Search results for "DNA Replication"

showing 10 items of 107 documents

Measurement of Lymphocyte Proliferation: Critical Analysis of Radioactive and Photometric Methods

1992

Different methods of lymphocyte proliferation are compared to identify a non-radioactive alternative to 3H-thymidine-test. The enzymatic assays evaluating the turnover of mitochondrial dehydrogenases (MTT-test) and lysosomal hexosaminidase (NAG-test) proved not sensitive enough to substitute for 3H-thymidine incorporation. The incorporation of the nucleotide analog 5-bromodeoxyuridine (BrdU) can be exploited using an ELISA-system (enzyme linked immunosorbent assay) employing a monoclonal anti-BrdU antibody to measure cell proliferation. An optimized test protocol of the BrdU-ELISA which fulfills the requirements for a sensitive and practicable non-radioactive alternative to 3H-thymidine-tes…

DNA ReplicationLymphocyteImmunologyDehydrogenaseLymphocyte proliferationLymphocyte ActivationImmunoenzyme TechniquesPhotometrymedicineHumansImmunology and AllergyHexosaminidaseCells Culturedchemistry.chemical_classificationbiologyChemistryCell growthDNAHematologyMolecular biologymedicine.anatomical_structureEnzymeBiochemistryMonoclonalbiology.proteinAutoradiographyColorimetryAntibodyCell DivisionImmunobiology
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How DNA lesions are turned into powerful killing structures: Insights from UV-induced apoptosis

2008

Mammalian cells treated with ultraviolet (UV) light provide one of the best-known experimental systems for depicting the biological consequences of DNA damage. UV irradiation induces the formation of DNA photoproducts, mainly cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts [(6-4)PPs], that drastically impairs DNA metabolism, culminating in the induction of cell death by apoptosis. While CPDs are the most important apoptosis-inducing lesions in DNA repair proficient cells, recent data indicates that (6-4)PPs also signals for apoptosis in DNA repair deficient cells. The toxic effects of these unrepaired DNA lesions are commonly associated with transcription …

DNA ReplicationMAPK/ERK pathwayProgrammed cell deathBase SequenceTranscription GeneticUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisMolecular Sequence DataApoptosisPyrimidine dimerBiologyCell biologychemistry.chemical_compoundchemistryBiochemistryApoptosisAutophagyGeneticsUltraviolet lightAnimalsHumansDNADNA DamageMutation Research/Reviews in Mutation Research
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Microenvironmental adaptation of experimental tumours to chronic vs acute hypoxia

2004

This study investigated long-term microenvironmental responses (oxygenation, perfusion, metabolic status, proliferation, vascular endothelial growth factor (VEGF) expression and vascularisation) to chronic hypoxia in experimental tumours. Experiments were performed using s.c.-implanted DS-sarcomas in rats. In order to induce more pronounced tumour hypoxia, one group of animals was housed in a hypoxic atmosphere (8% O(2)) for the whole period of tumour growth (chronic hypoxia). A second group was acutely exposed to inspiratory hypoxia for only 20 min prior to the measurements (acute hypoxia), whereas animals housed under normal atmospheric conditions served as controls. Acute hypoxia reduced…

DNA ReplicationMaleCancer ResearchPathologymedicine.medical_specialtyBiologyperfusionRats Sprague-Dawleychemistry.chemical_compoundOxygen ConsumptionVascularityIn vivomedicineAnimalsExperimental TherapeuticshypoxiaCell growthDNA NeoplasmNeoplasms ExperimentalOxygenationHypoxia (medical)VEGFCell HypoxiaRatsVascular endothelial growth factorDisease Models AnimalKineticscell proliferationBlood pressureOncologychemistryvascularityAcute DiseaseChronic Diseaseoxygenationmedicine.symptomPerfusionCell DivisionBritish Journal of Cancer
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The APC/C cofactor Cdh1 prevents replicative stress and p53-dependent cell death in neural progenitors

2013

The E3-ubiquitin ligase APC/C-Cdh1 is essential for endoreduplication but its relevance in the mammalian mitotic cell cycle is still unclear. Here we show that genetic ablation of Cdh1 in the developing nervous system results in hypoplastic brain and hydrocephalus. These defects correlate with enhanced levels of Cdh1 substrates and increased entry into the S phase in neural progenitors. However, cell division is prevented in the absence of Cdh1 due to hyperactivation of cyclin-dependent kinases, replicative stress, induction of p53, G2 arrest and apoptotic death of these progenitor cells. Concomitant ablation of p53 rescues apoptosis but not replicative stress, resulting in the presence of …

