2005
Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice
Uchida T, Nakamura T, Hashimoto N, Matsuda T, Kotani K, Sakaue H, Kido Y, Hayashi Y, Nakayama K, White M, Kasuga M. Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice. Nature Medicine 2005, 11: 175-182. PMID: 15685168, DOI: 10.1038/nm1187.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Cycle ProteinsCell NucleusCyclin-Dependent Kinase Inhibitor p27Diabetes Mellitus, Type 2Disease Models, AnimalEnzyme InhibitorsHyperglycemiaHyperinsulinismInsulin Receptor Substrate ProteinsInsulin-Like Growth Factor IIntracellular Signaling Peptides and ProteinsIslets of LangerhansLeptinMiceMice, KnockoutPhosphoproteinsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptors, Cell SurfaceReceptors, LeptinSignal TransductionTumor Suppressor ProteinsConceptsCyclin-dependent kinasesInsulin receptor substrate 2Cell cycle progressionPancreatic beta cell proliferationPotential new targetsCompensatory hyperinsulinemiaCycle progressionProtein p27Kip1Substrate 2Type 2 diabetes mellitusPancreatic beta cellsP27Kip1Beta-cell failureBeta-cell proliferationType 2 diabetesLong formNew targetsDeletionDiabetes mellitusDiabetic miceIslet massLeptin receptorBeta cellsAnimal modelsMice
1999
Stimulation of pancreatic beta-cell proliferation by growth hormone is glucose-dependent: signal transduction via janus kinase 2 (JAK2)/signal transducer and activator of transcription 5 (STAT5) with no crosstalk to insulin receptor substrate-mediated mitogenic signalling.
Cousin S, Hügl S, Myers M, White M, Reifel-Miller A, Rhodes C. Stimulation of pancreatic beta-cell proliferation by growth hormone is glucose-dependent: signal transduction via janus kinase 2 (JAK2)/signal transducer and activator of transcription 5 (STAT5) with no crosstalk to insulin receptor substrate-mediated mitogenic signalling. Biochemical Journal 1999, 344 Pt 3: 649-58. PMID: 10585851, PMCID: PMC1220686, DOI: 10.1042/0264-6021:3440649.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportAnimalsCell DivisionCell LineDNA-Binding ProteinsGlucoseGRB2 Adaptor ProteinGrowth HormoneInsulin Receptor Substrate ProteinsInsulin-Like Growth Factor IIntracellular Signaling Peptides and ProteinsIslets of LangerhansJanus Kinase 2Milk ProteinsMitogen-Activated Protein KinasesPhosphoproteinsPhosphorylationProteinsProtein-Tyrosine KinasesProto-Oncogene ProteinsRatsRibosomal Protein S6 KinasesShc Signaling Adaptor ProteinsSignal TransductionSon of Sevenless Protein, DrosophilaSrc Homology 2 Domain-Containing, Transforming Protein 1STAT5 Transcription FactorTrans-ActivatorsConceptsINS-1 cell proliferationSignal transduction pathwaysSignal transductionCell proliferationKinase 2Sevenless-1 proteinMitogenic signal transduction pathwaysJAK2/STAT5 pathwayMitogen-activated protein kinaseInsulin receptor substrateBeta-cell proliferationRat growth hormoneJAK2/STAT5Pancreatic beta cell proliferationMitogenic signalingS6 kinaseProtein kinaseProtein associationTranscription 5Beta-cell lineReceptor substrateDifferent mitogenicRat beta-cell lineDownstream activationIRS-2