Search results for "Glycosylase"

showing 10 items of 53 documents

Study of the Mode and Efficiency of DNA Binding in the Damage Induced by Photoactivated Water Soluble Porphyrins

2013

We have investigated the DNA binding interactions and in vitro photoactivated DNA damage induced by a neutral water soluble porphyrin derivative 5,10,15,20-tetrakis(2,4,6-trihydroxyphenyl)porphyrin (TTHPP) and its zinc derivative 5,10,15,20-tetrakis(2,4,6-trihydroxyphenyl)porphyrinato zinc(II) (Zn-TTHPP) upon visible light irradiation through various spectroscopic techniques and employing repair endonucleases. These porphyrin derivatives exhibited high affinity toward DNA through groove binding interactions as evidenced through the UV-vis absorption, emission, circular dichroism spectral and viscosity changes. Interestingly, the free base porphyrin derivative, TTHPP generated efficient sing…

HematoporphyrinCircular dichroismPorphyrinsSinglet oxygenDNA damageCircular DichroismSpectrum AnalysisWaterDNAGeneral MedicinePhotochemical ProcessesPhotochemistryBiochemistryPorphyrinchemistry.chemical_compoundchemistryDNA glycosylasePhotosensitizerPhysical and Theoretical ChemistryDNADNA DamagePhotochemistry and Photobiology
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Rapid inactivation and proteasome-mediated degradation of OGG1 contribute to the synergistic effect of hyperthermia on genotoxic treatments

2013

Inhibition of DNA repair has been proposed as a mechanism underlying heat-induced sensitization of tumour cells to some anticancer treatments. Base excision repair (BER) constitutes the main pathway for the repair of DNA lesions induced by oxidizing or alkylating agents. Here, we report that mild hyperthermia, without toxic consequences per se, affects cellular DNA glycosylase activities, thus impairing BER. Exposure of cells to mild hyperthermia leads to a rapid and selective inactivation of OGG1 (8-oxoguanine DNA glycosylase) associated with the relocalisation of the protein into a detergent-resistant cellular fraction. Following its inactivation, OGG1 is ubiquitinated and directed to pro…

HyperthermiaProteasome Endopeptidase ComplexPyrrolidinesDNA RepairDNA repairUbiquitin-Protein Ligases[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]BiochemistryDNA Glycosylases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineUbiquitinEnzyme StabilitymedicineHumans[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Molecular BiologyComputingMilieux_MISCELLANEOUSCell Proliferation030304 developmental biologyCell Nucleus0303 health sciencesPhotosensitizing AgentsbiologyCell growthUbiquitinationCell BiologyBase excision repairmedicine.diseaseMolecular biology[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Protein TransportProteasomechemistryDNA glycosylase030220 oncology & carcinogenesisProteolysisCancer researchbiology.proteinHeat-Shock ResponseQuinolizinesDNADNA DamageHeLa Cells
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The elemental role of iron in DNA synthesis and repair

2017

Iron is an essential redox element that functions as a cofactor in many metabolic pathways. Critical enzymes in DNA metabolism, including multiple DNA repair enzymes (helicases, nucleases, glycosylases, demethylases) and ribonucleotide reductase, use iron as an indispensable cofactor to function. Recent striking results have revealed that the catalytic subunit of DNA polymerases also contains conserved cysteine-rich motifs that bind iron–sulfur (Fe/S) clusters that are essential for the formation of stable and active complexes. In line with this, mitochondrial and cytoplasmic defects in Fe/S cluster biogenesis and insertion into the nuclear iron-requiring enzymes involved in DNA synthesis a…

Iron-Sulfur Proteins0301 basic medicineDNA RepairDNA polymeraseDNA damageDNA repairIronBiophysicsDNA repairEukaryotic DNA replicationSaccharomyces cerevisiaeBiochemistryDNA GlycosylasesBiomaterials03 medical and health sciencesRibonucleotide ReductasesHumansProtein–DNA interactionRibonucleotide reductaseReplication protein Achemistry.chemical_classificationDNA ligaseDeoxyribonucleasesDNA synthesis030102 biochemistry & molecular biologybiologyIron deficiencyDNA HelicasesMetals and AlloysHelicaseDNAYeast030104 developmental biologyIron cofactorBiochemistrychemistryChemistry (miscellaneous)biology.proteinIron-sulfur clusterMetallomics
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The Friedreich's Ataxia protein frataxin modulates DNA base excision repair in prokaryotes and mammals

