2005
Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents
Morino K, Petersen KF, Dufour S, Befroy D, Frattini J, Shatzkes N, Neschen S, White MF, Bilz S, Sono S, Pypaert M, Shulman GI. Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents. Journal Of Clinical Investigation 2005, 115: 3587-3593. PMID: 16284649, PMCID: PMC1280967, DOI: 10.1172/jci25151.Peer-Reviewed Original ResearchMeSH KeywordsBiopsyBlood GlucoseBlotting, WesternBody Mass IndexBody WeightDiabetes Mellitus, Type 2DNA, MitochondrialFamily HealthFemaleGene Expression RegulationGlucose Clamp TechniqueGlucose Tolerance TestHumansHyperinsulinismImmunoprecipitationInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceLipidsMaleMicroscopy, ElectronMicroscopy, Electron, TransmissionMitochondriaMusclesPhosphoproteinsPhosphorylationProtein Serine-Threonine KinasesReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSerineSignal TransductionTime FactorsTranscription, GeneticTriglyceridesConceptsInsulin-resistant offspringIR offspringType 2 diabetesInsulin-stimulated muscle glucose uptakeType 2 diabetic parentsIntramyocellular lipid contentHyperinsulinemic-euglycemic clampMuscle glucose uptakeIRS-1 serine phosphorylationMuscle mitochondrial densityMitochondrial densityMuscle biopsy samplesSerine kinase cascadeInsulin-stimulated Akt activationDiabetic parentsInsulin resistanceControl subjectsBiopsy samplesGlucose uptakeLipid accumulationMitochondrial dysfunctionInsulin signalingAkt activationEarly defectsMuscle
2002
Interleukin-4-mediated Protection of Primary B Cells from Apoptosis through Stat6-dependent Up-regulation of Bcl-xL*
Wurster A, Rodgers V, White M, Rothstein T, Grusby M. Interleukin-4-mediated Protection of Primary B Cells from Apoptosis through Stat6-dependent Up-regulation of Bcl-xL*. Journal Of Biological Chemistry 2002, 277: 27169-27175. PMID: 12023955, DOI: 10.1074/jbc.m201207200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBcl-X ProteinBlotting, NorthernB-LymphocytesCell DeathCells, CulturedImmunoblottingInterleukin-4LuciferasesLymphocytesMicePromoter Regions, GeneticPropidiumProtein BindingProto-Oncogene Proteins c-bcl-2RetroviridaeSignal TransductionSTAT6 Transcription FactorTime FactorsTrans-ActivatorsTranscription, GeneticTransfectionUp-RegulationConceptsFas-induced cell deathIL-4B cellsPrimary B cellsBcl-xLCell deathBcl-2 family membersBcl-xL transcriptionB lymphocyte developmentB lymphocyte apoptosisSTAT6-dependent mannerAnti-apoptotic cytokinesActivation of STAT6Splenic B cellsAnti-apoptotic activityIL-4 stimulationInterleukin-4Lymphocyte apoptosisBcl-xL.B lymphocytesMolecular eventsSubsequent transcriptionCytokine receptorsLymphocyte developmentCell survival
1998
Insulin receptor substrate-2 amino acid polymorphisms are not associated with random type 2 diabetes among Caucasians.
Bernal D, Almind K, Yenush L, Ayoub M, Zhang Y, Rosshani L, Larsson C, Pedersen O, White M. Insulin receptor substrate-2 amino acid polymorphisms are not associated with random type 2 diabetes among Caucasians. Diabetes 1998, 47: 976-979. PMID: 9604879, DOI: 10.2337/diabetes.47.6.976.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceDiabetes Mellitus, Type 2ExonsFemaleFetusGene Expression RegulationHumansInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsMaleMolecular Sequence DataOrgan SpecificityPhosphoproteinsPolymorphism, GeneticReceptor, InsulinRNA, MessengerSequence AlignmentSequence Homology, Amino AcidTranscription, GeneticWhite People