2018
Radio-sensitizing effects of VE-821 and beyond: Distinct phosphoproteomic and metabolomic changes after ATR inhibition in irradiated MOLT-4 cells
Šalovská B, Janečková H, Fabrik I, Karlíková R, Čecháková L, Ondrej M, Link M, Friedecký D, Tichý A. Radio-sensitizing effects of VE-821 and beyond: Distinct phosphoproteomic and metabolomic changes after ATR inhibition in irradiated MOLT-4 cells. PLOS ONE 2018, 13: e0199349. PMID: 30001349, PMCID: PMC6042708, DOI: 10.1371/journal.pone.0199349.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid MotifsAtaxia Telangiectasia Mutated ProteinsBinding SitesBiomarkersCell Cycle CheckpointsCell Line, TumorComputational BiologyGamma RaysGene OntologyHumansMetabolomeMetabolomicsPhosphoproteinsPhosphorylationProtein BindingProtein Kinase InhibitorsProteomeProteomicsPyrazinesRadiation ToleranceRadiation-Sensitizing AgentsSignal TransductionSulfonesTOR Serine-Threonine KinasesConceptsVE-821MOLT-4 cellsCellular metabolismOncogene-induced replication stressATR inhibitionATM-deficient cellsDNA damage responseATR/Chk1 pathwayCell biology techniquesDownregulation of mTORAnti-cancer strategyCurrent anti-cancer strategiesReplication stressPhosphorylation sitesDamage responseIrradiation-induced oxidative stressQuantitative proteomicsDNA repairChk1 pathwayCellular eventsBiology techniquesSpecific inhibitorMain regulatorTumor-specific abnormalitiesMTOR inhibition
2015
Chemical inhibition of DNA repair kinases as a promising tool in oncology
Durisova K, Salovska B, Pejchal J, Tichy A. Chemical inhibition of DNA repair kinases as a promising tool in oncology. Biomedical Papers 2015, 160: 11-19. PMID: 26498210, DOI: 10.5507/bp.2015.046.Peer-Reviewed Original ResearchMeSH KeywordsAtaxia Telangiectasia Mutated ProteinsCDC2 Protein KinaseDNA Breaks, Double-StrandedDNA RepairDNA-Activated Protein KinaseHumansNeoplasmsProtein Kinase InhibitorsConceptsDNA-dependent protein kinaseDNA repair pathwaysRepair pathwaysDNA repairSpecific DNA repair pathwaysKey DNA repairDNA-damaging agentsSmall molecule inhibitorsATM-Rad3Protein kinaseAtaxia telangiectasiaChemical inhibitionKinaseMolecule inhibitorsSpecific inhibitorPathwayPotent inhibitorInhibitorsRecent studiesTumor resistanceTumor cellsMajor roleRadiotherapy efficiencyRepairCells
2014
Radiosensitization of Human Leukemic HL-60 Cells by ATR Kinase Inhibitor (VE-821): Phosphoproteomic Analysis
Šalovská B, Fabrik I, Ďurišová K, Link M, Vávrová J, Řezáčová M, Tichý A. Radiosensitization of Human Leukemic HL-60 Cells by ATR Kinase Inhibitor (VE-821): Phosphoproteomic Analysis. International Journal Of Molecular Sciences 2014, 15: 12007-12026. PMID: 25003641, PMCID: PMC4139827, DOI: 10.3390/ijms150712007.Peer-Reviewed Original ResearchMeSH KeywordsAtaxia Telangiectasia Mutated ProteinsCell Line, TumorGamma RaysHumansPhosphorylationProtein Kinase InhibitorsProteomePyrazinesRadiation-Sensitizing AgentsSulfonesConceptsDNA-dependent protein kinaseVE-821HL-60 cellsNano-liquid chromatography-tandem mass spectrometry analysisCell cycleSequence motif analysisDNA damage responseRadiation-induced double-strand breaksATR kinase inhibitorsDNA damage repairDNA damaging agentsHuman leukemic HL-60 cellsDouble-strand breaksSpecific ATR inhibitorActivity of kinasesInhibitor VE-821Leukemic HL-60 cellsCell cycle arrestQuantitative phosphoproteomicsATR kinaseMotif analysisPhosphorylation sitesCellular processesDamage responsePhosphoproteomic analysis