2016
G protein-coupled receptors (GPCRs) That Signal via Protein Kinase A (PKA) Cross-talk at Insulin Receptor Substrate 1 (IRS1) to Activate the phosphatidylinositol 3-kinase (PI3K)/AKT Pathway*
Law N, White M, Hunzicker-Dunn M. G protein-coupled receptors (GPCRs) That Signal via Protein Kinase A (PKA) Cross-talk at Insulin Receptor Substrate 1 (IRS1) to Activate the phosphatidylinositol 3-kinase (PI3K)/AKT Pathway*. Journal Of Biological Chemistry 2016, 291: 27160-27169. PMID: 27856640, PMCID: PMC5207145, DOI: 10.1074/jbc.m116.763235.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCells, CulturedCyclic AMP-Dependent Protein KinasesFemaleGranulosa CellsHumansInsulin Receptor Substrate ProteinsOvarian FolliclePhosphatidylinositol 3-KinasePhosphorylationProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledSignal TransductionThyroid NeoplasmsConceptsG protein-coupled receptorsInsulin receptor substrate-1PI3K/Akt cascadeProtein-coupled receptorsAkt cascadeSer/ThrReceptor substrate-1PI3K/Akt activationInsulin-like growth factor-1PI3K/Akt pathwayGranulosa cellsConserved mechanismPI3K/AktCellular functionsProtein kinaseSer residuesSubstrate-1Myosin phosphataseSubunit 1Akt activationCell survivalAutocrine/paracrine mannerViral oncoproteinsAkt pathwayPreantral granulosa cells
2003
cAMP promotes pancreatic β-cell survival via CREB-mediated induction of IRS2
Jhala U, Canettieri G, Screaton R, Kulkarni R, Krajewski S, Reed J, Walker J, Lin X, White M, Montminy M. cAMP promotes pancreatic β-cell survival via CREB-mediated induction of IRS2. Genes & Development 2003, 17: 1575-1580. PMID: 12842910, PMCID: PMC196130, DOI: 10.1101/gad.1097103.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell LineCell SurvivalColforsinCyclic AMPCyclic AMP Response Element-Binding ProteinDiabetes MellitusGene Expression RegulationGlucagonGlucagon-Like Peptide 1GlucoseGlucose IntoleranceHumansInsulinInsulin Receptor Substrate ProteinsInsulin-Like Growth Factor IIntracellular Signaling Peptides and ProteinsIslets of LangerhansMiceMice, TransgenicPeptide FragmentsPhosphoproteinsPhosphorylationPromoter Regions, GeneticProtein PrecursorsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSignal TransductionTransfectionTransgenesTumor Cells, CulturedConceptsPancreatic β-cell survivalActivity of CREBSecond messenger cAMPSurvival kinase AktΒ-cell survivalKinase AktPathway componentsA-CREBCREB actionExpression of IRS2Cell survivalBeta-cell apoptosisDirect targetIslet cell survivalNovel mechanismCREBIRS2ExpressionCAMPInductionTransgeneAktIGF-1ApoptosisSurvival
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