Search results for "DNA Repair"

showing 10 items of 295 documents

The radiosensitization effect of titanate nanotubes as a new tool in radiation therapy for glioblastoma: A proof-of-concept

2013

Abstract Background and purpose One of the new challenges to improve radiotherapy is to increase the ionizing effect by using nanoparticles. The interest of titanate nanotubes (TiONts) associated with radiotherapy was evaluated in two human glioblastoma cell lines (SNB-19 and U87MG). Materials and methods Titanate nanotubes were synthetized by the hydrothermal treatment of titanium dioxide powder in a strongly basic NaOH solution. The cytotoxicity of TiONts was evaluated on SNB-19 and U87MG cell lines by cell proliferation assay. The internalization of TiONts was studied using Transmission Electron Microscopy (TEM). Finally, the effect of TiONts on cell radiosensitivity was evaluated using …

Radiation-Sensitizing AgentsCell SurvivalDNA repairCellApoptosisFlow cytometryCell Line TumormedicineHumansRadiology Nuclear Medicine and imagingRadiosensitivityClonogenic assayCytotoxicityTitaniumNanotubesmedicine.diagnostic_testBrain NeoplasmsChemistryCell growthCell CycleHematologyCell cyclemedicine.anatomical_structureOncologyBiophysicsGlioblastomaReactive Oxygen SpeciesDNA DamageRadiotherapy and Oncology
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A radiosensitizing effect of artesunate in glioblastoma cells is associated with a diminished expression of the inhibitor of apoptosis protein surviv…

2011

Abstract Background and purpose Novel strategies to overcome an irradiation resistant phenotype may help to increase therapeutic efficacy in glioblastoma multiforme. The present study aimed to elucidate radiation sensitizing properties of artesunate, a semi synthetic derivate of artemisinin and to assess factors involved in this effect. Materials and methods LN229 and U87MG cells were treated with various concentrations of artesunate and radiation response was determined by a colony forming assay. Cell numbers, apoptosis induction, cell cycle distribution, and DNA repair following combined modality treatment were monitored by MTT-, caspase 3/7 assay, cytofluorometry, and γ-H2AX foci formati…

Radiation-Sensitizing AgentsDNA RepairCell SurvivalSurvivinArtesunateDown-RegulationCaspase 3ApoptosisInhibitor of apoptosisInhibitor of Apoptosis Proteinschemistry.chemical_compoundCell Line TumorSurvivinHumansRadiology Nuclear Medicine and imagingClonogenic assayDose-Response Relationship DrugBrain NeoplasmsCell CycleHematologyCell cycleArtemisininsXIAPNeoplasm ProteinsOncologychemistryArtesunateApoptosisCancer researchGlioblastomaRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
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DICER and ZRF1 contribute to chromatin decondensation during nucleotide excision repair

2016

Abstract Repair of damaged DNA relies on the recruitment of DNA repair factors in a well orchestrated manner. As a prerequisite, the chromatin needs to be decondensed by chromatin remodelers to allow for binding of repair factors and for DNA repair to occur. Recent studies have implicated members of the SWI/SNF and INO80 families as well as PARP1 in nucleotide excision repair (NER). In this study, we report that the endonuclease DICER is implicated in chromatin decondensation during NER. In response to UV irradiation, DICER is recruited to chromatin in a ZRF1-mediated manner. The H2A–ubiquitin binding protein ZRF1 and DICER together impact on the chromatin conformation via PARP1. Moreover, …

Ribonuclease III0301 basic medicineDNA RepairUltraviolet RaysDNA damageDNA repairgenetic processesPoly (ADP-Ribose) Polymerase-1Genome Integrity Repair and ReplicationBiologyChromatin remodelingCell LineDEAD-box RNA HelicasesHistones03 medical and health scienceschemistry.chemical_compoundUbiquitinCell Line TumorGeneticsAnimalsHumansCaenorhabditis elegansOncogene ProteinsOsteoblastsUbiquitinfungiRNA-Binding ProteinsFibroblastsChromatin Assembly and DisassemblyMolecular biologyChromatinChromatinDNA-Binding Proteinsenzymes and coenzymes (carbohydrates)HEK293 Cells030104 developmental biologychemistrybiology.proteinDNADNA DamageMolecular ChaperonesNucleotide excision repairDicerNucleic Acids Research
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Yeast gene CMR1/YDL156W is consistently co-expressed with genes participating in DNA-metabolic processes in a variety of stringent clustering experim…

2013

© 2013 The Authors. Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0/, which permits unrestricted use, provided the original author and source are credited. The binarization of consensus partition matrices (Bi-CoPaM) method has, among its unique features, the ability to perform ensemble clustering over the same set of genes from multiple microarray datasets by using various clustering methods in order to generate tunable tight clusters. Therefore, we have used the Bi-CoPaM method to the most synchronized 500 cell-cycle-regulated yeast genes from different microarray datasets to produce four tight, specific …

Saccharomyces cerevisiae ProteinsCMR1/YDL156W1004Biomedical EngineeringBiophysicsG1/S transitionDNA repairBioengineeringDNA-Directed DNA PolymeraseSaccharomyces cerevisiaeBiologyDNA replication2244BiochemistryYeast geneBiomaterialschemistry.chemical_compoundReplication Protein Abinarization of consensus partition matrixCluster AnalysisCluster analysisGeneDNA-directed DNA polymeraseLicenseResearch Articlesta113GeneticsModels GeneticGene Expression ProfilingDNACreative commonsMicroarray AnalysisDNA-Binding ProteinsGenes cdcGene expression profilingchemistryDNABiotechnology
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Expression of yeast but not human apurinic/apyrimidinic endonuclease renders Chinese hamster cells more resistant to DNA damaging agents.

