2016
Down-regulation of Insulin Receptor Substrate 1 during Hyperglycemia Induces Vascular Smooth Muscle Cell Dedifferentiation*
Xi G, Wai C, White M, Clemmons D. Down-regulation of Insulin Receptor Substrate 1 during Hyperglycemia Induces Vascular Smooth Muscle Cell Dedifferentiation*. Journal Of Biological Chemistry 2016, 292: 2009-2020. PMID: 28003360, PMCID: PMC5290970, DOI: 10.1074/jbc.m116.758987.Peer-Reviewed Original ResearchConceptsInsulin receptor substrate-1Receptor substrate-1IRS-1Differentiated stateSubstrate-1Aberrant signalingMetabolic stressVascular smooth muscle cell dedifferentiationIGF-I stimulationIRS-1 expressionVascular smooth muscle cell migrationScaffold proteinSHPS-1Transcription factorsSmooth muscle cell dedifferentiationSmooth muscle cell migrationMuscle cell dedifferentiationMuscle cell migrationReceptor signalsVSMC dedifferentiationCell migrationInsulin-like growth factor ICell dedifferentiationMajor risk factorDevelopment of atherosclerosis
2011
IRS-2 Deficiency Impairs NMDA Receptor-Dependent Long-term Potentiation
Martín E, Sánchez-Perez A, Trejo J, Martin-Aldana J, Jaimez M, Pons S, Umanzor C, Menes L, White M, Burks D. IRS-2 Deficiency Impairs NMDA Receptor-Dependent Long-term Potentiation. Cerebral Cortex 2011, 22: 1717-1727. PMID: 21955917, PMCID: PMC3388895, DOI: 10.1093/cercor/bhr216.Peer-Reviewed Original ResearchConceptsLong-term potentiationInduction of LTPInsulin receptor substrate 2Activation of FynPotential new componentSynaptic transmissionSynaptic plasticityWild-type controlsSubstrate 2Alzheimer's diseasePostsynaptic N-methyl-D-aspartate receptorsIRS2 expressionN-methyl-D-aspartate receptorsImpairs long-term potentiationInsulin-like growth factor IMechanistic linkNMDA receptor-dependent long-term potentiationType 2 diabeticsBasal synaptic transmissionExpression of NR2AGroups of miceGrowth factor IPaired-pulse facilitationNeurodegenerative disordersTetanus stimulation
1998
Differential Regulation of Insulin Receptor Substrate-2 and Mitogen-Activated Protein Kinase Tyrosine Phosphorylation by Phosphatidylinositol 3-Kinase Inhibitors in SH-SY5Y Human Neuroblastoma Cells*This work was supported by NIH Grants R29-NS-32843 and R01-NS-36778, grants from the American Diabetes Association and Juvenile Diabetes Foundation (to E.L.F.), and a grant from the Millie Schembechler Adrenal Research Fund of the University of Michigan Comprehensive Cancer Center (to E.L.F. and P.S.L.).
Kim B, Leventhal P, White M, Feldman E. Differential Regulation of Insulin Receptor Substrate-2 and Mitogen-Activated Protein Kinase Tyrosine Phosphorylation by Phosphatidylinositol 3-Kinase Inhibitors in SH-SY5Y Human Neuroblastoma Cells*This work was supported by NIH Grants R29-NS-32843 and R01-NS-36778, grants from the American Diabetes Association and Juvenile Diabetes Foundation (to E.L.F.), and a grant from the Millie Schembechler Adrenal Research Fund of the University of Michigan Comprehensive Cancer Center (to E.L.F. and P.S.L.). Endocrinology 1998, 139: 4881-4889. PMID: 9832424, DOI: 10.1210/endo.139.12.6348.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportCalcium-Calmodulin-Dependent Protein KinasesElectrophoresis, Polyacrylamide GelEnzyme InhibitorsGRB2 Adaptor ProteinHumansInsulin Receptor Substrate ProteinsInsulin-Like Growth Factor IIntracellular Signaling Peptides and ProteinsIsoenzymesMitogen-Activated Protein Kinase 1NeuritesNeuroblastomaPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphoproteinsPhosphorylationProteinsShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1Tumor Cells, CulturedTyrosineConceptsInsulin receptor substrate 2IRS-2 tyrosine phosphorylationMitogen-activated protein kinase activationTyrosine phosphorylationProtein kinase activationKinase activationSerine/threonine phosphorylationSubstrate 2Association of Grb2Neurite outgrowthSH-SY5Y human neuroblastomaThreonine phosphorylationNegative regulationSH-SY5Y human neuroblastoma cellsIRS-1Grb2Nervous system growthDifferential regulationPhosphorylationHuman neuroblastoma cellsNeuronal cellsPhosphatidylinositolPI 3Concentration-dependent mannerInsulin-like growth factor IInsulin-like Growth Factor I (IGF-I)-stimulated Pancreatic β-Cell Growth Is Glucose-dependent SYNERGISTIC ACTIVATION OF INSULIN RECEPTOR SUBSTRATE-MEDIATED SIGNAL TRANSDUCTION PATHWAYS BY GLUCOSE AND IGF-I IN INS-1 CELLS*
Hügl S, White M, Rhodes C. Insulin-like Growth Factor I (IGF-I)-stimulated Pancreatic β-Cell Growth Is Glucose-dependent SYNERGISTIC ACTIVATION OF INSULIN RECEPTOR SUBSTRATE-MEDIATED SIGNAL TRANSDUCTION PATHWAYS BY GLUCOSE AND IGF-I IN INS-1 CELLS*. Journal Of Biological Chemistry 1998, 273: 17771-17779. PMID: 9651378, DOI: 10.1074/jbc.273.28.17771.Peer-Reviewed Original ResearchConceptsInsulin-like growth factor IGrowth factor IBeta-cell proliferationINS-1 cell proliferationCell proliferationFactor IMM glucoseCombination of IGFPancreatic β-cell growthPancreatic beta-cell lineBeta-cell lineΒ-cell growthINS-1 cellsNM IGFBeta-cell mitogenesisCertain growth factorsSignaling mechanismSignal transduction pathwaysGlucose metabolismIGFCell proliferation rateGrowth factorIRS-2Transduction pathwaysGlucose concentration