2014
Phenotypic differences in hiPSC NPCs derived from patients with schizophrenia
Brennand K, Savas J, Kim Y, Tran N, Simone A, Hashimoto-Torii K, Beaumont K, Kim H, Topol A, Ladran I, Abdelrahim M, Matikainen-Ankney B, Chao S, Mrksich M, Rakic P, Fang G, Zhang B, Yates J, Gage F. Phenotypic differences in hiPSC NPCs derived from patients with schizophrenia. Molecular Psychiatry 2014, 20: 361-368. PMID: 24686136, PMCID: PMC4182344, DOI: 10.1038/mp.2014.22.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsAntipsychotic AgentsCell DifferentiationCell MovementCells, CulturedFemaleGene ExpressionHumansMaleMiceMice, Inbred C57BLMice, TransgenicMitochondriaNeural Cell Adhesion MoleculesNeural Stem CellsOxidative StressPhenotypePluripotent Stem CellsProsencephalonProteomicsReactive Oxygen SpeciesSchizophreniaYoung AdultConceptsHiPSC neural progenitor cellsNeural progenitor cellsHuman-induced pluripotent stem cellsHiPSC-derived neuronsGene expressionGene expression comparisonsStable isotope labelingProteomic mass spectrometry analysisAbnormal gene expressionPluripotent stem cellsOxidative stressCytoskeletal remodelingMass spectrometry analysisCellular phenotypesExpression comparisonsDevelopmental mechanismsIsotope labelingPhenotypic differencesBrainSpan AtlasDisease predispositionAmino acidsScalable assayNPC phenotypeStem cellsProgenitor cells
2001
JNK3 contributes to c‐Jun activation and apoptosis but not oxidative stress in nerve growth factor‐deprived sympathetic neurons
Bruckner S, Tammariello S, Kuan C, Flavell R, Rakic P, Estus S. JNK3 contributes to c‐Jun activation and apoptosis but not oxidative stress in nerve growth factor‐deprived sympathetic neurons. Journal Of Neurochemistry 2001, 78: 298-303. PMID: 11461965, DOI: 10.1046/j.1471-4159.2001.00400.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisCells, CulturedGenes, junGenotypeIsoenzymesMiceMice, KnockoutMitogen-Activated Protein Kinase 10Mitogen-Activated Protein KinasesNerve Growth FactorNerve Tissue ProteinsNeuronsOxidative StressPhosphorylationProtein-Tyrosine KinasesProto-Oncogene Proteins c-junReverse Transcriptase Polymerase Chain ReactionSuperior Cervical GanglionConceptsJun kinaseC-Jun phosphorylationC-JunDominant negative proteinSympathetic neuronal deathProtein kinase pathwayOxidative stressC-jun inductionC-Jun activationPhosphorylated c-JunApoptotic roleJNK kinaseKinase pathwayNegative proteinJNK isoformsJNK pathwayOverall pathwayNeuronal deathSympathetic neuronsApoptosisJNK3NGF deprivationKinasePhosphorylationCritical roleBcl-XL–Caspase-9 Interactions in the Developing Nervous System: Evidence for Multiple Death Pathways
Zaidi A, D'Sa-Eipper C, Brenner J, Kuida K, Zheng T, Flavell R, Rakic P, Roth K. Bcl-XL–Caspase-9 Interactions in the Developing Nervous System: Evidence for Multiple Death Pathways. Journal Of Neuroscience 2001, 21: 169-175. PMID: 11150333, PMCID: PMC6762421, DOI: 10.1523/jneurosci.21-01-00169.2001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBcl-2-Associated X ProteinBcl-X ProteinCaspase 3Caspase 9CaspasesCells, CulturedCytarabineGanglia, SpinalGenes, LethalHeterozygoteHomozygoteImmunohistochemistryIn Situ Nick-End LabelingLiverMiceMice, KnockoutNervous SystemNeuronsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2TelencephalonTumor Suppressor Protein p53ConceptsGene family membersCaspase-9 deficiencyCaspase-9Telencephalic neural precursor cellsCell deathDouble homozygous mutantsCaspase family membersMultiple death pathwaysNormal nervous system developmentBcl-2Nervous system developmentBax-deficient neuronsNeuronal apoptosisTelencephalic neuronsDeficient embryosNeural precursor cellsDeath pathwaysFamily membersHomozygous mutantsApoptotic pathwayObligate pathwayBcl-xLApoptosis inducersDeficient neuronsTargeted disruption
