Search results for " DNA Damage"

showing 10 items of 41 documents

Potential role of oxidative DNA damage in the impact of PNPLA3 variant (rs 738409 CG) in hepatocellular carcinoma risk.

2014

International audience

Carcinoma HepatocellularHepatologybusiness.industry[SDV]Life Sciences [q-bio]Liver NeoplasmsMembrane ProteinsLipasemedicine.disease3. Good healthOxidative dna damageHepatocellular carcinomamedicineCancer researchHumansbusinessComputingMilieux_MISCELLANEOUS[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyHepatology (Baltimore, Md.)
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Cytolethal distending toxin (CDT): a bacterial weapon to control host cell proliferation ?

2001

Cytolethal distending toxins (CDT) constitute a family of genetically related bacterial protein toxins able to stop the proliferation of numerous cell lines. This effect is due to their ability to trigger in target cells a signaling pathway that normally prevents the transition between the G2 and the M phase of the cell cycle. Produced by several unrelated Gram-negative mucosa-associated bacterial species, CDTs are determined by a cluster of three adjacent genes (cdtA, cdtB, cdtC) encoding proteins whose respective role is not yet fully elucidated. The CDT-B protein presents sequence homology to several mammalian and bacterial phosphodiesterases, such as DNase I. The putative nuclease activ…

Cell cycle checkpointCell divisionCytolethal distending toxinCell growthBacterial ToxinsCell cycleG2-M DNA damage checkpointBiologyMicrobiologyMicrobiologyCell biologyCell Line[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyGram-Negative BacteriaGeneticsAnimalsHumansSignal transductionGram-Negative Bacterial InfectionsMolecular BiologyGene[SDV.MP] Life Sciences [q-bio]/Microbiology and ParasitologyCell Division
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Cisplatin sensitivity is related to late DNA damage processing and checkpoint control rather than to the early DNA damage response

2008

The present study aimed at elucidating mechanisms dictating cell death triggered by cisplatin-induced DNA damage. We show that CL-V5B hamster mutant cells, a derivative of V79B, are hypersensitive to cisplatin-induced apoptotic death. CL-V5B cells are characterized by attenuated cisplatin-induced early (2-6 h) stress response, such as phosphorylation of stress-activated protein kinases (SAPK/JNK), ATM and Rad3-related (ATR) protein kinase, histone H2AX and checkpoint kinase-1 (Chk-1). Human FANCC cells also showed a reduced phosphorylation of H2AX and SAPK/JNK at early time point after cisplatin treatment. This was not the case for BRCA2-defective VC-8 hamster cells, indicating that the FA …

Cell cycle checkpointCisplatin-DNA adducts ; DNA repair ; Interstrand cross links ; DNA damage response ; Cell cycle checkpoint ; Cell deathDNA damageDNA repairHealth Toxicology and MutagenesisApoptosisCell LineHistonesDNA AdductsCricetinaeGeneticsmedicineAnimalsHumansCHEK1PhosphorylationMolecular BiologyChromosome AberrationsCisplatinbiologyJNK Mitogen-Activated Protein KinasesDNA replicationG2-M DNA damage checkpointMolecular biologyCell biologyHistonebiology.proteinCisplatinDNA DamageMutagensmedicine.drug
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Deinococcus radiodurans' SRA-HNH domain containing protein Shp (Dr1533) is involved in faithful genome inheritance maintenance following DNA damage

2018

WOS:000452343100012; International audience; Background: Deinococcus radiodurans R1 (DR) survives conditions of extreme desiccation, irradiation and exposure to genotoxic chemicals, due to efficient DNA breaks repair, also through Mn2+ protection of DNA repair enzymes. Methods: Possible annotated domains of the DR1533 locus protein (Shp) were searched by bioinformatic analysis. The gene was cloned and expressed as fusion protein. Band-shift assays of Shp or the SRA and HNH domains were performed on oligonucleotides, genomic DNA from E. coif and DR. slip knock-out mutant was generated by homologous recombination with a kanamycin resistance cassette. Results: DR1533 contains an N-terminal SRA…

