Search results for " REPLICATION"

showing 10 items of 406 documents

Fen1 is induced p53 dependently and involved in the recovery from UV-light-induced replication inhibition.

2005

Mouse embryonic fibroblasts (MEFs) that lack p53 are hypersensitive to the cytotoxic and genotoxic effect of ultraviolet (UV-C) light. They also display a defect in the recovery from UV-C-induced DNA replication inhibition. An enzyme involved in processing stalled DNA replication forks is flap endonuclease 1 (Fen1). Gene expression profiling of UV-C-irradiated MEFs revealed fen1 to be upregulated, which was confirmed by RT-PCR and Western blot experiments. Increased Fen1 levels upon UV-C exposure are due to transcriptional activation, as revealed by inhibitor studies. Fen1 induction was dose- and time-dependent; it occurred on protein level already 3 h after irradiation. Induction of Fen1 b…

DNA ReplicationCancer ResearchDNA damageDNA repairFlap EndonucleasesUltraviolet RaysMolecular Sequence DataGene ExpressionCHO CellsBiologyTransfectionchemistry.chemical_compoundMiceCricetinaeGeneticsNull cellAnimalsPromoter Regions GeneticMolecular BiologyCell ProliferationBase SequenceCell growthDNA replicationTransfection3T3 CellsDNAMolecular biologyDNA Replication InhibitionchemistryEnzyme InductionTumor Suppressor Protein p53DNAOncogene
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Determination of DNA single strand breaks and selective DNA amplification by N-nitrodimethylamine and analogs, and estimation of the indicator cells'…

1986

N-nitrodimethylamine is metabolized oxidatively to N-nitrohydroxymethylmethylamine, which decomposes to yield formaldehyde and N-nitromethylamine. All four compounds and N-nitromethylamine were tested for their ability to induce DNA single strand breaks in hepatocytes and in SV 40-transformed Chinese hamster embryo cell lines. Only the two monoalkylnitramines were positive. They induced single strand breaks in hepatocytes, but were not effective in the other cells. Formaldehyde and N-nitrohydroxymethylmethylamine were toxic to the cells. None of the compounds tested was able to induce selective DNA amplification in the two transformed cell lines. Enzymes involved in drug metabolism were ass…

DNA ReplicationCancer ResearchHamsterDNA Single-StrandedSimian virus 40BiologyChinese hamsterCell Linechemistry.chemical_compoundCricetulusCricetinaeFormaldehydeAnimalsEpoxide hydrolaseCells Culturedchemistry.chemical_classificationDose-Response Relationship DrugDNA replicationGene AmplificationGeneral Medicinebiology.organism_classificationCell Transformation ViralEmbryo MammalianRatsEnzymeOncologychemistryBiochemistryLiverCell cultureDrug metabolismDNADimethylaminesJournal of cancer research and clinical oncology
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Lovastatin protects human endothelial cells from the genotoxic and cytotoxic effects of the anticancer drugs doxorubicin and etoposide

2006

Background and purpose: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they exert pleiotropic effects on cellular stress responses and death. Here, we analysed whether lovastatin affects the sensitivity of primary human endothelial cells (HUVEC) to the anticancer drug doxorubicin. Experimental approach: We investigated whether pretreatment of HUVEC with low dose of lovastatin influences the cellular sensitivity to doxorubicin. To this end, cell viability, proliferation and apoptosis as well as DNA damage-triggered stress response were analysed. Key results: Lovastatin reduced the cytotoxic potency of doxorub…

DNA ReplicationCell SurvivalDNA damageApoptosisBiologyPharmacologypolycyclic compoundsmedicineHumansTopoisomerase II InhibitorsDoxorubicinLovastatinEtoposideEtoposideFluorescent DyesPharmacologyAntibiotics AntineoplasticReverse Transcriptase Polymerase Chain ReactionTopoisomeraseCell CycleEndothelial Cellsnutritional and metabolic diseasesAntimutagenic AgentsFibroblastsCell cycleResearch PapersAntineoplastic Agents PhytogenicDoxorubicinDrug Resistance NeoplasmHMG-CoA reductasebiology.proteinlipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsTopoisomerase-II InhibitorReactive Oxygen SpeciesFluorescein-5-isothiocyanateDNA Damagemedicine.drugBritish Journal of Pharmacology
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On the relevance of genotoxicity for fish populations II: genotoxic effects in zebrafish (Danio rerio) exposed to 4-nitroquinoline-1-oxide in a compl…

