Search results for " DNA Damage"

showing 10 items of 41 documents

Inter-laboratory validation of procedures for measuring 8-oxo-7,8-dihydroguanine/8-oxo-7,8-dihydro-2’-deoxyguanosine in DNA.

2002

The aim of ESCODD, a European Commission funded Concerted Action, is to improve the precision and accuracy of methods for measuring 8-oxo-7,8-dihydroguanine (8-oxoGua) or the nucleoside (8-oxodG). On two occasions, participating laboratories received samples of different concentrations of 8-oxodG for analysis. About half the results returned (for 8-oxodG) were within 20% of the median values. Coefficients of variation (for three identical samples) were commonly around 10%. A sample of calf thymus DNA was sent, dry, to all laboratories. Analysis of 8-oxoGua/8-oxodG in this sample was a test of hydrolysis methods. Almost half the reported results were within 20% of the median value, and half …

GuanineAnalytical chemistryTest sensitivityThymus GlandSensitivity and SpecificityBiochemistryGas Chromatography-Mass SpectrometryMass SpectrometryOxidative dna damagechemistry.chemical_compound8 oxo 7 8 dihydroguanineAnimalsHumansEuropean commissionInter-laboratoryChromatography High Pressure LiquidChromatographyChemistry8 oxo 7 8 dihydro 2 deoxyguanosineDNAGeneral MedicineCattleBiomarkersDNAChromatography LiquidDNA Damage
researchProduct

Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
researchProduct

Oxidative DNA damage induced by visible light in mammalian cells: extent, inhibition by antioxidants and genotoxic effects

1998

The extent of the indirect DNA damage generated in mammalian cells by visible light because of the presence of endogenous photosensitizers was studied by means of repair endonucleases. In immortalized human keratinocytes (HaCaT cells) exposed to low doses of natural sunlight, the yield of oxidative DNA base modifications sensitive to the repair endonuclease formamidopyrimidine-DNA glycosylase (Fpg protein) generated by this indirect mechanism was 10% of that of pyrimidine dimers (generated by direct DNA excitation). A similar yield of Fpg-sensitive modifications, which include 8-hydroxyguanine, was observed in primary keratinocytes. The relative yield of oxidative base modifications decreas…

KeratinocytesMalePorphyrinsLightDNA damageRiboflavinPyrimidine dimerAscorbic AcidBiologyToxicologyIndirect DNA damageAntioxidantsMiceCricetinaeGeneticsAnimalsHumansN-Glycosyl HydrolasesMolecular BiologyCells CulturedMutagenesisInfant NewbornInfantEndonucleasesAscorbic acidHaCaTDNA-Formamidopyrimidine GlycosylaseBiochemistryMutagenesisDNA glycosylaseChild PreschoolBiophysicsL1210 cellsOxidation-ReductionDNA DamageMutation Research/DNA Repair
researchProduct

Upon oxidative stress, the antiapoptotic Hsp60/procaspase-3 complex persists in mucoepidermoid carcinoma cells.

2008

Hsp60, a mitochondrial chaperonin highly conserved during evolution, has been found elevated in the cytosol of cancer cells, both in vivo and in vitro, but its role in determining apoptosis during oxidative stress (OS) has not yet been fully elucidated. The aim of the present work was to study the effects of OS on Hsp60 levels and its interactions with procaspase- 3 (p-C3) and p53 in tumor cells. NCI-H292 (mucoepidermoid carcinoma) cells were exposed to various concentrations of hydrogen peroxide (H2O2) for 24 hours. Cell viability was determined by Trypan blue and MTT assays. DNA damage was assessed by the Comet assay, and apoptosis was measured by the AnnexinV cytofluorimetric test. Expos…

Lung Neoplasmsanimal structuresHistologyCell SurvivalDNA damageBlotting WesternBiophysicsHsp60;procaspase-3;mucoepidermoid carcinomaGene ExpressionTetrazolium SaltsApoptosisBiologymedicine.disease_causechemistry.chemical_compoundCell Line TumormedicineHumansChaperonin Hsp60 Cpn60 procaspase-3 caspase- 3 DNA damage p53 apoptosis.Viability assaylcsh:QH301-705.5FormazansCaspase 3Settore BIO/16 - Anatomia UmanaChaperonin 60DNAHydrogen PeroxideTrypan BlueCell BiologyImmunohistochemistryMolecular biologyComet assayOxidative Stresslcsh:Biology (General)chemistryApoptosisCancer cellCarcinoma MucoepidermoidHSP60Trypan blueComet AssayTumor Suppressor Protein p53Oxidative stressDNA Damage
researchProduct

