2009
Early gene expression changes induced by the bacterial superantigen staphylococcal enterotoxin B and its modulation by a proteasome inhibitor
Rajagopalan G, Tilahun A, Asmann Y, David C. Early gene expression changes induced by the bacterial superantigen staphylococcal enterotoxin B and its modulation by a proteasome inhibitor. Physiological Genomics 2009, 37: 279-293. PMID: 19336531, PMCID: PMC2685500, DOI: 10.1152/physiolgenomics.90385.2008.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBoronic AcidsBortezomibCytokinesEnterotoxinsGene Expression ProfilingGene Expression RegulationHLA-DR alpha-ChainsHLA-DR AntigensInflammation MediatorsMiceMice, TransgenicOligonucleotide Array Sequence AnalysisProtease InhibitorsPyrazinesReceptors, ChemokineReceptors, CytokineSignal TransductionSuperantigensConceptsToxic shock syndromePathogenesis of TSSStaphylococcal enterotoxin BBacterial superantigen staphylococcal enterotoxin BSuperantigen staphylococcal enterotoxin BEnterotoxin BAdministration of bortezomibAnti-inflammatory mediatorsTh17-type cytokinesProteasome inhibitorsCytokines/chemokinesSerious systemic illnessTransgenic mouse modelSuitable animal modelEarly gene expression changesNF-kappaB pathwaySystemic illnessSerum levelsShock syndromeImmunoregulatory cytokinesBacterial superantigensCC chemokinesMouse modelVivo administrationAnimal models
2008
p21-Activated Kinase Signaling Regulates Oxidant-Dependent NF-&kgr;B Activation by Flow
Orr AW, Hahn C, Blackman BR, Schwartz MA. p21-Activated Kinase Signaling Regulates Oxidant-Dependent NF-&kgr;B Activation by Flow. Circulation Research 2008, 103: 671-679. PMID: 18669917, PMCID: PMC2697905, DOI: 10.1161/circresaha.108.182097.Peer-Reviewed Original ResearchConceptsNF-kappaB activationReactive oxygen speciesProinflammatory transcription factor nuclear factorTranscription factor nuclear factorInflammatory gene expressionNF-kappaB pathwayAbility of ROSP21-activated kinaseDisturbed blood flowBlood flowSensitivity of cellsNuclear factorEndothelial cellsROS productionActivationOxygen speciesCellsDisturbed flowGene expressionCollagenTargeted inactivation of the COP9 signalosome impairs multiple stagesof T cell development
Panattoni M, Sanvito F, Basso V, Doglioni C, Casorati G, Montini E, Bender JR, Mondino A, Pardi R. Targeted inactivation of the COP9 signalosome impairs multiple stagesof T cell development. Journal Of Experimental Medicine 2008, 205: 465-477. PMID: 18268034, PMCID: PMC2271025, DOI: 10.1084/jem.20070725.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisbcl-X ProteinCell CycleCell LineCell ProliferationCOP9 Signalosome ComplexCyclin-Dependent Kinase Inhibitor p16DNA RepairFemaleHomeodomain ProteinsIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, KnockoutMultiprotein ComplexesNF-kappa BPeptide HydrolasesProto-Oncogene Proteins c-bcl-2Receptors, Antigen, T-CellRNA, MessengerT-LymphocytesTumor Suppressor Protein p53Ubiquitin-Protein LigasesConceptsCOP9 signalosomeCSN5/Jab1Genetic programBcl-2 family membersGenetic complementation analysisBcl-xL/BclS-phase progressionDistinct developmental stagesCell cycle progressionT cell developmentComplementation analysisLower organismsCatalytic subunitPositive selectionTranscription factorsDNA repairCycle progressionCell developmentThymocyte survivalDevelopmental stagesNF-kappaB pathwayTransgenic backgroundPhase progressionRapid turnoverEffector molecules
2004
IκB Kinase Complex α Kinase Activity Controls Chemokine and High Endothelial Venule Gene Expression in Lymph Nodes and Nasal-Associated Lymphoid Tissue
Drayton DL, Bonizzi G, Ying X, Liao S, Karin M, Ruddle NH. IκB Kinase Complex α Kinase Activity Controls Chemokine and High Endothelial Venule Gene Expression in Lymph Nodes and Nasal-Associated Lymphoid Tissue. The Journal Of Immunology 2004, 173: 6161-6168. PMID: 15528353, DOI: 10.4049/jimmunol.173.10.6161.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationChemokinesEndothelium, LymphaticEnzyme ActivationGene Expression Regulation, DevelopmentalI-kappa B KinaseLigandsLymph NodesLymphoid TissueLymphotoxin beta ReceptorMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsNasal MucosaProtein Serine-Threonine KinasesProtein SubunitsReceptors, Tumor Necrosis FactorConceptsHigh endothelial venulesSecondary lymphoid organogenesisLymph nodesAlternative NF-kappaB pathwayPeripheral node addressinNF-kappaB pathwayLymphoid tissueLymphoid organogenesisNasal-associated lymphoid tissueCell adhesion molecule-1Lymphoid chemokines CCL19Adhesion molecule-1GlyCAM-1Lymphotoxin beta receptorPathway activityNALT developmentChemokines CCL19Endothelial venulesBeta receptorsMolecule-1Mutant miceTarget genesCritical roleGene expressionReduced expression
1998
MyD88 Is an Adaptor Protein in the hToll/IL-1 Receptor Family Signaling Pathways
Medzhitov R, Preston-Hurlburt P, Kopp E, Stadlen A, Chen C, Ghosh S, Janeway C. MyD88 Is an Adaptor Protein in the hToll/IL-1 Receptor Family Signaling Pathways. Molecular Cell 1998, 2: 253-258. PMID: 9734363, DOI: 10.1016/s1097-2765(00)80136-7.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsAntigens, DifferentiationDrosophilaDrosophila ProteinsHumansInterleukin-1 Receptor-Associated KinasesMembrane GlycoproteinsMembrane ProteinsMyeloid Differentiation Factor 88NF-kappa BProtein KinasesProteinsReceptors, Cell SurfaceReceptors, ImmunologicReceptors, Interleukin-1Signal TransductionTNF Receptor-Associated Factor 6Toll-Like ReceptorsTranscription Factor AP-1ConceptsIL-1R familyNF-kappaB activationNF-kappaB pathwayImmune response genesToll/IL-1R familyAP-1 activationImmune responseIL-1RTRAF6 proteinInnate immunityNF-kappaBMyD88Drosophila Toll proteinReceptor familyToll receptorAdaptor proteinSignaling pathwaysReceptorsActivationToll proteinRegulator moleculesResponse genesAdult DrosophilaPathwayProtein
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply