2001
Bcl-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
1997
Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene
Yang D, Kuan C, Whitmarsh A, Rinócn M, Zheng T, Davis R, Rakic P, Flavell R. Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene. Nature 1997, 389: 865-870. PMID: 9349820, DOI: 10.1038/39899.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisDrug ResistanceExcitatory Amino Acid AgonistsGene ExpressionGene TargetingGlutamic AcidHippocampusKainic AcidMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 10Mitogen-Activated Protein KinasesNeuronsPhosphorylationProtein KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junSeizuresSignal TransductionTranscription Factor AP-1ConceptsKainic acidGlutamate receptor agonist kainic acidAgonist kainic acidExcitotoxicity-induced apoptosisExcitatory amino acidsHippocampal neuron apoptosisHippocampus of miceStress-induced neuronal apoptosisObserved neuroprotectionGlutamate neurotoxicitySeizure activityNeuron apoptosisGlutamate toxicityNeuronal apoptosisAP-1 transcription factor complexJNK3 geneMutant miceMiceMembrane depolarizationNoxious stressTranscription factor complexApoptosisC-JunRecent studiesTranscriptional activity