DNA ReplicationMaleProgrammed cell deathCell divisionNeurogenesisGeneral Physics and AstronomyApoptosisCell Cycle ProteinsBiologyAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineNeural Stem CellsAnimalsProgenitor cell030304 developmental biologyProgenitorMice KnockoutNeuronschemistry.chemical_classification0303 health sciencesDNA ligaseMultidisciplinaryCell CycleNeurogenesisBrainOrgan SizeGeneral ChemistryCell cycle3. Good healthCell biologyMice Inbred C57BLchemistrySynaptic plasticityFemaleTumor Suppressor Protein p53Cell Division030217 neurology & neurosurgeryNature Communications
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Are the leukocyte telomere length attrition and telomerase activity alteration potential predictor biomarkers for sporadic TAA in aged individuals?

2014

A large variability in occurrence, complications, and age/gender manifestations characterizes individual susceptibility of sporadic thoracic aortic aneurysms (TAA), even in subjects with the same risk factor profiles. The reasons are poorly understood. On the other hand, TAA pathophysiology mechanisms remain unclear than those involved in abdominal aorta aneurysms. However, recent evidence is suggesting a crucial role of biological ageing in inter-individual risk variation of cardiovascular diseases, including sporadic TAA. Biological age rather than chronological age is a better predictor of vascular risk. Relevant assumptions support this concept. In confirming this evidence and our preli…

DNA ReplicationMaleTelomerasePathologymedicine.medical_specialtyAgingGenotypeEnzyme-Linked Immunosorbent AssayBiologyPolymerase Chain ReactionArticleAortic aneurysmRisk FactorsGenotypemedicineIn Situ Nick-End LabelingLeukocytesSporadic TAA. Biological ageing . Leukocyte telomere length attrition . Telomere activity alteration . Predictor TAAbiomarkersSettore MED/05 - Patologia ClinicaHumansGenetic Predisposition to DiseaseRisk factorTelomere ShorteningSettore MED/04 - Patologia GeneraleAortic Aneurysm ThoracicSettore MED/23 - Chirurgia CardiacaGeneral MedicineDNAMiddle AgedTelomeremedicine.diseaseMolecular medicineImmunohistochemistryPathophysiologyTelomereAgeingImmunologyFemaleGeriatrics and GerontologyBiomarkersAge (Dordrecht, Netherlands)
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Asynchronous replication dynamics of imprinted and non-imprinted chromosome regions in early mouse embryos.

2008

We have used interphase FISH to analyze the replication behavior of four imprinted chromosome regions (Snrpn, Zim1-Peg3, Dlk1-Gtl2, and Igf2r) and five non-imprinted regions in mouse one-cell to morula-stage embryos and embryonic fibroblasts. In general, imprinted chromosome regions showed the expected asynchronous pattern of replication throughout all analyzed stages of preimplantation development and in differentiated cells. The Dlk1-Gtl2 locus which is not expressed and Igf2r which is biallelically expressed in early embryos showed a relaxation of replication asynchrony at the morula stage. Asynchronous replication in zygotes and two-cell embryos was not specific to imprinted regions. Th…

DNA ReplicationMaleTranscriptional ActivationRNA UntranslatedTime FactorsSomatic cellZygoteEmbryonic DevelopmentLocus (genetics)BiologyGenomeMorulaChromosomesGenomic InstabilityEpigenesis GeneticGenomic ImprintingMiceChromosome regionsAnimalsImprinting (psychology)GeneCells CulturedIn Situ Hybridization FluorescenceGeneticsZygoteChromosome MappingCell BiologyEmbryo MammalianMice Inbred C57BLFertilizationembryonic structuresFemalePloidyCell DivisionExperimental cell research
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Chromosomal instability, reproductive cell death and apoptosis induced by O6-methylguanine in Mex−, Mex+ and methylation-tolerant mismatch repair com…

1998

O6-Methylguanine (O6-MeG) is induced in DNA by methylating environmental carcinogens and various cytostatic drugs. It is repaired by O6-methylguanine-DNA methyltransferase (MGMT). If not repaired prior to replication, the lesion generates gene mutations and leads to cell death, sister chromatid exchanges (SCEs), chromosomal aberrations and malignant transformation. To address the question of how O6-MeG is transformed into genotoxic effects, isogenic Chinese hamster cell lines either not expressing MGMT (phenotypically Mex-), expressing MGMT (Mex+) or exhibiting the tolerance phenotype (Mex-, methylation resistant) were compared as to their clastogenic response. Mex- cells were more sensitiv…

