2022
UVB-mediated DNA damage induces matrix metalloproteinases to promote photoaging in an AhR- and SP1-dependent manner
Kim DJ, Iwasaki A, Chien AL, Kang S. UVB-mediated DNA damage induces matrix metalloproteinases to promote photoaging in an AhR- and SP1-dependent manner. JCI Insight 2022, 7: e156344. PMID: 35316219, PMCID: PMC9090247, DOI: 10.1172/jci.insight.156344.Peer-Reviewed Original ResearchConceptsSpecificity protein 1DNA damageSp1-dependent mannerProtein 1Activator protein-1HaCaT human immortalized keratinocytesExtracellular matrix componentsTranscription factorsAryl hydrocarbon receptorHuman immortalized keratinocytesMatrix componentsHydrocarbon receptorPotential targetImmortalized keratinocytesROSSun-exposed skinType IV collagenMMP2 expressionAhRMatrix metalloproteinasesMechanistic studiesMMP2IV collagenTopical treatmentMMP-1
2021
ICBP90 Regulates MIF Expression, Glucocorticoid Sensitivity, and Apoptosis at the MIF Immune Susceptibility Locus
Yao J, Leng L, Fu W, Li J, Bronner C, Bucala R. ICBP90 Regulates MIF Expression, Glucocorticoid Sensitivity, and Apoptosis at the MIF Immune Susceptibility Locus. Arthritis & Rheumatology 2021, 73: 1931-1942. PMID: 33844457, DOI: 10.1002/art.41753.Peer-Reviewed Original ResearchMeSH KeywordsAllelesApoptosisCCAAT-Enhancer-Binding ProteinsCell LineFibroblastsGene Expression RegulationGenetic LociGenetic Predisposition to DiseaseGenotypeGlucocorticoidsHumansIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsPromoter Regions, GeneticReceptors, GlucocorticoidUbiquitin-Protein LigasesConceptsMacrophage migration inhibitory factorAutoimmune disease severityMIF -794 CATTRheumatoid synovial fibroblastsMIF expressionGlucocorticoid receptorGlucocorticoid sensitivitySynovial fibroblastsT cellsDisease severityPeripheral blood T cellsBlood T cellsMigration inhibitory factorGlucocorticoid-treated cellsAP-1Glucocorticoid immunosuppressionMIF promoterMIF genotypeMIF polymorphismsFactor antibodyInflammatory responseT lymphocytesActivator protein-1Glucocorticoid responsivenessInhibitory factor
2019
LMO7 Is a Negative Feedback Regulator of Transforming Growth Factor β Signaling and Fibrosis
Xie Y, Ostriker AC, Jin Y, Hu H, Sizer AJ, Peng G, Morris AH, Ryu C, Herzog EL, Kyriakides T, Zhao H, Dardik A, Yu J, Hwa J, Martin KA. LMO7 Is a Negative Feedback Regulator of Transforming Growth Factor β Signaling and Fibrosis. Circulation 2019, 139: 679-693. PMID: 30586711, PMCID: PMC6371979, DOI: 10.1161/circulationaha.118.034615.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell ProliferationCells, CulturedDisease Models, AnimalExtracellular MatrixFeedback, PhysiologicalFibrosisHyperplasiaIntegrin alphaVbeta3LIM Domain ProteinsMaleMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaSignal TransductionTranscription Factor AP-1Transcription FactorsTransforming Growth Factor beta1Vascular RemodelingVascular System InjuriesConceptsSmooth muscle cellsActivator protein-1 (AP-1) transcription factorExtracellular matrixProtein-1 transcription factorTransforming Growth Factor β SignalingGrowth factor β signalingMouse smooth muscle cellsTGF-β1 target genesHuman smooth muscle cellsActivator protein-1Muscle-specific deletionNegative feedback regulatorTGF-β pathwayECM protein expressionSmad3 phosphorylationNegative feedback regulationTranscription factorsArteriovenous fistulaECM depositionDomain interactsTGF-β proteinTarget genesLMO7TGF-β treatmentGrowth factor β
2016
TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions
Rai R, Chen Y, Lei M, Chang S. TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions. Nature Communications 2016, 7: 10881. PMID: 26941064, PMCID: PMC4785230, DOI: 10.1038/ncomms10881.Peer-Reviewed Original ResearchConceptsRepressor/activator protein 1Telomere length controlTranscriptional gene regulationRepair of telomeresTelomere end protectionNon-homologous endActivator protein-1Myb domainChromosome fusionsYeast Rap1Gene regulationHDR pathwayEnd protectionBasic domainTelomere lossTelomeresHuman cellsHR factorsProtein 1Length controlPARP1Free fusionInappropriate processingTRF2Important role
2012
Polycystin-1 regulates amphiregulin expression through CREB and AP1 signalling: implications in ADPKD cell proliferation
Aguiari G, Bizzarri F, Bonon A, Mangolini A, Magri E, Pedriali M, Querzoli P, Somlo S, Harris PC, Catizone L, del Senno L. Polycystin-1 regulates amphiregulin expression through CREB and AP1 signalling: implications in ADPKD cell proliferation. Journal Of Molecular Medicine 2012, 90: 1267-1282. PMID: 22570239, PMCID: PMC4028691, DOI: 10.1007/s00109-012-0902-3.Peer-Reviewed Original ResearchMeSH KeywordsAmphiregulinAnimalsCell ProliferationCyclic AMPCyclic AMP Response Element-Binding ProteinEGF Family of ProteinsGene SilencingGlycoproteinsHEK293 CellsHumansIntercellular Signaling Peptides and ProteinsMiceMutagenesisMutationOligonucleotide Array Sequence AnalysisPhosphorylationPolycystic Kidney, Autosomal DominantPromoter Regions, GeneticSignal TransductionTranscription Factor AP-1TRPP Cation ChannelsConceptsActivator protein-1Cystic cellsCell proliferationFull-length PC1ADPKD cell proliferationCell growthEpidermal growth factor-like peptidesGrowth factor-like peptidesAutosomal dominant polycystic kidney diseaseRenal cyst developmentAbnormal cell proliferationChromatin immunoprecipitationPolycystin-1Key activatorEGFR activityMicroarray analysisAmphiregulin genesNew potential therapeutic targetsLuciferase assayFactor-like peptidesProtein 1Potential therapeutic targetCell linesAmphiregulin expressionCyst development
