Search results for "replica"

showing 10 items of 576 documents

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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Alteration of nuclear (2'-5')oligoriboadenylate synthetase and nuclease activities preceding replication of human immunodeficiency virus in H9 cells.

1988

After infection of the respective target cells with the human immunodeficiency virus (HIV-1) viral progeny is produced only after a short temporary delay of some days, depending on cell type. After this period of time a sudden onset of HIV-1 protein synthesis with a dramatic increase in virus release occurs. (2'-5')Oligoriboadenylates [(2'-5')A], capable to activate a latent ribonuclease (RNase L) degrading both mRNA and rRNA, are known mediators involved in the early response of cells to virus infection. Here we show that the (2'-5')A-synthesizing (2'-5')A synthetase, which is inducible by interferon and activated by double-stranded RNA, as well as a (2'-5')A nuclease (2',3'-exoribonucleas…

DNA ReplicationRNase PNuclear EnvelopeVirus ReplicationBiochemistryVirusCell LineSubstrate SpecificityInterferonExoribonucleaseEndoribonucleasesmedicine2'5'-Oligoadenylate SynthetaseHumansRibonucleaseCell NucleusMessenger RNAbiologyChemistryNucleic Acid HybridizationCell Transformation ViralVirologyMolecular biologyVirus ReleaseKineticsbiology.proteinHIV-1Exoribonuclease activitymedicine.drugBiological chemistry Hoppe-Seyler
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Chromatin remodeling regulation by small molecules and metabolites.

2010

The eukaryotic genome is a highly organized nucleoprotein structure comprising of DNA, histones, non-histone proteins, and RNAs, referred to as chromatin. The chromatin exists as a dynamic entity, shuttling between the open and closed forms at specific nuclear regions and loci based on the requirement of the cell. This dynamicity is essential for the various DNA-templated phenomena like transcription, replication, and repair and is achieved through the activity of ATP-dependent chromatin remodeling complexes and covalent modifiers of chromatin. A growing body of data indicates that chromatin enzymatic activities are finely and specifically regulated by a variety of small molecules derived f…

DNA ReplicationS-AdenosylmethionineTranscription GeneticInositol PhosphatesBiophysicsBiochemistryChromatin remodelingchemistry.chemical_compoundAdenosine TriphosphateStructural BiologyAcetyl Coenzyme AGeneticsAnimalsHumansMolecular Biologychromatin small moleculesbiologyGenome HumanDNA replicationDNAChromatin Assembly and DisassemblyNADMi-2/NuRD complexChromatinNucleoproteinChromatinHistoneBiochemistrychemistrybiology.proteinNAD+ kinaseDNABiochimica et biophysica acta
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Genotoxicity of the fungicide dichlofluanid in seven assays

1991

Seven different endpoints for detection of genotoxicity have been used to demonstrate the DNA-altering properties of Dichlofluanid, a fungicide commonly used in viticulture pest control. Each endpoint (DNA synthesis inhibition test, alkaline viscosimetry, umu-test, alkaline filter elution, FADU-test, 32P-postlabeling, and electron microscopy) shows clear evidence of genotoxicity. These data indicate that application of the fungicide dichlofluanid may be mutagenic and/or carcinogenic for exposed humans.

DNA ReplicationSalmonella typhimuriumDNA AlterationEpidemiologyHealth Toxicology and MutagenesisDichlofluanidmedicine.disease_causeCell LineMicechemistry.chemical_compoundmedicineAnimalsHumansBioassayGenetics (clinical)CaptanCarcinogenAniline CompoundsMutagenicity TestsFishesDNAPesticideFungicides IndustrialFungicideBiochemistrychemistryGenotoxicityDNA DamageHeLa CellsMutagensEnvironmental and Molecular Mutagenesis
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Inhibition of human T-cell leukemia virus type I replication in primary human T cells that express antisense RNA

1989

The human T-cell leukemia virus type I is associated with adult T-cell leukemia-lymphoma in humans, a disease which is induced by a malignant transformation of T lymphocytes. Retrovirus vectors carrying human T-cell leukemia virus type I-derived sequences in reversed transcriptional orientation were used to express antisense RNA transcripts in primary human leukocytes. Human T-cell leukemia virus type I replication and virus-mediated immortalization were inhibited in cells harboring antisense constructs. This study suggests that retrovirus-mediated antisense RNA inhibition can be used to protect primary human T-lymphocytes from human T-cell leukemia virus type I-mediated cell transformation.

DNA ReplicationT-LymphocytesvirusesGenetic VectorsImmunologyViral transformationVirus ReplicationMicrobiologyVirusCell LineRetrovirushemic and lymphatic diseasesVirologymedicineHumansRNA AntisenseHuman T-lymphotropic virus 1biologyRNAbiology.organism_classificationmedicine.diseaseVirologyMolecular biologyAntisense RNALeukemiaGene Expression RegulationViral replicationInsect ScienceHuman T-lymphotropic virus 1RNACell DivisionResearch ArticleJournal of Virology
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