2010

DNA-repair mechanisms enable cells to maintain their genetic information by protecting it from mutations that may cause malignant growth. Recent evidence suggests that specific DNA-repair enzymes contain ISCs (iron–sulfur clusters). The nuclearencoded protein frataxin is essential for the mitochondrial biosynthesis of ISCs. Frataxin deficiency causes a neurodegenerative disorder named Friedreich's ataxia in humans. Various types of cancer occurring at young age are associated with this disease, and hence with frataxin deficiency. Mice carrying a hepatocyte-specific disruption of the frataxin gene develop multiple liver tumours for unresolved reasons. In the present study, we show that frata…

Iron-Sulfur ProteinsDNA Repairmedicine.disease_causeBiochemistryDNA Glycosylases8-oxoG 78-dihydro-8-oxoguanineMice0302 clinical medicineIron-Binding Proteinsoxidative stressBER base excision repairCells CulturedMammalsMice Knockout0303 health sciencesfrataxinDMEM Dulbecco's modified Eagle's mediumbiologyLiver NeoplasmsSalmonella entericairon–sulfur clusterLife SciencesIron-binding proteinsTransfection3. Good healthLB Luria–BertaniOGG1 8-oxoguanine DNA glycosylase 1ISC iron–sulfur clusterFpg formamido-pyrimidine DNA glycosylaseHPRT hypoxanthine phosphoribosyltransferaseResearch ArticleDNA damageDNA repairSSB DNA single-strand breakTransfectionCell Line03 medical and health sciencesFRDA Friedreich's ataxiaROS reactive oxygen speciesmedicineAnimalsHumansMUTYH human mutY homologue (Escherichia coli)Molecular BiologyGene030304 developmental biologyFriedreich's ataxiaCell BiologyFibroblastsMolecular biologytumorigenesisProkaryotic CellsFriedreich AtaxiaDNA base excision repairDNA glycosylaseMutationHepatocytesFrataxinbiology.proteinInstitut für ErnährungswissenschaftCarcinogenesisMAPK mitogen-activated protein kinase030217 neurology & neurosurgeryDNA Damage
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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
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Meta-analysis of mismatch repair polymorphisms within the cogent consortium for colorectal cancer susceptibility

2013

In the last four years, Genome-Wide Association Studies (GWAS) have identified sixteen low-penetrance polymorphisms on fourteen different loci associated with colorectal cancer (CRC). Due to the low risks conferred by known common variants, most of the 35% broad-sense heritability estimated by twin studies remains unexplained. Recently our group performed a case-control study for eight Single Nucleotide Polymorphisms (SNPs) in 4 CRC genes. The present investigation is a followup of that study. We have genotyped six SNPs that showed a positive association and carried out a meta-analysis based on eight additional studies comprising in total more than 8000 cases and 6000 controls. The estimate…

Linkage disequilibriumGenotypeReparació de l'ADNlcsh:MedicineDNA repairGenome-wide association studySingle-nucleotide polymorphismBiologyGenetic polymorphismsDNA Mismatch RepairPolymorphism Single NucleotideDNA Glycosylases03 medical and health sciences0302 clinical medicineMUTYHCàncer colorectalHumansGenetic Predisposition to Diseaselcsh:ScienceGenetic Association Studies030304 developmental biologyGenetic associationGenetics0303 health sciencesMultidisciplinaryGenetic heterogeneityPolimorfisme genèticlcsh:RCase-control studyOdds ratioColorectal cancer3. Good health030220 oncology & carcinogenesisCase-Control Studieslcsh:QColorectal NeoplasmsResearch Article
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Stable Oxidative Cytosine Modifications Accumulate in Cardiac Mesenchymal Cells From Type2 Diabetes Patients

2018

Rationale: Human cardiac mesenchymal cells (CMSCs) are a therapeutically relevant primary cell population. Diabetes mellitus compromises CMSC function as consequence of metabolic alterations and incorporation of stable epigenetic changes. Objective: To investigate the role of α-ketoglutarate (αKG) in the epimetabolic control of DNA demethylation in CMSCs. Methods and Results: Quantitative global analysis, methylated and hydroxymethylated DNA sequencing, and gene-specific GC methylation detection revealed an accumulation of 5-methylcytosine, 5-hydroxymethylcytosine, and 5-formylcytosine in the genomic DNA of human CMSCs isolated from diabetic donors. Whole heart genomic DNA analysis reveale…

Male0301 basic medicinePhysiologyPopulationheartBiologyMixed Function OxygenasesCytosineMice03 medical and health sciencesProto-Oncogene ProteinsfibroblastsHuman Umbilical Vein Endothelial CellsAnimalsHumansMyocytes CardiacEpigeneticsEnzyme InhibitorseducationCells CulturedEpigenomicsDemethylationeducation.field_of_studyDNA methylationDNA methylation; epigenomics; fibroblasts; heart; hyperglycemia; metabolism; physiology; cardiology and cardiovascular medicineMesenchymal Stem CellsSettore MED/13 - ENDOCRINOLOGIABase excision repairMolecular biologyThymine DNA GlycosylaseMice Inbred C57BLHEK293 Cells030104 developmental biologyDNA demethylationDiabetes Mellitus Type 2epigenomicsDNA methylationKetoglutaric AcidshyperglycemiaThymine-DNA glycosylaseCardiology and Cardiovascular MedicineOxidation-ReductionmetabolismCirculation Research
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Constitutive expression and inducibility of O6-methylguanine-DNA methyltransferase and N-methylpurine-DNA glycosylase in rat liver cells exhibiting d…