2002
Activation Time Course of Activator Protein-1 and Effect of Proline Dithiocarbamate During Ischemia-Reperfusion in Rat Skeletal Muscle
Lefler SR, Lille ST, Huemer G, Tucker R, Murray T, Schoeller T, Mulligan DC. Activation Time Course of Activator Protein-1 and Effect of Proline Dithiocarbamate During Ischemia-Reperfusion in Rat Skeletal Muscle. Annals Of Plastic Surgery 2002, 49: 654-659. PMID: 12461450, DOI: 10.1097/00000637-200212000-00016.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryAP-1 activationRat skeletal muscleActivator protein-1Nuclear factor-kappa B (NF-κB) inhibitorSkeletal muscleAP-1Hours of reperfusionProtein 1Proline dithiocarbamateIschemia reperfusionIschemic periodIntravenous administrationBiphasic patternB inhibitorReperfusionActivation time courseFurther elucidationTime courseInjuryExpression of genesPerfusionDeleterious effectsMuscleHours
2000
Role of mitogen-activated protein kinases in pulmonary endothelial cells exposed to cyclic strain
Kito H, Chen E, Wang X, Ikeda M, Azuma N, Nakajima N, Gahtan V, Sumpio B. Role of mitogen-activated protein kinases in pulmonary endothelial cells exposed to cyclic strain. Journal Of Applied Physiology 2000, 89: 2391-2400. PMID: 11090594, DOI: 10.1152/jappl.2000.89.6.2391.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCattleCell MovementCells, CulturedEndothelium, VascularEnzyme ActivationEnzyme InhibitorsFlavonoidsImidazolesJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphorylationPromoter Regions, GeneticPulmonary ArteryPyridinesResponse ElementsStress, MechanicalTetradecanoylphorbol AcetateTranscription Factor AP-1ConceptsPD 98059Activator protein-1SB 203580Protein kinaseBovine pulmonary arterial endothelial cellsPulmonary arterial endothelial cellsArterial endothelial cellsMAPK kinase kinase-1Mitogen-activated protein kinase activationMitogen-activated protein kinaseExtracellular signal-regulated kinaseTerminal protein kinaseKinase kinase 1AP-1/Cell alignmentERK kinase inhibitorProtein kinase activationSignal-regulated kinaseEndothelial cellsTranscriptional activationInactive mutantActivated MAPKsKinase activationKinase 1Transient transfection
1995
Cyclic strain causes heterogeneous induction of transcription factors, AP-1, CRE binding protein and NF-kB, in endothelial cells: Species and vascular bed diversity
Du W, Mills I, Sumpio B. Cyclic strain causes heterogeneous induction of transcription factors, AP-1, CRE binding protein and NF-kB, in endothelial cells: Species and vascular bed diversity. Journal Of Biomechanics 1995, 28: 1485-1491. PMID: 8666588, DOI: 10.1016/0021-9290(95)00096-8.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 2AnimalsAortaCattleCell DivisionCyclic AMP Response Element-Binding ProteinEndothelium, VascularEpoprostenolGene Expression RegulationGenes, Immediate-EarlyHumansNF-kappa BNuclear ProteinsPhenotypeProtein Kinase CSpecies SpecificityStress, MechanicalTime FactorsTranscription Factor AP-1Transcription FactorsUmbilical VeinsConceptsHuman umbilical vein endothelial cellsBovine aortic endothelial cellsActivator protein-1NF-kBEndothelial cellsVascular bedDifferent vascular bedsUmbilical vein endothelial cellsAortic endothelial cellsCultured endothelial cellsTranscription factor activator protein-1Vein endothelial cellsProstacyclin secretionStretch-induced activationImmediate early genesEC exposureNuclear factorTime pointsHeterogeneous inductionCAMP response elementProtein 1Biphasic mannerSignificant inductionDivergent effectsHuman aorta
1994
Exposure of Endothelial Cells to Cyclic Strain Induces c-fos, fosB and c-jun But not jun B or jun D and Increases the Transcription Factor AP-1
Sumpio B, Du W, Xu W. Exposure of Endothelial Cells to Cyclic Strain Induces c-fos, fosB and c-jun But not jun B or jun D and Increases the Transcription Factor AP-1. Endothelium 1994, 2: 149-156. DOI: 10.3109/10623329409088469.Peer-Reviewed Original ResearchActivator protein-1Gel shiftHuman umbilical vein ECTranscriptional activator AP-1Fos family genesTranscription factor AP-1Intracellular regulatory eventsC-jun geneFactor AP-1Protein kinase CC-fosFamily genesSteady-state levelsActivation of PKCNuclear proteinsRegulatory eventsJun genesExpression of JUNGene expressionKinase CC-JunNorthern blotEndothelial cell proliferationDownstream inductionGenes
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