2001
Programmed Cell Death of Developing Mammalian Neurons after Genetic Deletion of Caspases
Oppenheim R, Flavell R, Vinsant S, Prevette D, Kuan C, Rakic P. Programmed Cell Death of Developing Mammalian Neurons after Genetic Deletion of Caspases. Journal Of Neuroscience 2001, 21: 4752-4760. PMID: 11425902, PMCID: PMC6762357, DOI: 10.1523/jneurosci.21-13-04752.2001.Peer-Reviewed Original ResearchConceptsCell deathGenetic deletionExtensive cytoplasmic vacuolizationPro-apoptotic proteasesCaspase familySpecific caspasesChromatin condensationNonapoptotic pathwaysPostmitotic neuronsCaspase-9Mammalian neuronsCell typesDeath processSpecific perturbationsCaspase-3Altered morphologyCaspasesNuclear changesKey membersDeletionUTP nickCytoplasmic vacuolizationElectron microscopic levelTerminal deoxynucleotidyl transferase-mediated biotinylated UTP nickNeuronal populationsCaspases and Their Regulation in Apoptosis during Brain Development
Kuan C, Flavell R, Rakic P. Caspases and Their Regulation in Apoptosis during Brain Development. Research And Perspectives In Neurosciences 2001, 75-88. DOI: 10.1007/978-3-662-04333-2_7.Peer-Reviewed Original ResearchJun N-terminal kinasePost-mitotic neuronsMammalian brain developmentCaspase-3 activationCell deathC. elegansCaspase familyDeath gene ced-3Caspase-3Caspase-9Mammalian caspase familyGene ced-3Ectopic cell deathGene ced-9Complex regulation mechanismsNematode C. elegansCell death pathwaysNormal mouse brain developmentN-terminal kinaseBrain developmentCell death cascadeMouse brain developmentCaspase-3 deficiencyCED-3CED-9Bcl-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
1998
Reduced Apoptosis and Cytochrome c–Mediated Caspase Activation in Mice Lacking Caspase 9
Kuida K, Haydar T, Kuan C, Gu Y, Taya C, Karasuyama H, Su M, Rakic P, Flavell R. Reduced Apoptosis and Cytochrome c–Mediated Caspase Activation in Mice Lacking Caspase 9. Cell 1998, 94: 325-337. PMID: 9708735, DOI: 10.1016/s0092-8674(00)81476-2.Peer-Reviewed Original ResearchConceptsCritical upstream activatorUpstream activatorCaspase-9Cell death machineryCytochrome cDeath machineryApoptotic stimuliCaspase activationCaspase cascadeDNA fragmentationPrevents activationCytosolic extractsEmbryonic brainCaspasesReduced apoptosisCASP9ApoptosisActivatorCASP3Brain developmentKnockout miceEssential componentCleavageActivationVivo