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
2004
Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy
McMullen J, Shioi T, Zhang L, Tarnavski O, Sherwood M, Dorfman A, Longnus S, Pende M, Martin K, Blenis J, Thomas G, Izumo S. Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy. Molecular And Cellular Biology 2004, 24: 6231-6240. PMID: 15226426, PMCID: PMC434247, DOI: 10.1128/mcb.24.14.6231-6240.2004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibiotics, AntineoplasticAortaCardiomegalyFemaleFetusGene Expression Regulation, DevelopmentalMiceMice, KnockoutMice, TransgenicOrgan SizePhosphatidylinositol 3-KinasesPhysical Conditioning, AnimalReceptor, IGF Type 1Ribosomal Protein S6 Kinases, 90-kDaSignal TransductionSirolimusStress, MechanicalSwimmingConceptsRibosomal S6 kinaseS6 kinaseOverexpression of S6K1PI3K mutantCritical downstream effectorRibosomal proteinsTransgenic miceCardiac hypertrophyDownstream effectorsK mutantS6KsGrowth factor pathwaysGenetic relationshipsPathological stressProtein synthesisCritical effectorS6K1K pathwayIGF1 receptorFactor 1Factor pathwayPhysiological stressInsulin-like growth factor-1Physiological stimuliKinase
2003
The mTOR/p70 S6K1 pathway regulates vascular smooth muscle cell differentiation
Martin K, Rzucidlo E, Merenick B, Fingar D, Brown D, Wagner R, Powell R. The mTOR/p70 S6K1 pathway regulates vascular smooth muscle cell differentiation. American Journal Of Physiology - Cell Physiology 2003, 286: c507-c517. PMID: 14592809, DOI: 10.1152/ajpcell.00201.2003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAorta, ThoracicBiomarkersCattleCell Cycle ProteinsCell DifferentiationCells, CulturedCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27CyclinsEndothelium, VascularExtracellular Matrix ProteinsImmunosuppressive AgentsMuscle ContractionMuscle, Smooth, VascularPhenotypeProtein KinasesRibosomal Protein S6 Kinases, 70-kDaSignal TransductionSirolimusTOR Serine-Threonine KinasesTumor Suppressor ProteinsConceptsVascular smooth muscle cellsVSMC differentiationVascular smooth muscle cell differentiationSmooth muscle cell differentiationVSMC gene expressionRapamycin-sensitive mTORMuscle cell differentiationContractile morphologyCyclin-dependent kinase inhibitorCell cycle withdrawalExtracellular matrix protein synthesisContractile proteinsMTOR pathway inhibitor rapamycinMuscle alpha-actinTranscriptional controlMatrix protein synthesisNovel functionGene expressionMigratory phenotypeRapamycin inductionMultiple speciesCell differentiationInhibitor rapamycinS6K1 pathwayProtein synthesis