2013
Metabotropic Glutamate Receptor 5 Is a Coreceptor for Alzheimer Aβ Oligomer Bound to Cellular Prion Protein
Um JW, Kaufman AC, Kostylev M, Heiss JK, Stagi M, Takahashi H, Kerrisk ME, Vortmeyer A, Wisniewski T, Koleske AJ, Gunther EC, Nygaard HB, Strittmatter SM. Metabotropic Glutamate Receptor 5 Is a Coreceptor for Alzheimer Aβ Oligomer Bound to Cellular Prion Protein. Neuron 2013, 79: 887-902. PMID: 24012003, PMCID: PMC3768018, DOI: 10.1016/j.neuron.2013.06.036.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCalciumCells, CulturedElongation Factor 2 KinaseHEK293 CellsHumansMiceNeuronsOocytesPhosphorylationPost-Synaptic DensityProto-Oncogene Proteins c-fynPrPC ProteinsReceptor, Metabotropic Glutamate 5Receptors, Metabotropic GlutamateSignal TransductionXenopusConceptsDisease pathophysiologyHuman AD brain extractsCellular prion proteinMetabotropic glutamate receptor 5Postsynaptic densityDendritic spine lossAD brain extractsMetabotropic glutamate receptorsGlutamate receptor 5Alzheimer's disease pathophysiologyExtracellular AβOsMGluR5 antagonismPrion proteinSpine lossSynapse densityGlutamate receptorsIntracellular calciumMGluR5Receptor 5Neuronal functionAβOsBrain extractsAβ oligomersFyn kinasePSD proteins
2000
Brain‐Derived Neurotrophic Factor Induces Excitotoxic Sensitivity in Cultured Embryonic Rat Spinal Motor Neurons Through Activation of the Phosphatidylinositol 3‐Kinase Pathway
Fryer H, Wolf D, Knox R, Strittmatter S, Pennica D, O'Leary R, Russell D, Kalb R. Brain‐Derived Neurotrophic Factor Induces Excitotoxic Sensitivity in Cultured Embryonic Rat Spinal Motor Neurons Through Activation of the Phosphatidylinositol 3‐Kinase Pathway. Journal Of Neurochemistry 2000, 74: 582-595. PMID: 10646509, DOI: 10.1046/j.1471-4159.2000.740582.x.Peer-Reviewed Original ResearchConceptsHerpes simplex virusBrain-derived neurotrophic factorNeurotrophic factorMotor neuronsGlial-derived neurotrophic factorRat spinal motor neuronsEffects of BDNFRat motor neuronsSpinal motor neuronsActivation of TrkBPI3K pathwayExcitotoxic deathNeurotrophin-3Receptor p75NTRBDNFSimplex virusIntracellular Ca2Cardiotrophin-1NeuronsReceptor-mediated cell deathK pathwayPI3KDominant negative p85 subunitTrkBCell death
1999
Excitotoxic Death of a Subset of Embryonic Rat Motor Neurons In Vitro
Fryer HJ, Knox RJ, Strittmatter SM, Kalb RG. Excitotoxic Death of a Subset of Embryonic Rat Motor Neurons In Vitro. Journal Of Neurochemistry 1999, 72: 500-513. PMID: 9930721, DOI: 10.1046/j.1471-4159.1999.0720500.x.Peer-Reviewed Original ResearchMeSH Keywords6-Cyano-7-nitroquinoxaline-2,3-dioneAlpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsCalciumCalcium ChannelsCalcium Channels, L-TypeCell Culture TechniquesCell DeathCells, CulturedDizocilpine MaleateDose-Response Relationship, DrugExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsFemaleGlutamic AcidGlutamineGlycineKainic AcidMembrane PotentialsMotor NeuronsN-MethylaspartateNerve Tissue ProteinsNeurotoxinsPotassiumPregnancyRatsRats, Sprague-DawleyReceptors, AMPAReceptors, Kainic AcidReceptors, N-Methyl-D-AspartateSpinal CordConceptsGlutamate receptor agonistsMotor neuronsReceptor agonistNon-NMDA glutamate receptor agonistsIntracellular Ca2Agonist-evoked intracellular Ca2Specific glutamate receptor agonistsIonotropic glutamate receptor activationReceptor subtype-specific antagonistsSpinal cord motor neuronsSubtype-specific antagonistsCultured motor neuronsGlutamate receptor expressionRat motor neuronsMost motor neuronsGlutamate receptor activationL-type Ca2Subunit-specific antibodiesTime-dependent mannerReceptor phenotypeChannel antagonistsReceptor expressionNeurotoxic effectsRoute of entryExtracellular Ca2
