Search results for "DNA Replication"

showing 10 items of 107 documents

Transformation of Aspergillus parasiticus using autonomously replicating plasmids from Aspergillus nidulans.

1994

A genetic transformation system for the aflatoxin-producing fungus Aspergillus parasiticus using two autonomously replicating plasmids from A. nidulans (ARp1 and pDHG25) is reported. Transformation frequencies using the plasmid pDHG25 were from 5 x 10(2) to 2.5 x 10(4) transformants per 10(6) viable protoplasts and microgram DNA. The stability of the plasmids in the transformants was also studied. This transformation system offers a new opportunity to clone genes related to aflatoxin production using appropriate aflatoxin-defective mutants.

DNA ReplicationArginine BAutonomously replicating sequenceMitosisLaboratorium voor ErfelijkheidsleerMicrobiologyAspergillus parasiticusAspergillus nidulansMicrobiologyGenetic transformationchemistry.chemical_compoundPlasmidTransformation GeneticAutonomous replicationAspergillus nidulansGeneticsDNA FungalMolecular BiologyGeneGeneticsAspergillus nidulans autonomous replicating plasmidbiologyProtoplastsfood and beveragesProtoplastbiology.organism_classificationAspergillus parasiticusTransformation (genetics)AspergilluschemistryLaboratory of GeneticsDNAPlasmidsFEMS microbiology letters
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Histone carbonylation occurs in proliferating cells

2012

12 páginas, 10 figuras (que no es encuentran en este documento, se pueden ver en: http://www.sciencedirect.com/science/article/pii/S0891584912000664)

DNA ReplicationBlotting WesternCarbonylationFree radicalsBiologyBiochemistryHistonesMicePhysiology (medical)Histone methylationHistone H2AAnimalsHistone codeEpigeneticsPhosphorylationPoly(ADP-ribosyl)ationCell proliferationEpigenomicsChromatinHistoneBiochemistryHistone methyltransferaseNIH 3T3 Cellsbiology.proteinEpigenetics
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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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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