2005
Experience-Driven Plasticity of Visual Cortex Limited by Myelin and Nogo Receptor
McGee AW, Yang Y, Fischer QS, Daw NW, Strittmatter SM. Experience-Driven Plasticity of Visual Cortex Limited by Myelin and Nogo Receptor. Science 2005, 309: 2222-2226. PMID: 16195464, PMCID: PMC2856689, DOI: 10.1126/science.1114362.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChondroitin Sulfate ProteoglycansDarknessDominance, OcularElectrophysiologyGamma-Aminobutyric AcidGene TargetingGPI-Linked ProteinsMiceMice, Inbred C57BLMutationMyelin Basic ProteinMyelin ProteinsMyelin SheathMyelin-Associated GlycoproteinNeuritesNeuronal PlasticityNeuronsNogo ProteinsNogo Receptor 1Photic StimulationReceptors, Cell SurfaceSignal TransductionVisual CortexConceptsOcular dominanceOcular dominance plasticityNogo-66 receptorExperience-dependent plasticityPostnatal critical periodCritical periodFunctional recoveryAxonal regenerationMonocular deprivationNogo receptorDays postnatalVisual cortexNeural circuitryPathological traumaJuvenile ageMyelinReceptorsNGRPlasticityPostnatalCortexOMgpTraumaNogoCessation
1998
GAP‐43 Augmentation of G Protein‐Mediated Signal Transduction Is Regulated by Both Phosphorylation and Palmitoylation
Nakamura F, Strittmatter P, Strittmatter S. GAP‐43 Augmentation of G Protein‐Mediated Signal Transduction Is Regulated by Both Phosphorylation and Palmitoylation. Journal Of Neurochemistry 1998, 70: 983-992. PMID: 9489717, DOI: 10.1046/j.1471-4159.1998.70030983.x.Peer-Reviewed Original ResearchConceptsG protein activationG-protein mediated signal transductionProtein kinase C phosphorylation sitesG-protein-coupled receptor stimulationKinase C phosphorylation sitesProtein activationG-protein-coupled signalsNeuronal protein GAP-43C phosphorylation sitesSignal transduction processesProtein kinase CGrowth cone membranePhosphorylation sitesSignal transductionXenopus laevis oocytesGAP-43Transduction processesKinase CResidues 41Second domainLaevis oocytesCone membraneCalmodulinProtein GAP-43Oocytes
1993
Functional expression of sodium channel mutations identified in families with periodic paralysis
Cannon S, Strittmatter S. Functional expression of sodium channel mutations identified in families with periodic paralysis. Neuron 1993, 10: 317-326. PMID: 8382500, DOI: 10.1016/0896-6273(93)90321-h.Peer-Reviewed Original ResearchConceptsSodium channel alpha subunitChannel alpha subunitAlpha subunitFunctional expressionMammalian cell linesSame functional defectSodium channel mutationsBenign polymorphismsSingle-channel conductanceMutationsChannel mutationsCell linesSubunitsMyotubesFunctional defectsPeriodic paralysisProcess of inactivationPotassium dependenceNoninactivating componentNew regionsInactivationExpressionPolymorphismSodium currentFamily