1995
An activated mutant of the a subunit of Go increases neurite outgrowth via protein kinase C
Xie R, Li L, Goshima Y, Strittmatter S. An activated mutant of the a subunit of Go increases neurite outgrowth via protein kinase C. Brain Research 1995, 87: 77-86. PMID: 7554235, DOI: 10.1016/0165-3806(95)00061-h.Peer-Reviewed Original ResearchMeSH KeywordsAlkaloidsAnimalsCalciumCalcium Channel BlockersCalcium-Transporting ATPasesDose-Response Relationship, DrugEnzyme InhibitorsEthers, CyclicGallic AcidGTP-Binding ProteinsMutationNeuritesOkadaic AcidPC12 CellsProtein Kinase CRatsSecond Messenger SystemsStaurosporineTerpenesThapsigarginTransfectionConceptsProtein kinase CAlpha oKinase CNeurite outgrowthNeuronal growth cone membraneProtein phosphatase inhibitorSignal transduction cascadeDifferent signal transduction cascadesNeurite extensionGrowth cone membranePhorbol ester treatmentPhosphatase inhibitorTransduction cascadeOkadaic acidEster treatmentPhorbol esterCone membraneNeurite elongationMutantsIntracellular mechanismsKinase inhibitorsOutgrowthSubunitsIntracellular calcium levelsPresence of agents
1993
GAP-43 augments G protein-coupled receptor transduction in Xenopus laevis oocytes.
Strittmatter SM, Cannon SC, Ross EM, Higashijima T, Fishman MC. GAP-43 augments G protein-coupled receptor transduction in Xenopus laevis oocytes. Proceedings Of The National Academy Of Sciences Of The United States Of America 1993, 90: 5327-5331. PMID: 7685122, PMCID: PMC46709, DOI: 10.1073/pnas.90.11.5327.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAnimalsCalciumCattleChloride ChannelsFemaleGAP-43 ProteinGrowth SubstancesGTP-Binding ProteinsHumansInositol 1,4,5-TrisphosphateIon Channel GatingIon ChannelsKineticsMembrane GlycoproteinsMembrane PotentialsMembrane ProteinsNerve Tissue ProteinsOocytesReceptors, MuscarinicRecombinant ProteinsSignal TransductionXenopus laevisConceptsGAP-43Receptor transductionG protein-coupled receptor agonistsCalcium-activated chloride channelXenopus laevis oocytesProtein GAP-43Neuronal protein GAP-43Receptor agonistInjection of inositolLaevis oocytesReceptor stimulationOocyte responseGrowth cone motilityChloride channelsSignal transductionIntracellular regulatorsIntracellular signalsMolecular mechanismsTransductionOocytesHigh levelsAgonists
1991
The neuronal growth cone as a specialized transduction system
Strittmatter S, Fishman M. The neuronal growth cone as a specialized transduction system. BioEssays 1991, 13: 127-134. PMID: 1831353, DOI: 10.1002/bies.950130306.Peer-Reviewed Original ResearchConceptsGene programGrowth conesNeuronal growth conesExtracellular stimuliEnvironmental signalsExtracellular signalsMembrane proteinsTransduction systemCell shapeGrowth cone behaviorExtracellular matrixGrowth cone activityCone behaviorGrowth programMechanical forcesNeuronal growthProteinTransduction devicesIntrinsic factorsGAP-43Molecular sitesGTPPossible componentsSitesCone activity