2000
Amyloid Beta-Induced Neuronal Death is Bax-Dependent but Caspase-Independent
Selznick L, Zheng T, Flavell R, Rakic P, Roth K. Amyloid Beta-Induced Neuronal Death is Bax-Dependent but Caspase-Independent. Journal Of Neuropathology & Experimental Neurology 2000, 59: 271-279. PMID: 10759182, DOI: 10.1093/jnen/59.4.271.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid Chloromethyl KetonesAmyloid beta-PeptidesAnimalsApoptosisBcl-2-Associated X ProteinCaspase 3Caspase InhibitorsCaspasesCell DeathCells, CulturedCysteine Proteinase InhibitorsDose-Response Relationship, DrugFemaleGlycoproteinsIn Situ Nick-End LabelingMaleMiceMice, KnockoutMicrotubule-Associated ProteinsMicrotubulesNeuronsPaclitaxelProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2TelencephalonConceptsNeuronal deathNeuronal apoptosisCaspase-3 activationTelencephalic neuronsFibrillar amyloid-beta (Abeta) peptidesAbeta-induced neuronal apoptosisAD treatment strategiesAbeta-induced neuronal deathPathogenesis of ADAlzheimer's disease brainEffects of AbetaAmyloid-beta peptideApoptotic nuclear featuresUnderlying pathophysiologyTreatment strategiesDisease brainSenile plaquesNeurotoxic effectsAmyloid betaCalpain inhibitionPharmacological inhibitionBeta peptideNuclear featuresAbetaCaspase-3
1999
Contact-Dependent Inhibition of Cortical Neurite Growth Mediated by Notch Signaling
Šestan N, Artavanis-Tsakonas S, Rakic P. Contact-Dependent Inhibition of Cortical Neurite Growth Mediated by Notch Signaling. Science 1999, 286: 741-746. PMID: 10531053, DOI: 10.1126/science.286.5440.741.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell CommunicationCell CountCell DifferentiationCell MovementCell NucleusCell SizeCells, CulturedCerebral CortexContact InhibitionHumansLigandsMembrane ProteinsMiceMitosisNeuritesNeuronsProtein Structure, TertiaryReceptor, Notch1Receptor, Notch2Receptors, Cell SurfaceSignal TransductionTranscription FactorsTranscriptional ActivationUp-RegulationConceptsNeurite growthMouse cerebral cortexCapacity of neuronsCortical neurite growthStudy of neuronsInhibition of NotchCerebral cortexNotch signalingCortical neuronsNotch activityMature neuronsInterneuronal contactsRetraction of neuritesHigh Notch activityNeuronsNeuronal growthNeuritesContact-dependent inhibitionExuberant growthNeurite extensionNotch receptorsInhibitionLow Notch activitySignalingActivityProcessing of the Notch Ligand Delta by the Metalloprotease Kuzbanian
Qi H, Rand M, Wu X, Sestan N, Wang W, Rakic P, Xu T, Artavanis-Tsakonas S. Processing of the Notch Ligand Delta by the Metalloprotease Kuzbanian. Science 1999, 283: 91-94. PMID: 9872749, DOI: 10.1126/science.283.5398.91.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsCell LineCells, CulturedDisintegrinsDrosophilaDrosophila ProteinsFemaleIntracellular Signaling Peptides and ProteinsLigandsMaleMembrane ProteinsMetalloendopeptidasesMolecular Sequence DataMutationNeuronsProtein Processing, Post-TranslationalReceptors, NotchSignal TransductionTransfectionConceptsLigand DeltaMetalloprotease KuzbanianCell fate determinationNotch ligand DeltaFate determinationNotch proteinsTransmembrane ligandsNotch activityProcessing eventsExtracellular fragmentGenetic analysisNotch ligandsSurface receptorsKuzbanianAdjacent cellsSoluble formBroad spectrumNotchSignalingProteinLigandsCellsFragmentsVivoReceptors
