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
2017
Opposing Actions of AKT (Protein Kinase B) Isoforms in Vascular Smooth Muscle Injury and Therapeutic Response
Jin Y, Xie Y, Ostriker AC, Zhang X, Liu R, Lee MY, Leslie KL, Tang W, Du J, Lee SH, Wang Y, Sessa WC, Hwa J, Yu J, Martin KA. Opposing Actions of AKT (Protein Kinase B) Isoforms in Vascular Smooth Muscle Injury and Therapeutic Response. Arteriosclerosis Thrombosis And Vascular Biology 2017, 37: 2311-2321. PMID: 29025710, PMCID: PMC5699966, DOI: 10.1161/atvbaha.117.310053.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesCell Cycle ProteinsCell DifferentiationCell MovementCell ProliferationCells, CulturedDisease Models, AnimalForkhead Transcription FactorsGene Expression RegulationGenetic Predisposition to DiseaseHumansMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaNuclear ProteinsPhenotypePromoter Regions, GeneticProto-Oncogene Proteins c-aktRNA InterferenceRNA, MessengerSignal TransductionSirolimusTime FactorsTrans-ActivatorsTranscription FactorsTransfectionVascular System InjuriesConceptsIntimal hyperplasiaTherapeutic inhibitionVascular smooth muscle injurySmooth muscle-specific deletionSmooth muscle cell proliferationSystemic vascular diseaseSevere intimal hyperplasiaSmooth muscle injuryNew treatment strategiesWild-type miceAkt isoformsMuscle cell proliferationMuscle-specific deletionMechanism of actionVascular smooth muscle cell differentiationCoronary revascularizationSmooth muscle cell differentiationDiabetes mellitusDiabetic patientsControl miceRapamycin therapyVascular diseaseMuscle injuryTherapeutic responseSevere thrombosis
2006
Rapamycin inhibits cell motility by suppression of mTOR-mediated S6K1 and 4E-BP1 pathways
Liu L, Li F, Cardelli J, Martin K, Blenis J, Huang S. Rapamycin inhibits cell motility by suppression of mTOR-mediated S6K1 and 4E-BP1 pathways. Oncogene 2006, 25: 7029-7040. PMID: 16715128, DOI: 10.1038/sj.onc.1209691.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCattleCell Cycle ProteinsCell LineCell MovementCytoprotectionDown-RegulationEnzyme ActivationHumansInsulin-Like Growth Factor IMicePhosphoproteinsPhosphorylationProtein KinasesRibosomal Protein S6 Kinases, 70-kDaSerumSignal TransductionSirolimusTOR Serine-Threonine KinasesTranscription FactorsConceptsCell motilityRNA interferenceEukaryotic initiation factor 4EDownregulation of RaptorType I insulin-like growth factorMTOR kinase activityInitiation factor 4ES6 kinase 1Rapamycin inhibitionTumor cell motilityResistant mutantsSuppression of mTORP70 S6K1Kinase activityKinase 1S6K1Mammalian targetRapamycinProtein 1Effect of rapamycinConsequence of inhibitionCell linesMutantsRaptorsMotility
1997
A Competitive Mechanism of CArG Element Regulation by YY1 and SRF: Implications for Assessment of Phox1/MHox Transcription Factor Interactions at CArG Elements
Martin K, Gualberto A, Kolman M, Lowry J, Walsh K. A Competitive Mechanism of CArG Element Regulation by YY1 and SRF: Implications for Assessment of Phox1/MHox Transcription Factor Interactions at CArG Elements. DNA And Cell Biology 1997, 16: 653-661. PMID: 9174170, DOI: 10.1089/dna.1997.16.653.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCells, CulturedChick EmbryoDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsGene Expression RegulationHomeodomain ProteinsMuscle, SkeletalNuclear ProteinsPoint MutationPromoter Regions, GeneticSequence Analysis, DNASerum Response FactorTranscription FactorsYY1 Transcription FactorConceptsSerum response factorMuscle-specific expressionCArG elementsTranscription factor serum response factorTranscription factor interactionsDNA regulatory elementsMuscle-specific genesSkeletal alpha-actinImmediate early genesCArG boxSRF bindingTranscriptional activationRegulatory elementsPoint mutantsYY1 repressionSerum inductionYY1Regulatory factorsEarly genesYY1 overexpressionAlpha-actinRepressionPoint mutationsResponse factorMutants