Search results for "RIMI"

showing 10 items of 3981 documents

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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Poly(ADP-ribosyl)ation accelerates DNA repair in a pathway dependent on Cockayne syndrome B protein

2003

Activation of poly(ADP-ribose)polymerases 1 and 2 (PARP-1 and PARP-2) is one of the earliest responses of mammalian cells to DNA damage by numerous genotoxic agents. We have analysed the influence of PARP inhibition, either achieved by over-expression of the DNA binding domain of PARP-1 or by treatment with 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone, on the repair of single-strand breaks (SSB), pyrimidine dimers and oxidative base modifications sensitive to Fpg protein (mostly 8-hydroxyguanine) in mammalian cells at very low, non-cytotoxic levels of DNA damage. The data show that the repair rates of all three types of DNA damage are significantly lower in PARP-inhibited c…

DNA RepairDNA damageDNA repairPoly ADP ribose polymerase[SDV]Life Sciences [q-bio]Pyrimidine dimerBiologyPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorCockayne syndromeDexamethasone03 medical and health sciencesMice0302 clinical medicinePiperidinesCricetinaeGeneticsmedicineAnimalsPoly-ADP-Ribose Binding ProteinsComputingMilieux_MISCELLANEOUS030304 developmental biologyCell Line TransformedMice Knockout0303 health sciencesDNA HelicasesArticlesDNADNA repair protein XRCC4Fibroblastsmedicine.diseaseIsoquinolinesMolecular biology3. Good healthDNA Repair Enzymes030220 oncology & carcinogenesisPoly(ADP-ribose) PolymerasesNucleotide excision repairDNA DamageSignal Transduction
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APE/Ref-1 and the mammalian response to genotoxic stress.

2003

Human apurinic/apyrimidinic endonuclease/redox factor-1 (hAPE/Ref-1) is a multifunctional protein involved in the repair of DNA damaged by oxidative or alkylating compounds as well as in the regulation of stress inducible transcription factors such as AP-1, NF-kappaB, HIF-1 and p53. With respect to transcriptional regulation, both redox dependent and independent mechanisms have been described. APE/Ref-1 also acts as a transcriptional repressor. Recent data indicate that APE/Ref-1 negatively regulates the activity of the Ras-related GTPase Rac1. How these different physiological activities of APE/Ref-1 are coordinated is poorly understood. So far, convincing evidence is available that the ex…

DNA RepairDNA repairRAC1Genotoxic StressTransfectionBiologyToxicologymedicine.disease_causeMolecular biologyCell biologyCell killingDNA Repair EnzymesGene Expression RegulationNeoplasmsmedicineTranscriptional regulationDNA-(Apurinic or Apyrimidinic Site) LyaseAnimalsHumansAmino Acid SequenceTranscription factorOxidative stressMutagensToxicology
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Molecular and functional analysis of the (6-4) photolyase from the hexactinellid Aphrocallistes vastus.

2003

The hexactinellid sponges (phylum Porifera) represent the phylogenetically oldest metazoans that evolved 570-750 million years ago. At this period exposure to ultraviolet (UV) light exceeded that of today and it may be assumed that this old taxon has developed a specific protection system against UV-caused DNA damage. A cDNA was isolated from the hexactinellid Aphrocallistes vastus which comprises high sequence similarity to genes encoding the protostomian and deuterostomian (6-4) photolyases. Subsequently functional studies were performed. It could be shown that the sponge gene, after transfection into mutated Escherichia coli, causes resistance of the bacteria against UV light. Recombinan…

DNA RepairDNA repairUltraviolet RaysMolecular Sequence DataBiophysicsPyrimidine dimerBiochemistryAnalytical Chemistrychemistry.chemical_compoundComplementary DNAAnimalsAmino Acid SequencePhotolyaseMolecular BiologyGenePhylogenyGeneticsbiologyHexactinellidbiology.organism_classificationRecombinant ProteinsPoriferaSpongechemistryBiochemistryDeoxyribodipyrimidine Photo-LyaseSequence AlignmentDNADNA DamageBiochimica et biophysica acta
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Oxidative stress triggers the preferential assembly of base excision repair complexes on open chromatin regions