Is the Mean Blood Leukocyte Telomere Length a Predictor for Sporadic Thoracic Aortic Aneurysm? Data from a Preliminary Study

2012

Telomeres have been postulated as a universal clock that shortens in parallel with cellular aging. They are specialized DNA-protein structures at the ends of chromosome with remarkable functions--preventing their recognition as double-stranded DNA breaks, protecting their recombination and degradation, and avoiding a DNA damage cellular response. Telomere shortening is currently considered the best aging marker, but is also a predictor for age-related diseases, including cardiovascular diseases. Biological age clearly seems to be a better predictor of vascular risk rather than chronological age. This concept is supported by key assumptions that peripheral blood leukocyte telomere content ac…

MaleAgingPathologymedicine.medical_specialtyThoracicBiological ageVascular riskBiologyBioinformaticsThoracic aortic aneurysmGeneticLeukocytesmedicineHumansSettore MED/05 - Patologia ClinicaAged; Aging; Aortic Aneurysm Thoracic; Case-Control Studies; Cellular Senescence; DNA; DNA Damage; Female; Humans; Leukocytes; Male; Middle Aged; Recombination Genetic; Telomere; Vascular DiseasesVascular DiseasesCellular Senescencevascular ageingAgedRecombination GenetictelomereAortic Aneurysm ThoracicVascular diseaseChromosomeSettore MED/23 - Chirurgia CardiacaDNAMiddle Agedmedicine.diseaseRecombinationPeripheral bloodAortic AneurysmTAATelomereCellular AgingCase-Control StudiesFemaleGeriatrics and GerontologyDNA DamageRejuvenation Research
researchProduct

Deregulation of the G1 to S-phase cell cycle checkpoint is involved in the pathogenesis of human osteosarcoma.

2004

Osteosarcoma (OS) displays complex karyotypes with numerical changes as well as structural abnormalities suggesting that several oncogenes and tumor suppressor genes may be implicated in the biology of OS. The aim of our study was to investigate the possible implication of the molecular alterations of the G1 to S-phase checkpoint genes in the pathogenesis of OS. We analyzed samples from 29 patients and found molecular alterations of the RB and TP53 genes in 6 (21%) and 3 (10%) cases, respectively. Homozygous deletion of the INK4A/ARF locus and methylation of INK4A was detected in 3 (10%) and 2 (7%) cases, respectively. CDK4 and MDM2 co-amplification was observed in 1 case (3%). Cyclin D3 is…

MaleCell cycle checkpointAdolescentLocus (genetics)Bone NeoplasmsBiologyPathology and Forensic MedicineS PhasePathogenesisGene duplicationmedicineHumansCHEK1Cyclin D3ChildMolecular BiologyAgedOsteosarcomaReverse Transcriptase Polymerase Chain ReactionCell CycleAge FactorsG1 PhaseGene AmplificationCell BiologyG2-M DNA damage checkpointMiddle Agedmedicine.diseaseGenes cdcHistory 16th CenturyCancer researchOsteosarcomaFemaleChromosomes Human Pair 9Diagnostic molecular pathology : the American journal of surgical pathology, part B
researchProduct

CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination

2015

Artículo escrito por un elevado número de autores, solo se referencian el que aparece en primer lugar, el nombre del grupo de colaboración, si le hubiere, y los autores pertenecientes a la UAM

MaleProgrammed cell deathMicrocephalyGeneral Physics and AstronomyCell Cycle ProteinsDwarfismBiologyReal-Time Polymerase Chain ReactionArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineChromosome structureSpermatocytesmedicineAnimalscentrioleHomologous Recombination030304 developmental biologyRecombination GeneticfertilityGeneticsCentrosomeMeiotic recombination0303 health sciencesMultidisciplinarySperm CountProtein cep63FaciesGeneral Chemistrymedicine.diseaseBiología y Biomedicina / BiologíaImmunohistochemistryNeural stem cell3. Good healthCEP63MeiosisSeckel syndromeCentrosomeMicrocephalyTumor Suppressor Protein p53Homologous recombinationmicrocephaly ; DNA damage ; centrosome ; meiosis030217 neurology & neurosurgeryDNA Damage
researchProduct

Mitochondrial Oxidative Stress, Mitochondrial DNA Damage and Their Role in Age-Related Vascular Dysfunction