2003

In order to characterize the impact of genotoxic potentials on populations of aquatic organisms in surface waters, zebrafish (Danio rerio) were exposed to the model genotoxicant 4-nitroquinoline-1-oxide (NQO) in a complete life-cycle test. Fish exposed to mean NQO concentrations of 0, 0.1, 0.3, 1.1, and 2.9 microg/l were examined by several genotoxicity assays with different endpoints. Assays included the unscheduled DNA synthesis (UDS) test, the comet assay, the alkaline filter elution, and the micronucleus test. The genotoxicity assays revealed an increasing genotoxicity, ranging from induction of DNA repair (even at the lowest concentration tested) to primary and secondary DNA alteration…

DNA ReplicationDNA RepairDNA repairHealth Toxicology and Mutagenesis4-Nitroquinoline 1-oxideDanioAquatic ScienceBiologymedicine.disease_causechemistry.chemical_compoundmedicineEcotoxicologyAnimalsToxicity Tests ChronicZebrafishGeneticsMicronucleus TestsDose-Response Relationship DrugMutagenicity Testsbiology.organism_classificationMolecular biology4-Nitroquinoline-1-oxideComet assaychemistryMicronucleus testToxicityComet AssayGenotoxicityMutagensAquatic toxicology (Amsterdam, Netherlands)
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The autoradiographic test for unscheduled DNA synthesis: a sensitive assay for the detection of DNA repair in the HepG2 cell line

2004

International audience; We assessed the DNA-repair capacity of HepG2 cells, which were derived from a human hepatoma, by the unscheduled DNA synthesis assay, using the autoradiography protocol (UDS-AR). We evaluated DNA repair following exposure to direct mutagens (4-nitroquinoline-N-oxide (4-NQO), methyl methanesulfonate (MMS)), to mutagens requiring metabolic activation (benzo[a]pyrene (B[a]P), 2-acetylaminofluorene (2-AAF), N-dimethylnitrosoamine (NDMA)) or to structurally related non-mutagens such as pyrene and 4-acetylaminofluorene (4-AAF). All positive compounds tested induced UDS in HepG2 cells. With 4-NQO and MMS, a concentration-dependent increase in net nuclear grains per cell was…

DNA ReplicationDNA RepairEndpoint DeterminationDNA damageDNA repairHealth Toxicology and Mutagenesis[SDV]Life Sciences [q-bio]Mutagen[SDV.TOX.TCA]Life Sciences [q-bio]/Toxicology/Toxicology and food chainBiologymedicine.disease_causeHEPG203 medical and health scienceschemistry.chemical_compound0302 clinical medicineTumor Cells CulturedGeneticsmedicineHumansComputingMilieux_MISCELLANEOUS030304 developmental biologyGeneticsAnalysis of Variance0303 health sciencesfungiMolecular biologyMethyl methanesulfonate[SDV] Life Sciences [q-bio]chemistryCell culture030220 oncology & carcinogenesisAutoradiographyRegression AnalysisPyreneGenotoxicityDNAMutagens
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The high rate of endoreduplication in the repair deficient CHO mutant EM9 parallels a reduced level of methylated deoxycytidine in DNA

2008

It has been recently proposed that hypomethylation of DNA induced by 5-azacytidine (5-azaC) leads to reduced chromatid decatenation that ends up in endoreduplication, most likely due to a failure in topo II function [S. Mateos, I. Domínguez, N. Pastor, G. Cantero, F. Cortés, The DNA demethylating 5-azaC induces endoreduplication in cultured Chinese hamster cells, Mutat. Res. 578 (2005) 33-42]. The Chinese hamster mutant cell line EM9 has a high spontaneous frequency of endoreduplication as compared to its parental line AA8. In order to see if this is related to the degree of DNA methylation, we have investigated the basal levels of both endpoints in AA8 and EM9, as well as the effect of ext…

DNA ReplicationDNA RepairHealth Toxicology and MutagenesisMutantCHO CellsChromosome segregationamedicine.disease_causeDeoxycytidineChromosomesChinese hamsterHypomethylation of DNAchemistry.chemical_compoundCricetulusCricetinaeGeneticsmedicineAnimalsEndoreduplicationMolecular BiologyMutationbiologyChinese hamster ovary cellEndoreduplicationDNA Methylationbiology.organism_classificationTopoisomerase IIMolecular biologychemistryMutationDNA methylationAzacitidineChromatidDNAMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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A microplate version of the DNA-synthesis inhibition test for rapid detection of DNA-alteration potentials.