2010

How DNA repair machineries detect and access, within the context of chromatin, lesions inducing little or no distortion of the DNA structure is a poorly understood process. Removal of oxidized bases is initiated by a DNA glycosylase that recognises and excises the damaged base, initiating the base excision repair (BER) pathway. We show that upon induction of 8-oxoguanine, a mutagenic product of guanine oxidation, the mammalian 8-oxoguanine DNA glycosylase OGG1 is recruited together with other proteins involved in BER to euchromatin regions rich in RNA and RNA polymerase II and completely excluded from heterochromatin. The underlying mechanism does not require direct interaction of the prote…

DNA RepairHMG-boxDNA damageDNA repairGenome Integrity Repair and ReplicationCell LineDNA GlycosylasesEuchromatinDNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsHumansGuanosinebiologyBromatesBase excision repairChromatinProliferating cell nuclear antigenChromatinDNA-Binding ProteinsOxidative StressX-ray Repair Cross Complementing Protein 1BiochemistryDNA glycosylasebiology.proteinDNA DamageNucleotide excision repairNucleic Acids Research
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Oxidative stress impairs the repair of oxidative DNA base modifications in human skin fibroblasts and melanoma cells.

2008

Irradiation of mammalian cells with solar light is associated with the generation of reactive oxygen species (ROS) and oxidative stress, which is mediated in part by endogenous photosensitizers absorbing in the visible range of the solar spectrum. Accordingly, oxidative DNA base modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are the predominant types of DNA damage in cells irradiated at wavelengths >400 nm. We have analysed the repair of oxidative purine modifications in human skin fibroblasts and melanoma cells using an alkaline elution technique, both under normal conditions and after depletion of glutathione. Similar repair rates were observed in fibroblasts and melanoma cells f…

DNA RepairLightDNA damageUltraviolet RaysPyrimidine dimerOxidative phosphorylationBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundmedicineHumansMolecular BiologyMelanomaAgedSkinchemistry.chemical_classificationReactive oxygen speciesGuanosineCell BiologyBase excision repairGlutathioneMolecular biologyGlutathioneOxidative StresschemistryBiochemistryFemaleOxidative stressNucleotide excision repairDNA repair
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Nucleotide excision repair of abasic DNA lesions

2019

AbstractApurinic/apyrimidinic (AP) sites are a class of highly mutagenic and toxic DNA lesions arising in the genome from a number of exogenous and endogenous sources. Repair of AP lesions takes place predominantly by the base excision pathway (BER). However, among chemically heterogeneous AP lesions formed in DNA, some are resistant to the endonuclease APE1 and thus refractory to BER. Here, we employed two types of reporter constructs accommodating synthetic APE1-resistant AP lesions to investigate the auxiliary repair mechanisms in human cells. By combined analyses of recovery of the transcription rate and suppression of transcriptional mutagenesis at specifically positioned AP lesions, w…

DNA RepairTranscription GeneticDNA damageDNA repairGenome Integrity Repair and ReplicationGene Knockout Techniques03 medical and health sciencesEndonucleasechemistry.chemical_compoundTranscription (biology)CRISPR-Associated Protein 9DNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsHumansAP siteCell Line TransformedSkin030304 developmental biologyGene Editing0303 health sciencesBase SequencebiologyGenome Human030302 biochemistry & molecular biologyDNABase excision repairFibroblastsMolecular biologyXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinschemistryMutationbiology.proteinCRISPR-Cas SystemsDNADNA DamageProtein BindingNucleotide excision repairNucleic Acids Research
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UVA irradiation induces relocalisation of the DNA repair protein hOGG1 to nuclear speckles

