2017
Protein Tyrosine Phosphatase δ Mediates the Sema3A-Induced Cortical Basal Dendritic Arborization through the Activation of Fyn Tyrosine Kinase
Nakamura F, Okada T, Shishikura M, Uetani N, Taniguchi M, Yagi T, Iwakura Y, Ohshima T, Goshima Y, Strittmatter SM. Protein Tyrosine Phosphatase δ Mediates the Sema3A-Induced Cortical Basal Dendritic Arborization through the Activation of Fyn Tyrosine Kinase. Journal Of Neuroscience 2017, 37: 7125-7139. PMID: 28637841, PMCID: PMC6705738, DOI: 10.1523/jneurosci.2519-16.2017.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedCerebral CortexDendritesEnzyme ActivationFemaleGene Expression Regulation, EnzymologicMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeuronal PlasticityProtein-Tyrosine KinasesProto-Oncogene Proteins c-fynReceptor-Like Protein Tyrosine Phosphatases, Class 2Semaphorin-3AConceptsCortical dendritic growthBasal dendritesCultured dorsal root ganglion neuronsCortical layer V neuronsPrimary cultured dorsal root ganglion (DRG) neuronsDorsal root ganglion neuronsWild-type cortical neuronsBasal dendritic arborizationLayer V neuronsAxon guidanceDouble heterozygous mutantsSpecific guidance cuesProtein tyrosine phosphatase δAxon guidance cuesPoor arborizationV neuronsGuidance cuesGanglion neuronsDendritic arborizationCortical neuronsMutant miceSemaphorin 3ASrc kinaseActivation of FynGrowth cone collapse response
2010
MAG and OMgp Synergize with Nogo-A to Restrict Axonal Growth and Neurological Recovery after Spinal Cord Trauma
Cafferty WB, Duffy P, Huebner E, Strittmatter SM. MAG and OMgp Synergize with Nogo-A to Restrict Axonal Growth and Neurological Recovery after Spinal Cord Trauma. Journal Of Neuroscience 2010, 30: 6825-6837. PMID: 20484625, PMCID: PMC2883258, DOI: 10.1523/jneurosci.6239-09.2010.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsBiotinCells, CulturedDextransDisease Models, AnimalFemaleFunctional LateralityGanglia, SpinalGPI-Linked ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutMutationMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNerve Tissue ProteinsNeuronsNogo ProteinsPyramidal TractsReceptors, Cell SurfaceReceptors, SerotoninRecovery of FunctionSpinal Cord InjuriesConceptsAxonal growthSpinal Cord Injury StudyMutant miceGreater axonal growthGreater behavioral recoverySpinal cord traumaWild-type miceAxonal growth inhibitionHeterozygous mutant miceDeficient myelinNeurological recoveryCNS damageTriple-mutant miceBehavioral recoveryCord traumaFunctional recoveryNeurological functionMyelin inhibitorsAxonal regrowthReceptor mechanismsInjury studiesMyelin inhibitionDecoy receptorOptimal chanceMice
2004
Nogo Receptor Antagonism Promotes Stroke Recovery by Enhancing Axonal Plasticity
Lee JK, Kim JE, Sivula M, Strittmatter SM. Nogo Receptor Antagonism Promotes Stroke Recovery by Enhancing Axonal Plasticity. Journal Of Neuroscience 2004, 24: 6209-6217. PMID: 15240813, PMCID: PMC6729662, DOI: 10.1523/jneurosci.1643-04.2004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsBehavior, AnimalDisease Models, AnimalGPI-Linked ProteinsInfarction, Middle Cerebral ArteryMaleMiceMice, KnockoutMyelin ProteinsNeuronal PlasticityNogo ProteinsNogo Receptor 1RatsRats, Sprague-DawleyReceptors, Cell SurfaceReceptors, PeptideRecombinant Fusion ProteinsRecovery of FunctionStrokeTreatment OutcomeConceptsAxonal plasticityStroke recoveryIpsilateral cervical spinal cordMiddle cerebral artery occlusionFocal brain infarctionCerebral artery occlusionCervical spinal cordComplex motor functionContralateral red nucleusUndamaged cortexBrain infarctionArtery occlusionIschemic strokeAxonal sproutingIntracerebroventricular administrationArterial occlusionPharmacological blockadeMotor functionSpinal cordControl animalsRed nucleusAxonal connectionsBehavioral improvementMutant miceStroke