2013
Neuroprotection against neuroblastoma cell death induced by depletion of mitochondrial glutathione
Dukhande VV, Kawikova I, Bothwell AL, Lai JC. Neuroprotection against neuroblastoma cell death induced by depletion of mitochondrial glutathione. Apoptosis 2013, 18: 702-712. PMID: 23494481, PMCID: PMC3645366, DOI: 10.1007/s10495-013-0836-4.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisAzolesBcl-2-Associated X ProteinButhionine SulfoximineCell Line, TumorCell SurvivalCoculture TechniquesCytochromes cCytosolEthacrynic AcidGlioblastomaGlutathioneHumansIsoindolesMitochondriaNeuroblastomaNeuronsOrganoselenium CompoundsProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesConceptsSK-N-SH cellsMitochondrial glutathioneCell deathNeuroblastoma cell deathMitochondrial dysfunctionCellular reactive oxygen speciesMitochondrial glutathione poolPrevention of apoptosisMitochondrial glutathione depletionNeurodegenerative disordersOxidative stressGlutathione depletionReactive oxygen speciesGlutathione poolDistinct inhibitorsApoptotic deathGlutathione metabolismEthacrynic acidROS productionOxygen speciesBCL2 overexpressionGSH depletionApoptosisL-buthionineCells
2004
Qualitatively differential regulation of T cell activation and apoptosis by T cell receptor ζ chain ITAMs and their tyrosine residues
Chae WJ, Lee HK, Han JH, Kim SW, Bothwell AL, Morio T, Lee SK. Qualitatively differential regulation of T cell activation and apoptosis by T cell receptor ζ chain ITAMs and their tyrosine residues. International Immunology 2004, 16: 1225-1236. PMID: 15302845, DOI: 10.1093/intimm/dxh120.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinaseTCR zeta chainTyrosine phosphorylated proteinsTyrosine residuesZeta chainPhosphorylated proteinsT cell activationCell deathFirst tyrosine residueCell activationInfluence of mutationsActivation-induced cell deathProtein kinaseDistinctive regulationIntracellular signalsDifferential regulationITAMMAPK phosphorylationTCR stimulationStepwise deletionJurkat transfectantsDistinct signalsActivation signalsMutationsResidues