DNA RepairDNA cytosine-methylation; DNA damage; DR1533 locus; Genotoxic agents; Mn2+; SRA domain; Biophysics; Biochemistry; Molecular BiologyGenotoxic agents[SDV]Life Sciences [q-bio]DNA cytosine-methylationperspectiveSettore BIO/19 - Microbiologia GeneraleBiochemistrychemistry.chemical_compound0302 clinical medicineKanamycinCloning Molecularcytosine0303 health sciencesDR1533 locusbiologyChemistryGenotoxic agentuhrf1Mn(2+)Mn2+SRA domainDeinococcusrecognitionmanganese(ii)DNA BacterialDNA damageDNA repairoxidationUbiquitin-Protein LigasesBiophysicsSettore BIO/11 - Biologia Molecolareresistance03 medical and health sciencesBacterial ProteinsProtein DomainsDR1533 locuDrug Resistance BacterialEscherichia coliHumansfeaturesAmino Acid SequenceGeneMolecular Biology030304 developmental biologyOligonucleotideComputational BiologyDeinococcus radioduransDNA Methylationbiology.organism_classificationMolecular biologygenomic DNArepairMutationCCAAT-Enhancer-Binding ProteinsDNA damageHomologous recombination030217 neurology & neurosurgeryDNAGenome BacterialMutagens
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The bacterial cytolethal distending toxin (CDT) triggers a G2 cell cycle checkpoint in mammalian cells without preliminary induction of DNA strand br…

1999

The bacterial cytolethal distending toxin (CDT) was previously shown to arrest the tumor-derived HeLa cell line in the G2-phase of the cell cycle through inactivation of CDK1, a cyclin-dependent kinase whose state of activation determines entry into mitosis. We have analysed the effects induced in HeLa cells by CDT, in comparison to those induced by etoposide, a prototype anti-tumoral agent that triggers a G2 cell cycle checkpoint by inducing DNA damage. Both CDT and etoposide inhibit cell proliferation and induces the formation of enlarged mononucleated cells blocked in G2. In both cases, CDK1 from arrested cells could be re-activated both in vitro by dephosphorylation by recombinant Cdc25…

DNA ReplicationG2 PhaseCancer ResearchCAFFEINECell cycle checkpointCytolethal distending toxinDNA damageRecombinant Fusion Proteins[SDV]Life Sciences [q-bio]Bacterial ToxinsBiologyS Phase03 medical and health sciencesCDC2 Protein KinaseGeneticsHumanscdc25 PhosphatasesCHEK1PhosphorylationMolecular BiologyMitosisEtoposide030304 developmental biology0303 health sciences030306 microbiologyCell growthDNA NeoplasmG2-M DNA damage checkpointCell cycleAntineoplastic Agents PhytogenicNeoplasm Proteins3. Good healthCell biology[SDV] Life Sciences [q-bio]BiochemistryAGENT ANTITUMEURProtein Processing Post-TranslationalCell DivisionDNA DamageHeLa Cells
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The DNA topoisomerase II catalytic inhibitor merbarone is genotoxic and induces endoreduplication

2012

Abstract In the last years a number of reports have shown that the so-called topoisomerase II (topo II) catalytic inhibitors are able to induce DNA and chromosome damage, an unexpected result taking into account that they do not stabilize topo II-DNA cleavable complexes, a feature of topo II poisons such as etoposide and amsacrine. Merbarone inhibits the catalytic activity of topo II by blocking DNA cleavage by the enzyme. While it was first reported that merbarone does not induce genotoxic effects in mammalian cells, this has been challenged by reports showing that the topo II inhibitor induces efficiently chromosome and DNA damage, and the question as to a possible behavior as a topo II p…

DNA damageHealth Toxicology and MutagenesisTopoisomerase II; Catalytic inhibitor; Merbarone; DNA damage; Clastogens; EndoreduplicationCatalytic inhibitorCell Linechemistry.chemical_compoundCricetulusCricetinaeGeneticsmedicineEndoreduplicationAnimalsTopoisomerase II InhibitorsClastogenMolecular BiologyAmsacrineCell ProliferationbiologyDNA synthesisCell growthTopoisomeraseMerbaroneCell cycleEndoreduplicationThiobarbituratesMolecular biologyTopoisomerase IIchemistrybiology.proteinDNAmedicine.drugDNA Damage
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2α-Hydroxyalantolactone from Pulicaria undulata: activity against multidrug-resistant tumor cells and modes of action.