DNA ReplicationMethylnitronitrosoguanidineGuanineDNA RepairDNA damageHealth Toxicology and MutagenesisDrug ResistanceApoptosisCHO CellsGene mutationBiologyChromosomesDNA AdductsO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeChromosome instabilityGeneticsAnimalsSister chromatidsMolecular BiologyMitosisChromosome AberrationsCell DeathModels GeneticMutagenicity TestsDNA replicationDNA MethylationMolecular biologyDNA methylationDNA mismatch repairSister Chromatid ExchangeMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Replication origins and pause sites in sea urchin mitochondrial DNA

1992

We have used a combination of one- and two-dimensional agarose gel electrophoresis, and solution hybridization to strand-specific probes, to map the replication origin of sea urchin mitochondrial DNA and to investigate the structure of replication intermediates. These assays are consistent with replication initiating unidirectionally from the D-loop region by D-loop expansion, as in vertebrates. A prominent site of initiation of lagging-strand synthesis lies at, or near to, the boundary between the genes for ATPase 6 and COIII, which is also close to a pause site for leading-strand synthesis. These findings suggest a role for pause sites in the regulation of mitochondrial transcription and …

DNA ReplicationMitochondrial DNAMacromolecular SubstancesRestriction MappingEukaryotic DNA replicationBiologyOrigin of replicationPre-replication complexDNA MitochondrialDNA RibosomalGeneral Biochemistry Genetics and Molecular BiologyElectron Transport Complex IVRNA TransferControl of chromosome duplicationAnimalsElectrophoresis Gel Two-DimensionalGeneral Environmental ScienceElectrophoresis Agar GelGeneral Immunology and MicrobiologyTer proteinChromosome MappingNADH DehydrogenaseGeneral MedicineMolecular biologyCell biologyRNA RibosomalSea UrchinsNucleic Acid ConformationOrigin recognition complexSolution hybridizationGeneral Agricultural and Biological SciencesProceedings of the Royal Society of London. Series B: Biological Sciences
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Processing of O6-methylguanine into DNA double-strand breaks requires two rounds of replication whereas apoptosis is also induced in subsequent cell …

2009

The DNA adduct O(6)-methylguanine (O(6)MeG) induced by environmental genotoxins and anticancer drugs is a highly mutagenic, genotoxic and apoptotic lesion. Apoptosis induced by O(6)MeG requires mismatch repair (MMR) and proliferation. Models of O(6)MeG-triggered cell death postulate that O(6)MeG/T mispairs activate MMR giving rise to either direct genotoxic signaling or secondary lesions that trigger apoptotic signaling in the 2(nd) replication cycle. To test these hypotheses, we used a highly synchronized cell system competent and deficient for the repair of O(6)MeG adducts, which were induced by the S(N)1 methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). We show that DNA doub…

DNA ReplicationProgrammed cell deathMethylnitronitrosoguanidineCell cycle checkpointGuanineDNA repairBlotting WesternSuccinimidesApoptosisCHO CellsBiologychemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeDNA adductAnimalsDNA Breaks Double-StrandedMolecular BiologyCell CycleCell BiologyCell cycleFlow CytometryFluoresceinsMolecular biologyCell biologychemistryMicroscopy FluorescenceApoptosisDNA mismatch repairDNADevelopmental BiologyCell cycle (Georgetown, Tex.)
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Apoptotic death induced by the cyclophosphamide analogue mafosfamide in human lymphoblastoid cells: Contribution of DNA replication, transcription in…

2007

Cyclophosphamide is one of the most often used anticancer drugs. Although DNA interstrand cross-links are considered responsible for its cytotoxicity, the mechanism of initiation and execution of cell death is largely unknown. Using the cyclophosphamide analogue mafosfamide, which does not need metabolic activation, we show that mafosfamide induces apoptosis dose and time dependently in lymphoblastoid cells, with clearly more apoptosis in p53(wt) cells. We identified two upstream processes that initiate apoptosis, DNA replication blockage and transcriptional inhibition. In lymphoblastoid cells, wherein DNA replication can be switched off by tetracycline, proliferation is required for induci…

DNA ReplicationProgrammed cell deathTime FactorsTranscription GeneticDNA damageDrug ResistanceAntineoplastic AgentsApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesToxicologyCaspase-Dependent ApoptosisCell Linechemistry.chemical_compoundMafosfamideHumansCHEK1PhosphorylationCyclophosphamideCaspaseCell ProliferationPharmacologyDose-Response Relationship DrugbiologyTumor Suppressor ProteinsCell cycleDNA-Binding ProteinsCheckpoint Kinase 2chemistryApoptosisCaspasesCheckpoint Kinase 1Cancer researchbiology.proteinTumor Suppressor Protein p53Protein KinasesSignal TransductionToxicology and Applied Pharmacology
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