Search results for "N-Glycosyl Hydrolases"

showing 10 items of 13 documents

Genetic epidemiology of autosomal recessive hypercholesterolemia in Sicily: Identification by next-generation sequencing of a new kindred.

2017

Background Autosomal recessive hypercholesterolemia (ARH) is a rare inherited lipid disorder. In Sardinia, differently from other world regions, the mutated allele frequency is high. It is caused by mutations in the low-density lipoprotein receptor adaptor protein 1 gene. Fourteen different mutations have been reported so far; in Sardinia, 2 alleles (ARH1 and ARH2) explain most of the cases. Four ARH patients, all carriers of the ARH1 mutation, have been identified in mainland Italy and 2 in Sicily. Objective The objectives of the study were to improve the molecular diagnosis of familial hypercholesterolemia (FH) and to estimate the frequency of the ARH1 allele in 2 free-living Sicilian pop…

0301 basic medicineMaleSettore MED/09 - Medicina InternaEndocrinology Diabetes and MetabolismFamilial hypercholesterolemia030204 cardiovascular system & hematology0302 clinical medicineChildN-Glycosyl HydrolasesSicilyGeneticsAged 80 and overeducation.field_of_studyNutrition and DieteticsAllele frequencyHomozygoteHigh-Throughput Nucleotide SequencingAutosomal recessive hypercholesterolemiaMiddle AgedAutosomal Recessive HypercholesterolemiaSettore MED/26 - NeurologiaFemaleCardiology and Cardiovascular MedicineAdultAdolescentGenotypePopulationHypercholesterolemiaBiologyDNA sequencing03 medical and health sciencesYoung AdultARH1Internal MedicinemedicineHumansAlleleeducationGenotypingAllele frequencyAllelesAdaptor Proteins Signal TransducingAgedHeterozygous carrierSequence Analysis DNAmedicine.diseaseNGS-based gene panel030104 developmental biologyGenetic epidemiologyReceptors LDLJournal of clinical lipidology
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Expression of DNA repair proteins hMSH2, hMSH6, hMLH1,O6-methylguanine-DNA methyltransferase and N-methylpurine-DNA glycosylase in melanoma cells wit…

1999

Malignant melanoma is well known for its primary unresponsiveness to chemotherapy. The mechanisms conferring this intrinsic resistance are unclear. In this study, we investigated the role of genes involved in DNA repair in a panel of human melanoma cell variants exhibiting low and high levels of resistance to 4 commonly used drugs in melanoma treatment, i.e., vindesine, etoposide, fotemustine and cisplatin. We show that in melanoma cells exhibiting resistance to cisplatin, etoposide and vindesine, the nuclear content of each of the DNA mismatch repair (MMR) proteins hMLH1, hMSH2 and hMSH6 was reduced by 30–70%. A decreased expression level of up to 80% of mRNAs encoding hMLH1 and hMSH2 was …

Cancer ResearchDNA RepairTranscription GeneticVindesineDNA repairAntineoplastic AgentsBiologyNitrosourea CompoundsDNA GlycosylasesO(6)-Methylguanine-DNA MethyltransferaseOrganophosphorus CompoundsProto-Oncogene ProteinsmedicineHumansRNA MessengerPromoter Regions GeneticMelanomaN-Glycosyl HydrolasesneoplasmsEtoposideAdaptor Proteins Signal TransducingEtoposideCisplatinMelanomaNuclear Proteinsmedicine.diseaseMolecular biologyDrug Resistance Multipledigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinOncologyDNA glycosylaseFotemustineVindesineDNA mismatch repairCisplatinCarrier ProteinsMutL Protein Homolog 1medicine.drugInternational Journal of Cancer
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Influence of glutathione levels and heat-shock on the steady-state levels of oxidative DNA base modifications in mammalian cells

1999

The effects of thiols, ascorbic acid and thermal stress on the basal (steady-state) levels of oxidative DNA base modifications were studied. In various types of untreated cultured mammalian cells, the levels of total glutathione were found to be inversely correlated with the levels of DNA base modifications sensitive to the repair endonuclease Fpg protein, which include 8-hydroxyguanine (8-oxoG). A depletion of glutathione by treatment with buthionine sulphoximine increased the steady-state level in AS52 Chinese hamster cells by approximately 50%. However, additional thiols in the culture medium did not reduce the level of Fpg-sensitive base modifications: 0-10 mM N-acetylcysteine had no ef…

Cancer ResearchHot TemperatureDNA damageGlutathione reductaseOxidative phosphorylationmedicine.disease_causeCell LineMicechemistry.chemical_compoundHsp27CricetinaeTumor Cells CulturedmedicineAnimalsHumansEnzyme InhibitorsButhionine SulfoximineN-Glycosyl HydrolasesHeat-Shock ProteinsbiologyChemistryGeneral MedicineGlutathioneAscorbic acidGlutathioneOxidative StressDNA-Formamidopyrimidine GlycosylaseBiochemistrybiology.proteinOxidative stressDNA DamageHeLa CellsCysteineCarcinogenesis
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Overexpression of Ogg1 in mammalian cells: effects on induced and spontaneous oxidative DNA damage and mutagenesis

1999

Chinese hamster ovary cell lines (AA8 and AS52) were stably transfected to overexpress hOgg1 protein, the human DNA repair glycosylase for 7,8-dihydro-8-oxoguanine (8-oxoG). In the transfectants, the repair rate of 8-oxoG residues induced by either potassium bromate or the photosensitizer [R]-1-[(10-chloro-4-oxo-3-phenyl-4H-benzo[a]quinolizin-1-yl)-carbo nyl ]-2-pyrrolidinemethanolplus light was up to 3-fold more rapid than in the parental cells. However, the improved repair had little effect on the mutagenicity of potassium bromate in the guanine phosphoribosyl transferase (gpt) locus of the OGG1-transfected AS52 cells. The steady-state (background) levels of DNA base modifications sensiti…

