2000
Selective Inhibition of NF-κB Activation by a Peptide That Blocks the Interaction of NEMO with the IκB Kinase Complex
May M, D'Acquisto F, Madge L, Glöckner J, Pober J, Ghosh S. Selective Inhibition of NF-κB Activation by a Peptide That Blocks the Interaction of NEMO with the IκB Kinase Complex. Science 2000, 289: 1550-1554. PMID: 10968790, DOI: 10.1126/science.289.5484.1550.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAnti-Inflammatory Agents, Non-SteroidalCells, CulturedCOS CellsEndothelium, VascularE-SelectinGene Expression RegulationHeLa CellsHumansI-kappa B KinaseInflammationMiceMice, Inbred C57BLMolecular Sequence DataMutationNF-kappa BPeptidesPoint MutationProtein Serine-Threonine KinasesProtein Structure, TertiaryRecombinant Fusion ProteinsConceptsNF-kappaBBasal NF-kappaB activityExperimental mouse modelTranscription factor nuclear factorCytokine-induced NF-kappaB activationCell-permeable NBD peptideInhibitor of kappaBNF-κB activationNF-kappaB activityNF-kappaB activationAssociation of NEMOIKK complexAcute inflammationDevelopment of drugsProinflammatory activationInflammatory responseNBD peptideMouse modelProinflammatory stimuliIκB kinase (IKK) complexNuclear factorRegulatory protein NEMOInflammationSelective inhibitionExpression of genesCytoprotection of Human Umbilical Vein Endothelial Cells Against Apoptosis and CTL-Mediated Lysis Provided by Caspase-Resistant Bcl-2 Without Alterations in Growth or Activation Responses
Zheng L, Dengler T, Kluger M, Madge L, Schechner J, Maher S, Pober J, Bothwell A. Cytoprotection of Human Umbilical Vein Endothelial Cells Against Apoptosis and CTL-Mediated Lysis Provided by Caspase-Resistant Bcl-2 Without Alterations in Growth or Activation Responses. The Journal Of Immunology 2000, 164: 4665-4671. PMID: 10779771, DOI: 10.4049/jimmunol.164.9.4665.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCaspasesCell DivisionCell Line, TransformedCells, CulturedCulture Media, ConditionedCytotoxicity, ImmunologicEndothelial Growth FactorsEndothelium, VascularGenetic VectorsGreen Fluorescent ProteinsHumansLuminescent ProteinsProto-Oncogene Proteins c-bcl-2RetroviridaeT-Lymphocytes, CytotoxicTransduction, GeneticTransfectionUmbilical VeinsConceptsGraft endothelial cellsAllograft rejectionBcl-2Endothelial cellsAcute allograft rejectionClass I MHC moleculesNF-kappaB activationHuman umbilical vein endothelial cellsI MHC moleculesUmbilical vein endothelial cellsHost CTLVein endothelial cellsEndothelial injuryAnti-apoptotic gene Bcl-2MHC moleculesGene Bcl-2Induction of apoptosisBcl-2-transduced cellsClass IActivation responseApoptotic effectsCTLHUVECTNFGrowth factor withdrawalIL-11 Activates Human Endothelial Cells to Resist Immune-Mediated Injury
Mahboubi K, Biedermann B, Carroll J, Pober J. IL-11 Activates Human Endothelial Cells to Resist Immune-Mediated Injury. The Journal Of Immunology 2000, 164: 3837-3846. PMID: 10725745, DOI: 10.4049/jimmunol.164.7.3837.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, CDCells, CulturedComplement System ProteinsCytokine Receptor gp130Cytotoxicity, ImmunologicDNA-Binding ProteinsDose-Response Relationship, ImmunologicEndothelium, VascularEnzyme ActivationHumansImmunity, InnateInflammation MediatorsInterleukin-11Interleukin-11 Receptor alpha SubunitMembrane GlycoproteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesNF-kappa BPhosphorylationReceptors, InterleukinReceptors, Interleukin-11Signal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorT-Lymphocytes, CytotoxicTrans-ActivatorsTyrosineUmbilical VeinsConceptsIL-11Mitogen-activated protein kinaseP44 mitogen-activated protein kinaseImmune-Mediated InjuryCytolytic T lymphocytesNF-kappaB activationGp130-signaling cytokinesInflammatory injuryHuman endothelial cellsIL-11 receptorProinflammatory responseMolecule expressionT lymphocytesICAM-1Maximal responseE-selectinMHC AbsVivo modelNF-kappaBEndothelial cellsTyrosine phosphorylationPhospho-STAT3Cultured HUVECsInjuryKinase 1 inhibitor
1996
A Sustained Reduction in IκB-β May Contribute to Persistent NF-κB Activation in Human Endothelial Cells*
Johnson D, Douglas I, Jahnke A, Ghosh S, Pober J. A Sustained Reduction in IκB-β May Contribute to Persistent NF-κB Activation in Human Endothelial Cells*. Journal Of Biological Chemistry 1996, 271: 16317-16322. PMID: 8663191, DOI: 10.1074/jbc.271.27.16317.Peer-Reviewed Original ResearchMeSH KeywordsBase SequenceBinding SitesCell Adhesion MoleculesCell MembraneCell NucleusCells, CulturedConsensus SequenceCytosolDNADNA-Binding ProteinsEndothelium, VascularGene ExpressionHistocompatibility Antigens Class IHumansI-kappa B ProteinsIntercellular Adhesion Molecule-1Interleukin-1KineticsMolecular Sequence DataNF-kappa BOligodeoxyribonucleotidesTetradecanoylphorbol AcetateTumor Necrosis Factor-alphaUmbilical VeinsVascular Cell Adhesion Molecule-1ConceptsAdhesion molecule-1Vascular cell adhesion molecule-1Intercellular adhesion molecule-1Cell adhesion molecule-1Phorbol myristate acetateInterleukin-1alphaNF-kappaB activationMolecule-1Sustained reductionNF-kappaBEndothelial cellsIkappaB-alphaIkappaB-betaHuman endothelial cellsHuman leukocyte antigen (HLA) class INF-kappaB.Inhibitory protein IkappaB-alphaCell surface molecule expressionIkappaB-beta degradationPersistent NF-κB activationSurface molecule expressionAntigen class INF-κB activationIkappaB-beta levelsDe novo expression