TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts
Park E, Kim J, Ha T, Choi J, Soo Hong K, Rho J. TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts. Experimental & Molecular Medicine 2013, 45: e35-e35. PMID: 23928855, PMCID: PMC3789259, DOI: 10.1038/emm.2013.67.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisEmbryo, MammalianFibroblastsGene Expression RegulationIntracellular SpaceMiceMitogen-Activated Protein KinasesNF-kappa BOxidative StressReactive Oxygen SpeciesSignal TransductionTranscription FactorsConceptsMouse embryonic fibroblastsApoptotic cell deathCell deathOxidative stress-induced apoptotic cell deathReactive oxygen speciesPleckstrin homology-like domain familyPromotes oxidative stress-induced apoptosisActivation of caspase-3Stress responseStress-induced cell deathT-cell death-associated genePro-apoptotic functionOxidative stress-induced cell deathOxidative stress-induced apoptosisTDAG51 deficiencyDeath-associated genesStress-induced apoptosisReceptor-mediated cell deathPro-apoptotic genesResponse to oxidative stressCellular stress responseEndoplasmic reticulum stressOxygen speciesProduction of intracellular reactive oxygen speciesIntracellular reactive oxygen species