Featured Publications
Adenosine is required for sustained inflammasome activation via the A2A receptor and the HIF-1α pathway
Ouyang X, Ghani A, Malik A, Wilder T, Colegio OR, Flavell RA, Cronstein BN, Mehal WZ. Adenosine is required for sustained inflammasome activation via the A2A receptor and the HIF-1α pathway. Nature Communications 2013, 4: 2909. PMID: 24352507, PMCID: PMC3895487, DOI: 10.1038/ncomms3909.Peer-Reviewed Original ResearchMeSH KeywordsAdenosineAdenosine TriphosphateAnimalsCarrier ProteinsCyclic AMPCyclic AMP Response Element-Binding ProteinCyclic AMP-Dependent Protein KinasesHypoxia-Inducible Factor 1, alpha SubunitInflammasomesInterleukin-1betaLipopolysaccharidesLiverMacrophagesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinReceptor, Adenosine A2ASignal TransductionConceptsHIF-1α pathwayInflammasome activityInflammasome activationA2A receptorsIL-1β productionIL-1β responseReceptor-mediated signalingLack of responseTolerogenic stateChronic diseasesInflammatory responseInflammasome pathwayPrevious exposureLipopolysaccharideAdenosineReceptorsActivationKey regulatorInitial activationPathwaySignalingResponseInterleukinStimuliDisease
2009
AP-1 Activated by Toll-like Receptors Regulates Expression of IL-23 p19*
Liu W, Ouyang X, Yang J, Liu J, Li Q, Gu Y, Fukata M, Lin T, He JC, Abreu M, Unkeless JC, Mayer L, Xiong H. AP-1 Activated by Toll-like Receptors Regulates Expression of IL-23 p19*. Journal Of Biological Chemistry 2009, 284: 24006-24016. PMID: 19592489, PMCID: PMC2781995, DOI: 10.1074/jbc.m109.025528.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 2AnimalsAutoimmune DiseasesCell LineDendritic CellsGene Expression RegulationInterleukin-10Interleukin-23 Subunit p19LipopolysaccharidesMacrophages, PeritonealMAP Kinase Signaling SystemMiceMice, KnockoutMitogen-Activated Protein Kinase KinasesMutationMyeloid Differentiation Factor 88NF-kappa BProto-Oncogene Proteins c-junResponse ElementsToll-Like Receptor 4Transcription Factor AP-1ConceptsIL-23 p19Toll-like receptorsP19 expressionIL-10-deficient miceNF-kappaBMyD88-dependent Toll-like receptorIL-23 expressionRecombinant IL-10IL-12 familyC-JunWild-type miceAP-1 siteC-Fos bindsAP-1Promoter activationIL-23IL-10Dendritic cellsMyD88 pathwayAutoimmune diseasesImmune responseInflammatory signalsType miceLipopolysaccharide (LPS) stimulationNF-kappaB.
2007
Cooperation between MyD88 and TRIF pathways in TLR synergy via IRF5 activation
Ouyang X, Negishi H, Takeda R, Fujita Y, Taniguchi T, Honda K. Cooperation between MyD88 and TRIF pathways in TLR synergy via IRF5 activation. Biochemical And Biophysical Research Communications 2007, 354: 1045-1051. PMID: 17275788, DOI: 10.1016/j.bbrc.2007.01.090.Peer-Reviewed Original ResearchConceptsToll-like receptorsInterferon regulatory factor 5TLR synergyTRIF pathwayImmune systemMultiple Toll-like receptorsTranscription factor interferon regulatory factor 5Regulatory factor 5Agonist combinationsImmune cellsMyD88 adaptorInnate immunityIRF5 activationTRIF adaptorMyD88Synergistic inductionActivationFactor 5Target genesCross talkCellsAgonistsTRIFPathwayImmunity