2006

The DNA glycosylase hOGG1 initiates base excision repair (BER) of oxidised purines in cellular DNA. Using confocal microscopy and biochemical cell fractionation experiments we show that, upon UVA irradiation of human cells, hOGG1 is recruited from a soluble nucleoplasmic localisation to the nuclear matrix. More specifically, after irradiation, hOGG1 forms foci colocalising with the nuclear speckles, organelles that are interspersed between chromatin domains and that have been associated with transcription and RNA-splicing processes. The use of mutant forms of hOGG1 unable to bind the substrate showed that relocalisation of hOGG1 does not depend on the recognition of the DNA lesion by the en…

DNA RepairTranscription GeneticUltraviolet RaysDNA repairRecombinant Fusion ProteinsGreen Fluorescent ProteinsFluorescent Antibody TechniqueBiologyDNA GlycosylasesSubstrate Specificitychemistry.chemical_compoundDNA Repair ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseHumansCell NucleusGuanosineBiological TransportCell BiologyBase excision repairNuclear matrixMolecular biologyChromatinCell biologychemistryDNA glycosylaseCell fractionationReactive Oxygen SpeciesDNAHeLa CellsJournal of Cell Science
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Influences of histone deacetylase inhibitors and resveratrol on DNA repair and chromatin compaction

2013

Accessibility of DNA is a prerequisite for both DNA damage and repair. Therefore, the chromatin structure is expected to have major impact on both processes, with opposite consequences for the stability of the genome. To analyse the influence of chromatin compaction on the generation and repair of various types of DNA modifications, we modulated the global chromatin structure of AS52 Chinese hamster ovary cells and HeLa cells by treatment with either histone deacetylase inhibitors or resveratrol and measured the repair kinetics of (i) pyrimidine dimers induced by ultraviolet B, (ii) oxidised purines generated by photosensitisation and (iii) single-strand breaks induced by H2O2, using an alk…

DNA RepairUltraviolet RaysDNA damageDNA repairHealth Toxicology and MutagenesisCarbazolesCHO CellsHydroxamic AcidsToxicologyChromatin remodelingCricetulusStilbenesHistone H2AGeneticsmedicineAnimalsDeoxyribonuclease IHumansDNA Breaks Single-StrandedGenetics (clinical)EpigenomicsbiologyChemistryMolecular biologyChromatinCell biologyProliferating cell nuclear antigenChromatinHistone Deacetylase InhibitorsButyratesTrichostatin APyrimidine DimersResveratrolbiology.proteinHeLa Cellsmedicine.drugMutagenesis
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c-Fos is required for excision repair of UV-light induced DNA lesions by triggering the re-synthesis of XPF

2006

Cells deficient in c-Fos are hypersensitive to ultraviolet (UV-C) light. Here we demonstrate that mouse embryonic fibroblasts lacking c-Fos (fos-/-) are defective in the repair of UV-C induced DNA lesions. They show a decreased rate of sealing of repair-mediated DNA strand breaks and are unable to remove cyclobutane pyrimidine dimers from DNA. A search for genes responsible for the DNA repair defect revealed that upon UV-C treatment the level of xpf and xpg mRNA declined but, in contrast to the wild type (wt), did not recover in fos-/- cells. The observed decline in xpf and xpg mRNA is due to impaired re-synthesis, as shown by experiments using actinomycin D. Block of xpf transcription resu…

DNA RepairUltraviolet RaysDNA repairDNA damageRNA StabilityGene ExpressionPyrimidine dimerBiologyCell LineMicechemistry.chemical_compoundTranscription (biology)Gene expressionGeneticsAnimalsDNA Breaks Single-StrandedRNA MessengerMolecular BiologyTranscription factorMice KnockoutGenetic Complementation TestGenes fosNuclear ProteinsDNAEndonucleasesMolecular biologyDNA-Binding ProteinsTranscription Factor AP-1chemistryPyrimidine DimersDNADNA DamageTranscription FactorsNucleotide excision repairNucleic Acids Research
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