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
2000
Regulation of Ribosomal S6 Kinase 2 by Effectors of the Phosphoinositide 3-Kinase Pathway*
Martin K, Schalm S, Richardson C, Romanelli A, Keon K, Blenis J. Regulation of Ribosomal S6 Kinase 2 by Effectors of the Phosphoinositide 3-Kinase Pathway*. Journal Of Biological Chemistry 2000, 276: 7884-7891. PMID: 11108711, DOI: 10.1074/jbc.m006969200.Peer-Reviewed Original ResearchConceptsProtein kinase CzetaC-terminusPhosphoinositide-dependent kinase 1Ribosomal S6 kinase 2S6 kinase 2PI3K effectorsRibosomal S6 kinaseRibosomal protein S6Agonist-dependent activationS6 kinaseProtein S6Kinase activityKinase 2Kinase 1Translational capacityS6K2Terminal sequencePhysiological roleImportant regulatorRapamycin (mTOR) pathwayMammalian targetS6K1Basal activationTerminusHomolog