2019
Promoters to Study Vascular Smooth Muscle
Chakraborty R, Saddouk FZ, Carrao AC, Krause DS, Greif DM, Martin KA. Promoters to Study Vascular Smooth Muscle. Arteriosclerosis Thrombosis And Vascular Biology 2019, 39: 603-612. PMID: 30727757, PMCID: PMC6527360, DOI: 10.1161/atvbaha.119.312449.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCell LineCell LineageCell TransdifferentiationGene Expression RegulationGene Knockout TechniquesGene TargetingHumansMiceMicrofilament ProteinsMuscle ProteinsMuscle, Smooth, VascularMyocytes, Smooth MuscleMyofibroblastsMyosin Heavy ChainsNeovascularization, PathologicNeovascularization, PhysiologicPhenotypePromoter Regions, GeneticRecombinant Fusion ProteinsConceptsSmooth muscle cellsCre driver linesDiversity of phenotypesMuscle cell typesVisceral smooth muscle cellsSMC transdifferentiationActa2 promoterRemarkable plasticityExciting new eraSMC functionCell typesCre linesEmbryonic heartExciting discoveriesPhenotypeMuscle cellsPerivascular adipocytesPromoterVascular smooth muscleNonmuscular cellsExpressionMyeloid cellsCardiovascular phenotypesCellsBlood vessel wall
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
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 factorMutantsDown-Regulation of P2U-Purinergic Nucleotide Receptor Messenger RNA Expression During In Vitro Differentiation of Human Myeloid Leukocytes by Phorbol Esters or Inflammatory Activators
Martin K, Kertesy S, Dubyak G. Down-Regulation of P2U-Purinergic Nucleotide Receptor Messenger RNA Expression During In Vitro Differentiation of Human Myeloid Leukocytes by Phorbol Esters or Inflammatory Activators. Molecular Pharmacology 1997, 51: 97-108. PMID: 9016351, DOI: 10.1124/mol.51.1.97.Peer-Reviewed Original ResearchConceptsTHP-1 monocytesHL-60 cellsMRNA levelsMyeloid leukocytesReceptor messenger RNA expressionMonocyte/macrophage phenotypeMessenger RNA expressionInositol phospholipid hydrolysisNeutrophil phenotypeInflammatory activationHL-60 granulocytesUndifferentiated HL-60 cellsInflammatory activatorsInflammatory macrophagesAcute exposureMacrophage phenotypeNucleotide receptorsHuman epithelial cellsTissue-specific mechanismsEpithelial cellsRNA expressionLeukocytesDown regulationDibutyryl cAMPHuman keratinocytes