2021
PINK1 Inhibits Multimeric Aggregation and Signaling of MAVS and MAVS-Dependent Lung Pathology.
Kim SH, Shin HJ, Yoon CM, Lee SW, Sharma L, Dela Cruz CS, Kang MJ. PINK1 Inhibits Multimeric Aggregation and Signaling of MAVS and MAVS-Dependent Lung Pathology. American Journal Of Respiratory Cell And Molecular Biology 2021, 64: 592-603. PMID: 33577398, PMCID: PMC8086043, DOI: 10.1165/rcmb.2020-0490oc.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsBleomycinEpithelial CellsGene Expression RegulationHEK293 CellsHumansImmunity, InnateInflammasomesInfluenza A virusLungMiceMice, KnockoutMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinOrthomyxoviridae InfectionsPeroxisomesProtein AggregatesProtein BindingProtein KinasesPulmonary FibrosisSignal TransductionConceptsMAVS aggregationPINK1 deficiencyBimolecular fluorescence complementation analysisAntiviral innate immuneAppropriate cellular functionsKey molecular processesIntracellular signaling pathwaysInnate immune signalingComplementation analysisCellular functionsIntracellular perturbationsImmune signalingSignaling pathwaysPINK1Molecular processesMitochondria dysfunctionMAVSMAVS signalingMurine modelingSignalingFunctional significanceInnate immuneImportant roleRegulationNew role
2018
Salinomycin ameliorates oxidative hepatic damage through AMP-activated protein kinase, facilitating autophagy
Kim K, Lee S, Baek S, Lee E, Jang E, Lee J, Ahn S, Chang J, Oh T, Kim S, Ma J, Kim S, Park K, Kim Y. Salinomycin ameliorates oxidative hepatic damage through AMP-activated protein kinase, facilitating autophagy. Toxicology And Applied Pharmacology 2018, 360: 141-149. PMID: 30290169, DOI: 10.1016/j.taap.2018.10.002.Peer-Reviewed Original ResearchConceptsImportance of AMPKMitochondrial dysfunctionAcidic vesicle organellesOxidative stressProtein kinase activationReactive oxygen species productionProtein kinaseAMPK inhibitionKinase activationSevere oxidative stressOxygen species productionLiver injuryMolecular mechanismsIron-induced apoptosisHepatic protectantStreptomyces albusHuman diseasesAMPKCellular mechanismsLC3-IISalinomycin's effectsArachidonic acidMitochondrial impairmentROS productionAnti-cancer agents
2016
Silibinin induces mitochondrial NOX4-mediated endoplasmic reticulum stress response and its subsequent apoptosis
Kim S, Kim K, Yu S, Seo Y, Chun S, Yu H, Ahn S. Silibinin induces mitochondrial NOX4-mediated endoplasmic reticulum stress response and its subsequent apoptosis. BMC Cancer 2016, 16: 452. PMID: 27405931, PMCID: PMC4942927, DOI: 10.1186/s12885-016-2516-6.Peer-Reviewed Original ResearchConceptsReactive oxygen speciesNOX4 expressionDisruption of Ca2ER stress responseProstate cancer PC-3 cellsCancer PC-3 cellsRegulation of NOX4Inhibited tumor growthCell linesPC-3 cellsProstate cell linesSilibinin-induced apoptosisProduction of ROSEndoplasmic reticulum stress responseExpression of apoptosisCancer cell linesProstate cancerROS-dependent apoptosisChemopreventive effectsMitochondrial Nox4Mitochondrial reactive oxygen speciesReticulum stress responseTumor growthFlow cytometryMethodsThe effects
2013
Interplay of reactive oxygen species, intracellular Ca2+ and mitochondrial homeostasis in the apoptosis of prostate cancer cells by deoxypodophyllotoxin
Kim K, Cho H, Yu S, Kim S, Yu H, Park Y, Mirkheshti N, Kim S, Song C, Chatterjee B, Ahn S. Interplay of reactive oxygen species, intracellular Ca2+ and mitochondrial homeostasis in the apoptosis of prostate cancer cells by deoxypodophyllotoxin. Journal Of Cellular Biochemistry 2013, 114: 1124-1134. PMID: 23192945, DOI: 10.1002/jcb.24455.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisBcl-2-Associated X ProteinCalciumCaspase 3Cell Line, TumorCell ProliferationCell SurvivalCytochromes cDrug Screening Assays, AntitumorDrugs, Chinese HerbalEgtazic AcidEnzyme ActivationG2 Phase Cell Cycle CheckpointsHomeostasisHumansIntracellular SpaceM Phase Cell Cycle CheckpointsMaleMembrane Potential, MitochondrialMitochondriaModels, BiologicalPodophyllotoxinProstatic NeoplasmsProtein TransportReactive Oxygen SpeciesConceptsReactive oxygen speciesMitochondrial homeostasisProstate cancer cellsCaspase-3-dependent pathwayCytochrome c releasePC-3 cell modelBax protein translocationTurn induced apoptosisCancer cellsMitochondrial membrane potentialOxygen speciesCaspase-3 activationN-acetylcysteineIncrease of ROSProtein translocationProstate cancerHuman prostate cancer cellsGeneration of ROSC releaseAntioxidant N-acetylcysteineNew anti-neoplastic agentsROS accumulationMitochondrial functionRecurrent prostate cancerLimited treatment options