2005
Anaplasma phagocytophilum Modulates gp91phox Gene Expression through Altered Interferon Regulatory Factor 1 and PU.1 Levels and Binding of CCAAT Displacement Protein
Thomas V, Samanta S, Wu C, Berliner N, Fikrig E. Anaplasma phagocytophilum Modulates gp91phox Gene Expression through Altered Interferon Regulatory Factor 1 and PU.1 Levels and Binding of CCAAT Displacement Protein. Infection And Immunity 2005, 73: 208-218. PMID: 15618156, PMCID: PMC538944, DOI: 10.1128/iai.73.1.208-218.2005.Peer-Reviewed Original ResearchMeSH KeywordsAnaplasma phagocytophilumDNA-Binding ProteinsGene Expression RegulationHL-60 CellsHomeodomain ProteinsHumansInterferon Regulatory Factor-1Membrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesNuclear ProteinsPhosphoproteinsPhosphorylationPromoter Regions, GeneticProto-Oncogene ProteinsRepressor ProteinsSTAT1 Transcription FactorTrans-ActivatorsTranscription FactorsTranscription, GeneticConceptsCCAAT displacement proteinRegulatory factor 1IRF-1IRF-1 promoterRegulation of genesA. phagocytophilum-infected cellsFirst molecular mechanismFactor 1Interferon regulatory factor 1IFN-gamma signalingActivator proteinGene transcriptionAnaplasma phagocytophilumTranscriptional inhibitionGene expressionMolecular mechanismsNuclear extractsGamma interferon stimulationPhosphorylated STAT1Interferon stimulationGenesA. phagocytophilum infectionProteinProtein expressionReduced expression
2003
STAT3 deletion during hematopoiesis causes Crohn's disease-like pathogenesis and lethality: A critical role of STAT3 in innate immunity
Welte T, Zhang SS, Wang T, Zhang Z, Hesslein DG, Yin Z, Kano A, Iwamoto Y, Li E, Craft JE, Bothwell AL, Fikrig E, Koni PA, Flavell RA, Fu XY. STAT3 deletion during hematopoiesis causes Crohn's disease-like pathogenesis and lethality: A critical role of STAT3 in innate immunity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2003, 100: 1879-1884. PMID: 12571365, PMCID: PMC149927, DOI: 10.1073/pnas.0237137100.Peer-Reviewed Original ResearchConceptsDeletion of Stat3STAT3 deletionInnate immune responseKey transcriptional mediatorNormal embryonic developmentCell-autonomous proliferationAbsence of STAT3Tissue-specific disruptionImmune responseInnate immunityCritical roleTumor necrosis factor alphaNF-kappa B activationTranscriptional mediatorsEmbryonic developmentBowel wall thickeningHematopoiesis resultsInflammatory cell infiltrationSignal transducerNecrosis factor alphaTranscription 3NAPDH oxidase activityBone marrow cellsMyeloid lineageSTAT3
2000
Inhibition of Th1 Differentiation by IL-6 Is Mediated by SOCS1
Diehl S, Anguita J, Hoffmeyer A, Zapton T, Ihle J, Fikrig E, Rincón M. Inhibition of Th1 Differentiation by IL-6 Is Mediated by SOCS1. Immunity 2000, 13: 805-815. PMID: 11163196, DOI: 10.1016/s1074-7613(00)00078-9.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen-Presenting CellsCarrier ProteinsCell DifferentiationDNA-Binding ProteinsGene ExpressionInterferon-gammaInterleukin-12Interleukin-4Interleukin-6MiceReceptors, InterferonRepressor ProteinsSignal TransductionSTAT1 Transcription FactorSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTh1 CellsTrans-ActivatorsUp-RegulationConceptsIFNgamma gene expressionReceptor-mediated signalsIndependent molecular mechanismsFunctional pleiotropyTranscription 1 (STAT1) phosphorylationNovel functionNegative regulationSignal transducerGene expressionMolecular mechanismsCell differentiationCell typesT cell activationDifferentiationTh2 differentiationTh1 differentiationCell activationNonimmune cellsExpressionTh1 cell differentiationImportant roleCellsInhibitionPleiotropyPhosphorylation