1990

A microplate version of the DNA-synthesis inhibition test (DIT) for fast detection of DNA-alteration potentials has been developed. The DIT is based on the concept that DNA damage causes inhibition of DNA synthesis that becomes detectable some time after replicating cells have been in contact with genotoxic agents. In this test procedure human tissue culture cells (HeLa S3), prelabeled with [14C]thymidine, arfe exposed for 90 min to the substances in question. After the cells are rinsed, they are allowed to recover for 2 1/2 h in fresh culture medium, thereby unspecific interactions interfering with DNA replication are practically eliminated. Next, [3H]thymidine is added for 30 min, and the…

DNA ReplicationDNA damageBiophysicsBiologymedicine.disease_causeBiochemistryDNA Synthesis Inhibitionchemistry.chemical_compoundmedicineBenzo(a)pyreneHumansMolecular BiologyChromatographyAutoanalysisDNA synthesisMutagenicity TestsDNA replicationNitroquinolinesCell BiologyDNAMolecular biologychemistryCell cultureMutationThymidineDNAGenotoxicityDNA DamageHeLa CellsMutagensAnalytical biochemistry
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A neutralizing antibody against human DNA polymerase epsilon inhibits cellular but not SV40 DNA replication.

1999

The contribution of human DNA polymerase epsilon to nuclear DNA replication was studied. Antibody K18 that specifically inhibits DNA polymerase activity of human DNA polymerase epsilon in vitro significantly inhibits DNA synthesis both when microinjected into nuclei of exponentially growing human fibroblasts and in isolated HeLa cell nuclei. The capability of this neutralizing antibody to inhibit DNA synthesis in cells is comparable to that of monoclonal antibody SJK-132-20 against DNA polymerase alpha. Contrary to the antibody against DNA polymerase alpha, antibody K18 against DNA polymerase epsilon did not inhibit SV40 DNA replication in vitro. These results indicate that DNA polymerase e…

DNA ReplicationDNA polymeraseDNA polymerase IIDNA polymerase epsilonSimian virus 40Virus ReplicationDNA polymerase deltaAntibodiesCell LineNeutralization TestsCatalytic DomainGeneticsAnimalsHumansPolymeraseDNA clampbiologyDNA replicationDNA Polymerase IIFibroblastsMolecular biologyProliferating cell nuclear antigenBromodeoxyuridineDNA Viralbiology.proteinCattleRabbitsHeLa CellsResearch ArticleNucleic acids research
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A breakdown in macromolecular synthesis preceding differentiation in Streptomyces coelicolor A3(2)

1990

Summary: A transitory cessation of growth was recorded in Streptomyces coelicolor A3(2) at the end of vegetative mycelium formation on solid medium. In the same phase a striking reduction in protein and nucleic acid synthesis was detected. Growth and macromolecular synthesis resumed, nearly reaching the original values, when morphological differentiation occurred. It is concluded that a physiological stress occurs within the bacterial population just before the onset of the morphological differentiation.

DNA ReplicationDNA BacterialbiologyStreptomycetaceaeCell CycleStreptomyces coelicolorbiology.organism_classificationMicrobiologyStreptomycesKineticsRNA Bacterialchemistry.chemical_compoundBiochemistryBiosynthesischemistryProtein BiosynthesisNucleic acidActinomycetalesBacteriaMyceliumMacromoleculeJournal of General Microbiology
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Ras-Related GTPase RhoB Forces Alkylation-Induced Apoptotic Cell Death

2000

rhoB encoding a Ras-related GTPase is immediate-early inducible by genotoxic treatments. To address the question of the physiological role of RhoB in cellular defense, cells stably overexpressing wild-type RhoB protein were generated. Overexpression of RhoB renders cells hypersensitive to the killing effect of alkylating agents including antineoplastic drugs but not to UV-light and doxorubicin. As compared to control cells, RhoB overexpressing cells revealed an increase in the frequency of alkylation-induced apoptotic cell death. This indicates that RhoB is involved in modulating apoptotic signaling. Furthermore, overexpression of RhoB resulted in a prolonged transient block to DNA replicat…

DNA ReplicationDNA ComplementaryAlkylationDNA RepairUltraviolet RaysRHOBBiophysicsApoptosisGTPaseBiologyTransfectionBiochemistryMicechemistry.chemical_compoundRhoB GTP-Binding ProteinmedicineAnimalsDoxorubicinrhoB GTP-Binding ProteinCytotoxicityAntineoplastic Agents AlkylatingMolecular BiologyDNA replication3T3 CellsCell BiologyMethyl MethanesulfonateRatsCell biologychemistryApoptosisCancer researchDNADNA Damagemedicine.drugBiochemical and Biophysical Research Communications
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