2015

The prevalence of cardiovascular diseases is significantly increased in the older population. Risk factors and predictors of future cardiovascular events such as hypertension, atherosclerosis, or diabetes are observed with higher frequency in elderly individuals. A major determinant of vascular aging is endothelial dysfunction, characterized by impaired endothelium-dependent signaling processes. Increased production of reactive oxygen species (ROS) leads to oxidative stress, loss of nitric oxide (•NO) signaling, loss of endothelial barrier function and infiltration of leukocytes to the vascular wall, explaining the low-grade inflammation characteristic for the aged vasculature. We here disc…

Mitochondrial ROSmedicine.medical_specialtyMitochondrial DNADNA RepairInflammationReviewBiologyMitochondrionmedicine.disease_causeDNA MitochondrialCatalysisAntioxidantsNitric oxideInorganic Chemistrylcsh:Chemistrychemistry.chemical_compoundInternal medicinemedicineAnimalsHumansPhysical and Theoretical ChemistryEndothelial dysfunctionMolecular Biologylcsh:QH301-705.5Spectroscopychemistry.chemical_classificationReactive oxygen speciesmitochondrial oxidative stressOrganic Chemistryagingmitochondrial DNA damageGeneral Medicinevascular dysfunctionmedicine.diseaseComputer Science ApplicationsMitochondriaOxidative StressEndocrinologyBiochemistrychemistrylcsh:Biology (General)lcsh:QD1-999Cardiovascular Diseasesmedicine.symptomReactive Oxygen SpeciesOxidative stressDNA DamageInternational Journal of Molecular Sciences
researchProduct

A nanodosimetric model of radiation-induced clustered DNA damage yields

2010

International audience; We present a nanodosimetric model for predicting the yield of double strand breaks (DSBs) and non-DSB clustered damages induced in irradiated DNA. The model uses experimental ionization cluster size distributions measured in a gas model by an ion counting nanodosimeter or, alternatively, distributions simulated by a Monte Carlo track structure code developed to simulate the nanodosimeter. The model is based on a straightforward combinatorial approach translating ionizations, as measured or simulated in a sensitive gas volume, to lesions in a DNA segment of one-two helical turns considered equivalent to the sensitive volume of the nanodosimeter. The two model paramete…

Quantitative Biology::BiomoleculesAlgorithms Computer Simulation DNA/*radiation effects DNA Breaks[PHYS.PHYS.PHYS-MED-PH] Physics [physics]/Physics [physics]/Medical Physics [physics.med-ph][ PHYS.PHYS.PHYS-MED-PH ] Physics [physics]/Physics [physics]/Medical Physics [physics.med-ph]Genetic Monte Carlo Method Nanotechnology/instrumentation/*methods Plasmids/radiation effects Probability Protons/adverse effects Radiometry/instrumentation/*methods Reproducibility of Results Saccharomyces cerevisiae SoftwareDouble-Stranded/radiation effects DNA Damage/*radiation effects Helium/adverse effects *Models
researchProduct

Protein kinase C controls activation of the DNA integrity checkpoint

2014

The protein kinase C (PKC) superfamily plays key regulatory roles in numerous cellular processes. Saccharomyces cerevisiae contains a single PKC, Pkc1, whose main function is cell wall integrity maintenance. In this work, we connect the Pkc1 protein to the maintenance of genome integrity in response to genotoxic stresses. Pkc1 and its kinase activity are necessary for the phosphorylation of checkpoint kinase Rad53, histone H2A and Xrs2 protein after deoxyribonucleic acid (DNA) damage, indicating that Pkc1 is required for activation of checkpoint kinases Mec1 and Tel1. Furthermore, Pkc1 electrophoretic mobility is delayed after inducing DNA damage, which reflects that Pkc1 is post-translatio…

Saccharomyces cerevisiae ProteinsCell cycle checkpointCell Cycle ProteinsProtein Serine-Threonine KinasesGenome Integrity Repair and ReplicationBiologyGeneticsHumansCHEK1Kinase activityCheckpoint Kinase 2Protein Kinase CProtein kinase CDNA-PKcsDNA integrity checkpointIntracellular Signaling Peptides and ProteinsG2-M DNA damage checkpointCell biologyCheckpoint Kinase 2Protein Kinase C-deltaBiochemistryMutationProtein Processing Post-TranslationalDNA DamageHeLa CellsMutagensNucleic Acids Research
researchProduct