2020

Abstract Background Sesquiterpene lactones having α-methylene-γ-lactone moiety are promising natural metabolites showing various biological activity. One of the major metabolites isolated from Pulicaria undulata, 2α-hydroxyalantolactone (PU-1), has not been investigated in detail yet. Multidrug resistance (MDR) represents a major obstacle for cancer chemotherapy and the capability of novel natural products to overcoming MDR is of great interest. Purpose Exploring the molecular modes of action for potent natural product metabolites. Methods The resazurin reduction assay was employed to evaluate the cytotoxicity of PU-1 on sensitive and their corresponding drug-resistant cell lines (overexpre…

DNA damagePharmaceutical ScienceApoptosisPulicaria03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineCell Line TumorDrug DiscoveryHumansPI3K/AKT/mTOR pathway030304 developmental biologyPhosphoinositide-3 Kinase InhibitorsPharmacology0303 health sciencesLeukemiaCell growthChemistryCell cycleG2-M DNA damage checkpointMolecular biologyAntineoplastic Agents PhytogenicBlotGene expression profilingG2 Phase Cell Cycle CheckpointsGene Expression Regulation NeoplasticComplementary and alternative medicineApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisMolecular MedicineSesquiterpenesDNA DamagePhytomedicine : international journal of phytotherapy and phytopharmacology
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DNA damage-induced cell death: From specific DNA lesions to the DNA damage response and apoptosis

2011

DNA damaging agents are potent inducers of cell death triggered by apoptosis. Since these agents induce a plethora of different DNA lesions, it is firstly important to identify the specific lesions responsible for initiating apoptosis before the apoptotic executing pathways can be elucidated. Here, we describe specific DNA lesions that have been identified as apoptosis triggers, their repair and the signaling provoked by them. We discuss methylating agents such as temozolomide, ionizing radiation and cisplatin, all of them are important in cancer therapy. We show that the potentially lethal events for the cell are O(6)-methylguanine adducts that are converted by mismatch repair into DNA dou…

DNA re-replicationCancer ResearchGuanineDNA RepairDNA repairDNA damageSurvivinAntineoplastic AgentsApoptosisBiologyInhibitor of Apoptosis ProteinsDNA AdductsNeoplasmsRadiation IonizingmedicineAnimalsHumansPhosphorylationCisplatinCell DeathCell CycleNF-kappa BDNA replicationDNAG2-M DNA damage checkpointCell cycleOncologyCancer researchDNA mismatch repairProto-Oncogene Proteins c-aktDNA DamageSignal Transductionmedicine.drugCancer Letters
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Specific detection of cyclobutane pyrimidine dimers in phytoplankton DNA by a non-radioactive assay based on T4-endonuclease V digestion.

2001

The effect of artificial and natural UV irradiation on DNA in marine phytoplankton Isochrysis galbana monoculture was investigated. The presence of cyclobutane pyrimidine dimers (CPDs) in unlabelled I. galbana DNA was detected by a non-radiometric alkaline filter elution assay after T4-endonuclease V digestion. The quantity of CPDs was estimated by alkaline agarose gel electrophoresis. Precise determination of the amount of DNA in the presence of I. galbana pigments was achieved by oxazole yellow homodimer (YOYO) dye. T4-endonuclease V-sensitive sites frequency (ESS/kb), measured after exposure to 2-40 kJ m(-2) of artificial UV light, increased in a dose-dependent manner. Twelve hours after…

Environmental EngineeringDNA RepairDNA damageDNA repairUltraviolet RaysPyrimidine dimerIsochrysis galbanachemistry.chemical_compoundPigmentDeoxyribonuclease (Pyrimidine Dimer)Viral ProteinsEnvironmental ChemistryWaste Management and DisposalEndodeoxyribonucleasesbiologyAlkaline filter elution; crude oil; DNA damage; phytoplankton; UV; sunlightbiology.organism_classificationPollutionPetroleumBiochemistrychemistryCell culturePyrimidine Dimersvisual_artAgarose gel electrophoresisPhytoplanktonvisual_art.visual_art_mediumSunlightBiological AssayDNADNA DamageThe Science of the total environment
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Escherichia coli cytolethal distending toxin blocks the HeLa cell cycle at the G2/M transition by preventing cdc2 protein kinase dephosphorylation an…

1997

Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized HeLa cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes cell accumulation in G2 and not in M, that it does not slow the progression of cells th…

G2 PhaseCytolethal distending toxinBacterial toxins[SDV]Life Sciences [q-bio]ImmunologyBacterial ToxinsMitosisBiologyMicrobiologyCDTCDC2 Protein KinaseEscherichia coliHumansKinase activityPhosphorylationMitosisCyclin-dependent kinase 1Cell growthCell CycleCell cycleG2-M DNA damage checkpointFlow CytometryMicrobiologie et ParasitologieCell biology[SDV] Life Sciences [q-bio]Enzyme ActivationInfectious DiseasesCytolethal distending toxinsParasitologyCDC2 Protein KinaseHeLa CellsResearch Article
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