1995

AbstractWe have analyzed the expression of the DNA repair genes O6-methylguanine-DNA methyltransferase (MGMT) and N-methylpurine-DNA glycosylase (MPG) at RNA and protein activity level in primary rat hepatocytes in vitro and various rat hepatoma cell lines exhibiting different status of differentiation. The basal level of MGMT mRNA and activity correlated well with the degree of differentiation, as measured by tyrosine aminotransferase (TAT) mRNA expression. Induction of MGMT mRNA and protein activity by X-ray and Nmethyl-N′-nitro-N-nitrosoguanidine (MNNG) treatment was most pronounced in the well-differentiated hepatocytes and in various differentiated hepatoma cell lines (up to 6-fold). T…

MaleAlkylating AgentsMethyltransferaseDNA repairDNA repairBiology(Rat)DNA methyltransferaseCell LineDNA GlycosylasesRats Sprague-DawleyO(6)-Methylguanine-DNA MethyltransferaseTyrosine aminotransferaseGene expressionAnimalsHepatocyteRNA MessengerN-Glycosyl HydrolasesMolecular BiologyneoplasmsMessenger RNACell DifferentiationMethyltransferasesMolecular biologydigestive system diseasesRatsPerfusionLiverCell cultureDNA glycosylaseEnzyme InductionMolecular MedicineGene expressionMGMTMPGBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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DNA repair activity of 8-oxoguanine DNA glycosylase 1 (OGG1) in human lymphocytes is not dependent on genetic polymorphism Ser326/Cys326.

2001

8-oxoguanine DNA glycosylase 1 (OGG1) is a DNA repair enzyme that excises 7,8-dihydro-8-oxoguanine (8oxoG) from DNA. Since 8oxoG is a highly mispairing lesion, decreased OGG1 expression level could lead to a higher background mutation frequency and could possibly increase the cancer risk of an individual under oxidative stress. In order to analyse the natural variation of OGG1, we measured the DNA repair activity in human lymphocytes of healthy individuals by means of an 8oxoG-containing oligonucleotide assay. The data obtained revealed a two fold interindividual variation of OGG1 activity in lymphocytes. There was no difference in OGG1 activity due to gender and smoking behaviour. Transcri…

MaleDNA RepairDNA damageDNA repairBiologyIn Vitro TechniquesToxicologyDNA-formamidopyrimidine glycosylasechemistry.chemical_compoundGene FrequencyMUTYHGeneticsHumansAmino Acid SequenceLymphocytesMolecular BiologyGeneN-Glycosyl HydrolasesAllelesDNA PrimersPolymorphism GeneticBase SequenceOligonucleotideReverse Transcriptase Polymerase Chain ReactionMolecular biologyIsoenzymeschemistryDNA-Formamidopyrimidine GlycosylaseDNA glycosylaseDNADNA DamageMutation research
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The basal levels of 8-oxoG and other oxidative modifications in intact mitochondrial DNA are low even in repair-deficient (Ogg1(-/-)/Csb(-/-)) mice.

2007

Abstract Mitochondrial DNA (mtDNA) is assumed to be highly prone to damage by reactive oxygen species (ROS) because of its location in close proximity to the mitochondrial electron transport chain. Accordingly, mitochondrial oxidative DNA damage has been hypothesized to be responsible for various neurological diseases, ageing and cancer. Since 7,8-dihydro-8-oxoguanine (8-oxoG), one of the most frequent oxidative base modifications, is removed from the mitochondrial genome by the glycosylase OGG1, the basal levels of this lesion are expected to be highly elevated in Ogg1−/− mice. To investigate this hypothesis, we have used a mtDNA relaxation assay in combination with various repair enzymes …

MaleMitochondrial DNADNA RepairDNA repairHealth Toxicology and MutagenesisOxidative phosphorylationBiologyMitochondrionDNA MitochondrialDNA Glycosylaseschemistry.chemical_compoundMiceGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyMice KnockoutGuanosinePlant ExtractsCorticoviridaeMolecular biologyNuclear DNAMice Inbred C57BLDNA Repair EnzymeschemistryDNA glycosylaseDNA ViralFemaleDNANucleotide excision repairDNA DamageMutation research
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