2008
Interferon-γ Induces X-linked Inhibitor of Apoptosis-associated Factor-1 and Noxa Expression and Potentiates Human Vascular Smooth Muscle Cell Apoptosis by STAT3 Activation*
Bai Y, Ahmad U, Wang Y, Li JH, Choy JC, Kim RW, Kirkiles-Smith N, Maher SE, Karras JG, Bennett CF, Bothwell AL, Pober JS, Tellides G. Interferon-γ Induces X-linked Inhibitor of Apoptosis-associated Factor-1 and Noxa Expression and Potentiates Human Vascular Smooth Muscle Cell Apoptosis by STAT3 Activation*. Journal Of Biological Chemistry 2008, 283: 6832-6842. PMID: 18192275, DOI: 10.1074/jbc.m706021200.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsApoptosisApoptosis Regulatory ProteinsF-Box ProteinsGene Expression RegulationHumansInterferon-gammaIntracellular Signaling Peptides and ProteinsMiceModels, BiologicalMuscle, Smooth, VascularNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2Signal TransductionSTAT3 Transcription FactorTissue TransplantationConceptsVascular smooth muscle cellsInhibitor of apoptosisHuman vascular smooth muscle cellsSTAT3 activationNoxa expressionFactor 1Mouse vascular smooth muscle cellsExpression of XAF1Vascular smooth muscle cell apoptosisSmooth muscle cell apoptosisMuscle cell apoptosisApoptotic stimuliTranscription factorsTranscription (STAT) proteinsGene productsPro-apoptotic effectsHuman coronary artery graftsSignal transducerDeath receptorsMicroarray analysisHuman endothelial cellsChimeric animal modelPhenotypic modulationSTAT1 activationNuclear translocation
2005
Osteoporosis with increased osteoclastogenesis in hematopoietic cell-specific STAT3-deficient mice
Zhang Z, Welte T, Troiano N, Maher SE, Fu XY, Bothwell AL. Osteoporosis with increased osteoclastogenesis in hematopoietic cell-specific STAT3-deficient mice. Biochemical And Biophysical Research Communications 2005, 328: 800-807. PMID: 15694417, DOI: 10.1016/j.bbrc.2005.01.019.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone RemodelingBone ResorptionCarrier ProteinsCell DifferentiationCell ProliferationCells, CulturedDNA-Binding ProteinsHematopoietic Stem CellsMembrane GlycoproteinsMiceOsteoclastsOsteoporosisProto-Oncogene Proteins c-fosRANK LigandReceptor Activator of Nuclear Factor-kappa BSTAT3 Transcription FactorTrans-Activators
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 ResearchMeSH KeywordsAnimalsBone Marrow CellsCells, CulturedCrohn DiseaseDNA-Binding ProteinsGene DeletionHematopoiesisImmunityMiceSTAT3 Transcription FactorTrans-ActivatorsConceptsDeletion 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