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 role
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-3Caspase‐3 is required for apoptosis‐associated DNA fragmentation but not for cell death in neurons deprived of potassium
D'Mello S, Kuan C, Flavell R, Rakic P. Caspase‐3 is required for apoptosis‐associated DNA fragmentation but not for cell death in neurons deprived of potassium. Journal Of Neuroscience Research 2000, 59: 24-31. PMID: 10658182, DOI: 10.1002/(sici)1097-4547(20000101)59:1<24::aid-jnr4>3.0.co;2-8.Peer-Reviewed Original ResearchConceptsCell deathCaspase-3Apoptosis-associated DNA fragmentationDNA fragmentationCell death pathwaysRegulated cell deathPan-caspase inhibitorApoptosis-inducing stimuliDeath pathwaysChromatin condensationCaspase inhibitorsCaspase inhibitionApoptotic featuresCerebellar granule neuronsPotassium deprivationFmkCultured cerebellar granule neuronsCaspasesCrucial effectorNonneuronal cellsApoptosisSame extentGranule neuronsPivotal roleNeuronal death