1997
Developmental expression, pattern of distribution, and effect on cell aggregation implicate a neuron‐glial junctional domain protein in neuronal migration
Cameron R, Ruffin J, Cho N, Cameron P, Rakic P. Developmental expression, pattern of distribution, and effect on cell aggregation implicate a neuron‐glial junctional domain protein in neuronal migration. The Journal Of Comparative Neurology 1997, 387: 467-488. PMID: 9373008, DOI: 10.1002/(sici)1096-9861(19971103)387:4<467::aid-cne1>3.0.co;2-0.Peer-Reviewed Original ResearchConceptsRadial glial cellsGlial cellsRadial glial cell processesGlial cell processesMultiple brain regionsNeuronal cell migrationAstrocyte-astrocyteSubventricular zoneImmunofluorescent localization studiesAstroglial cellsNeuron-neuronCerebellar astrocytesBrain regionsMorphologic featuresNeuronal migrationMonoclonal antibodiesImmunoreactivityAntibodiesNeuronsAstrocytesCell migrationPresent studyDevelopmental expressionPattern of distributionCell migration processes
1996
Intracellular Ca2+ Fluctuations Modulate the Rate of Neuronal Migration
Komuro H, Rakic P. Intracellular Ca2+ Fluctuations Modulate the Rate of Neuronal Migration. Neuron 1996, 17: 275-285. PMID: 8780651, DOI: 10.1016/s0896-6273(00)80159-2.Peer-Reviewed Original Research
1994
Identification of membrane proteins that comprise the plasmalemmal junction between migrating neurons and radial glial cells
Cameron R, Rakic P. Identification of membrane proteins that comprise the plasmalemmal junction between migrating neurons and radial glial cells. Journal Of Neuroscience 1994, 14: 3139-3155. PMID: 8182462, PMCID: PMC6577439, DOI: 10.1523/jneurosci.14-05-03139.1994.Peer-Reviewed Original ResearchConceptsRadial glial cellsGlial cellsMembrane proteinsCell-cell recognitionFocal adhesion plaquesApparent molecular massRadial glial cell processesNeuronal cell migrationCerebellar glial cellsActin cytoskeletonGlial cell processesMicrotubule cytoskeletonNon-neural tissuesSurface microdomainsMembrane polypeptidesIndividual proteinsAdhesion plaquesProcess-bearing astrocytesIntact microtubulesAdult stageMolecular massCell migrationMigration eventsIntegrin subunitsJunctional complexes
1992
Selective Role of N-Type Calcium Channels in Neuronal Migration
Komuro H, Rakic P. Selective Role of N-Type Calcium Channels in Neuronal Migration. Science 1992, 257: 806-809. PMID: 1323145, DOI: 10.1126/science.1323145.Peer-Reviewed Original ResearchConceptsN-type calcium channelsCalcium channelsNeuronal migrationT-type calcium channelsCerebellar slice preparationGranule cell migrationImmature neuronsSelective blockadeSlice preparationPostmitotic granule cellsAdult brainGranule cellsSynaptic circuitsNeurotransmitter releasePotassium channelsPlasmalemmal surfaceIncubation mediumCell migrationSelective roleLaser scanning confocal microscopeScanning confocal microscopeBlockadeSpecific developmental roleNeuronsBrain