1997

Abasic sites represent ubiquitous DNA lesions that arise spontaneously or are induced by DNA-damaging agents. They block DNA replication and are considered to be cytotoxic and mutagenic. The key enzymes involved in the repair of abasic sites are apurinic/apyrimidinic (AP) endonucleases which process these lesions in an error-free mechanism. To analyze the role of AP endonuclease in the protection of mammalian cells against DNA damaging agents, we have transfected both the human (APE) and the yeast (APN1) AP endonuclease in Chinese hamster cells and compared the effects of expression of these genes in stable transfectants as to survival of cells and formation of chromosomal aberrations. Alth…

Saccharomyces cerevisiae ProteinsDNA RepairDNA repairCell SurvivalBlotting WesternCarbon-Oxygen LyasesChromosome DisordersCHO CellsToxicologyTransfectionAP endonucleaseDNA repair ; Apurinic endonuclease ; cellular defense mechanismschemistry.chemical_compoundCricetinaeGeneticsDNA-(Apurinic or Apyrimidinic Site) LyaseAnimalsHumansAP siteRNA MessengerFluorescent Antibody Technique IndirectMolecular BiologyCell NucleusChromosome AberrationsEndodeoxyribonucleasesbiologyCell DeathfungiNuclear ProteinsBase excision repairHydrogen PeroxideBlotting NorthernMethyl MethanesulfonateMolecular biologyDNA-(apurinic or apyrimidinic site) lyaseDNA Repair EnzymeschemistryGene Expression Regulationbiology.proteinChromosome breakageDNANucleotide excision repairDNA DamagePlasmidsMutation research
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DNA damage susceptibility and repair in correlation to calendric age and longevity.

2000

In two mouse strains, SAM P (senescence acceleration prone) and SAM R (senescence acceleration resistant), of different longevities, with a ratio of P/R=1:2), the DNA status in the course of aging has been investigated using the DNA Alkaline Filter Elution (AFE) technique. Six different organs (brain, liver, heart, lung, intestine, and muscle) have been used in each of the four animals of a given age. Earlier it had been shown, that DNA is damaged the more the higher the age of the animal. DNA damage susceptibility, measured after exposure of organ pieces to nitroquinoline-N-oxide (NQO), is also significantly increased at higher ages, while repair, measured of NQO damaged tissue after 3 h i…

SenescenceAgingDNA RepairDNA damageRatónmedia_common.quotation_subjectLongevityBiologyAndrologychemistry.chemical_compoundMicemedicineAnimalsIncubationmedia_commonGeneticsLungStrain (chemistry)LongevityDNA4-Nitroquinoline-1-oxideMice Mutant Strainsmedicine.anatomical_structurechemistryDNADevelopmental BiologyDNA DamageMutagensMechanisms of ageing and development
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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Long-term effects of delayed parenthood.

1998

The present study aims to define, characterize and compare the long-term effects on offspring of delayed parenthood. Data published so far on this topic show that maternal and paternal ageing may affect offspring by different mechanisms. Delayed motherhood is characterized by increased probability of obstetric complications and/or fetal and perinatal problems which, in turn, may increase the risks of mortality and morbidity in newborns and later life. Furthermore, maternal ageing is distinguished by a decreased ratio of male to female infants and higher odds of conceiving a trisomic child and/or an individual suffering from mitochondrial DNA disorders. In contrast, delayed fatherhood is ass…

SenescenceMaleMitochondrial DNAmedicine.medical_specialtyDNA RepairOffspringDiseaseBiologymedicine.disease_causePaternal AgeAndrologyPregnancyInternal medicinemedicineHumansFetusPregnancyRehabilitationPregnancy OutcomeObstetrics and Gynecologymedicine.diseasePregnancy ComplicationsEndocrinologyReproductive MedicineAgeingMutationFemaleOxidative stressMaternal AgeHuman reproduction (Oxford, England)
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The role of mitochondrial oxidative stress in aging.

2003

Mitochondria are both a major source of oxidants and a target for their damaging effects, and, therefore, mitochondrial oxidative stress appears to be a cause, rather than a consequence, of cell aging. Oxidative damage in aging is particularly high in specific molecular targets, such as mitochondrial DNA and aconitase, and mitochondrial oxidative stress may drive tissue aging through intrinsic apoptosis. Mitochondrial function and morphology are impaired upon aging, as judged by a decline in membrane potential as well as by an increase in peroxide production and size of the organelles. In view of the age-related decreases in mitochondrial protein synthesis, mitochondrial transcripts, and ex…

SenescenceMitochondrial DNAAgingDNA RepairMitochondrial TurnoverMitochondrionBiologymedicine.disease_causeBiochemistryDNA MitochondrialGlutathioneMitochondriaOxygenOxidative StressBiochemistrymitochondrial fusionLiverPhysiology (medical)medicineDNAJA3AnimalsHumansReactive Oxygen SpeciesCell agingOxidative stressFree radical biologymedicine
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Gene amplification in fibroblasts from ataxia telangiectasia (AT) patients and in X-ray hypersensitive AT-like Chinese hamster mutants

2001

In search of functions involved in the regulation of gene amplification, and given the relevance of chromosome breakage in initiating the process, we analyzed the gene amplification ability of cells hypersensitive to inducers of DNA double-strand breaks and defective in cell cycle control: two human fibroblast strains derived from patients affected by ataxia telangiectasia (AT) and two hamster mutant cell lines belonging to complementation group XRCC8 of the rodent X-ray-sensitive mutants. These mutants are considered hamster models of AT cells. To measure gene amplification, the frequency and the rate of occurrence of N-(phosphonacetyl)-l-aspartate resistant cells were determined. In both …

Settore BIO/18 - GeneticaCancer Research gene amplification DNA repair
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