasesTime FactorsTransfectionTyrosineConceptsC-SrcPI3-kinaseAkt phosphorylationSrc kinaseUpstream regulatorKinase-dead c-SrcC-Src associationActive c-SrcC-Src phosphorylationMurine embryonic fibroblastsBasal Akt phosphorylationC-Src expressionCritical upstream regulatorEndothelial nitric oxide synthaseSrc familyActive AktEmbryonic fibroblastsComplex formation resultsEndothelial cellsHuman endothelial cellsAkt activationPhosphorylationKinaseAktPhosphatidylinositol
2000
CD28 and LFA‐1 contribute to cyclosporin A‐resistant T cell growth by stabilizing the IL‐2 mRNA through distinct signaling pathways
Geginat J, Clissi B, Moro M, Dellabona P, Bender J, Pardi R. CD28 and LFA‐1 contribute to cyclosporin A‐resistant T cell growth by stabilizing the IL‐2 mRNA through distinct signaling pathways. European Journal Of Immunology 2000, 30: 1136-1144. PMID: 10760803, DOI: 10.1002/(sici)1521-4141(200004)30:4<1136::aid-immu1136>3.0.co;2-3.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, CDB7-2 AntigenCalcineurinCD28 AntigensCells, CulturedCyclosporineCytoskeletonDendritic CellsDNA-Binding ProteinsDrug SynergismHumansIntercellular Adhesion Molecule-1Interleukin-2Lymphocyte ActivationLymphocyte Function-Associated Antigen-1Membrane GlycoproteinsMitogen-Activated Protein KinasesNF-kappa BNFATC Transcription FactorsNuclear ProteinsPromoter Regions, GeneticProtein BindingRNA StabilityRNA, MessengerSignal TransductionSuperantigensT-LymphocytesTranscription FactorsConceptsIL-2 mRNALFA-1ICAM-1IL-2 dependentT cell proliferationSubsequent T cell proliferationCostimulatory molecule CD28TCR-induced proliferationSignaling pathwaysT cell growthIL-2 transcriptsGraft rejectionDendritic cellsIL-2Clinical transplantationT lymphocytesMolecule CD28Primary T lymphocytesNF-kappaBCD28Distinct signaling pathwaysLower transcriptional rateDifferent signaling pathwaysProtein kinase activationCell proliferationEstrogen Stimulates Heat Shock Protein 90 Binding to Endothelial Nitric Oxide Synthase in Human Vascular Endothelial Cells EFFECTS ON CALCIUM SENSITIVITY AND NO RELEASE*
Russell K, Haynes M, Caulin-Glaser T, Rosneck J, Sessa W, Bender J. Estrogen Stimulates Heat Shock Protein 90 Binding to Endothelial Nitric Oxide Synthase in Human Vascular Endothelial Cells EFFECTS ON CALCIUM SENSITIVITY AND NO RELEASE*. Journal Of Biological Chemistry 2000, 275: 5026-5030. PMID: 10671543, DOI: 10.1074/jbc.275.7.5026.Peer-Reviewed Original ResearchConceptsEndothelial nitric oxide synthaseNitric oxide synthaseHuman umbilical vein endothelial cellsENOS activationOxide synthaseEstrogen receptor antagonist ICINO releaseEndothelium-dependent vasodilationReceptor-mediated modulationReceptor antagonist ICINitric oxide releaseUmbilical vein endothelial cellsVein endothelial cellsAntagonist ICIHeat shock protein 90CGMP productionShock protein 90Oxide releaseEndothelial cellsEndothelial cell effectsCalcium sensitivityCalcium dependenceCell effectsEstrogenProtein 90