Cancer ResearchPyrrolidinesDNA RepairPhotochemistryDNA repairDNA damageBiologyTransfectionPolymerase Chain ReactionCell LineDNA-formamidopyrimidine glycosylasechemistry.chemical_compoundCricetulusGenes ReporterCricetinaeAnimalsheterocyclic compoundsN-Glycosyl HydrolasesPhotosensitizing AgentsBromatesChinese hamster ovary cellOvaryGeneral MedicineTransfectionDNA repair protein XRCC4OxidantsMolecular biologyOxidative StressDNA-Formamidopyrimidine GlycosylasechemistryGenes BacterialMutagenesisDNA glycosylaseEnzyme InductionFemaleQuinolizinesDNADNA DamageCarcinogenesis
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DNA oxidation products determined with repair endonucleases in mammalian cells: Types, basal levels and influence of cell proliferation

1999

Purified repair endonucleases such as Fpg protein, endonuclease III and IV allow a very sensitive quantification of various types of oxidative DNA modifications in mammalian cells. By means of these assays, the numbers of base modifications sensitive to Fpg protein, which include 8-hydroxyguanine (8-oxoG), were determined to be less than 0.3 per 10(6) bp in several types of untreated cultured mammalian cells and human lymphocytes and less than 10 per 10(6) bp in mitochondrial DNA from rat and porcine liver. Oxidative 5,6-dihydropyrimidine derivatives sensitive to endonuclease III and sites of base loss sensitive to endonuclease IV or exonuclease III were much less frequent than Fpg-sensitiv…

DNA RepairBase pairDNA repairDNA damageCarbon-Oxygen LyasesCHO CellsDeferoxamineBiochemistryDeoxyribonuclease (Pyrimidine Dimer)chemistry.chemical_compoundCricetinaeDNA-(Apurinic or Apyrimidinic Site) LyaseAnimalsHumansDimethyl SulfoxideBase PairingN-Glycosyl HydrolasesChromatography High Pressure LiquidMammalsExonuclease IIIEndodeoxyribonucleasesPhotosensitizing AgentsGuanosinebiologyEscherichia coli ProteinsAcridine orangeDNAGeneral MedicineDNA oxidationOxidantsMolecular biologyDNA-(apurinic or apyrimidinic site) lyaseDeoxyribonuclease IV (Phage T4-Induced)DNA-Formamidopyrimidine GlycosylasechemistryBiochemistrybiology.proteinOxidation-ReductionCell DivisionDNAHeLa CellsFree Radical Research
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Fanconi's anaemia cells have normal steady-state levels and repair of oxidative DNA base modifications sensitive to Fpg protein

1998

Abstract Cells from Fanconi's anaemia (FA) patients are abnormally sensitive to oxygen. However, a distinct genetic defect in either the cellular defence against reactive oxygen species (ROS) or in their metabolic generation has not been identified to date. Recently, the gene for the human 8-hydroxyguanine (8-oxoG) glycosylase, which removes this oxidative base modification from the genome, has been localized on chromosome 3p25, i.e., in the same region as the FA complementation group D (FAD) gene. We therefore studied the removal of photosensitization-induced 8-oxoG residues from the DNA of FA cells, using Fpg protein, the bacterial 8-oxoG glycosylase, to quantify the lesions by alkaline e…

GuanineDNA RepairLightDNA repairBiologyToxicologymedicine.disease_causechemistry.chemical_compoundFanconi anemiaGeneticsmedicineHumansN-Glycosyl HydrolasesMolecular BiologyGeneCells CulturedPhotosensitizing AgentsDNAmedicine.diseaseMolecular biologyNuclear DNAComplementationOxidative StressFanconi AnemiaDNA-Formamidopyrimidine GlycosylaseBiochemistrychemistryDNA glycosylaseCell DivisionOxidative stressDNAMutation Research/DNA Repair
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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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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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Expression of HIP/PAP mRNA in Human Hepatoma Cell Lines

2002

The present study attempts to shed more light on the role of hepatocarcinoma-intestine-pancreas/pancreatic associated protein (HIP/PAP) in hepatoma cells. We initially examined, by reverse transcription-polymerase chain reaction (RT-PCR), the HIP/PAP transcripts present in human hepatoma cell lines of different origins and with different grades of differentiation and genetic profiles. We also used DNA sequencing analysis to investigate the structure of the HIP/PAP gene. Further investigation is necessary to define the role of HIP/PAP during the development of human hepatocellular carcinoma and to ascertain whether the use of different transcripts is helpful in regulating HIP/PAP expression …

Pathologymedicine.medical_specialtyCarcinoma HepatocellularSettore MED/09 - Medicina InternaPancreatitis-Associated ProteinscarcinomaGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceAntigenAntigens NeoplasmHIP/PAPBiomarkers TumorTumor Cells CulturedmedicineCarcinomaHumansNeoplasmLectins C-TypeRNA MessengerPancreatitis-Associated ProteinsN-Glycosyl HydrolasesGenePlant ProteinsMessenger RNAbusiness.industryGeneral NeuroscienceLiver NeoplasmsAcute-phase proteinpancreatitihepatomamedicine.diseasePancreatitisHepatocellular carcinomaRibosome Inactivating Proteins Type 1Cancer researchproteinbusinessAcute-Phase ProteinsAnnals of the New York Academy of Sciences
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