Search results for "HeLa Cell"

showing 10 items of 281 documents

Nuclear Localization of PTEN by a Ran-dependent Mechanism Enhances Apoptosis: Involvement of an N-Terminal Nuclear Localization Domain and Multiple N…

2006

The targeting of the tumor suppressor PTEN protein to distinct subcellular compartments is a major regulatory mechanism of PTEN function, by controlling its access to substrates and effector proteins. Here, we investigated the molecular basis and functional consequences of PTEN nuclear/cytoplasmic distribution. PTEN accumulated in the nucleus of cells treated with apoptotic stimuli. Nuclear accumulation of PTEN was enhanced by mutations targeting motifs in distinct PTEN domains, and it was dependent on an N-terminal nuclear localization domain. Coexpression of a dominant negative Ran GTPase protein blocked PTEN accumulation in the nucleus, which was also affected by coexpression of importin…

Cèl·lulesAmino Acid MotifsMolecular Sequence DataNuclear Localization SignalsApoptosisBiologyModels BiologicalCatalysislaw.inventionMicelawChlorocebus aethiopsmedicineAnimalsHumansPTENAmino Acid SequenceProteïnes supressores de tumorsMolecular BiologyCells CulturedSequence DeletionCell NucleusCOS cellsEffectorPTEN Phosphohydrolase3T3 CellsArticlesCell BiologyProtein Structure TertiaryRatsTransport proteinProtein TransportCell nucleusran GTP-Binding Proteinmedicine.anatomical_structureCOS CellsRanbiology.proteinCancer researchSuppressorNuclear localization sequenceHeLa CellsMolecular Biology of the Cell
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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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EGFP Reporters for Direct and Sensitive Detection of Mutagenic Bypass of DNA Lesions

2020

The sustainment of replication and transcription of damaged DNA is essential for cell survival under genotoxic stress

DNA RepairTranscription GeneticDNA damageMutantGenetic VectorsGreen Fluorescent Proteinslcsh:QR1-502host cell reactivation (HCR)BiochemistryArticlelcsh:Microbiology03 medical and health scienceschemistry.chemical_compoundmutation assay0302 clinical medicinetranslesion synthesis (TLS)transcriptional mutagenesisTranscription (biology)Genes ReporterHumansCloning MolecularMolecular Biologyenhanced green fluorescent protein (EGFP)PolymeraseCells CulturedDNA damage tolerance030304 developmental biology0303 health sciencesbiologyDNA synthesisChemistryPoint mutationreporter assayRNACell biologyAmino Acid SubstitutionMutagenesis030220 oncology & carcinogenesisMutationbiology.proteinDNA damageDNAHeLa Cellsdamage bypassBiomolecules
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Excision of Uracil from Transcribed DNA Negatively Affects Gene Expression

2014

Uracil is an unavoidable aberrant base in DNA, the repair of which takes place by a highly efficient base excision repair mechanism. The removal of uracil from the genome requires a succession of intermediate products, including an abasic site and a single strand break, before the original DNA structure can be reconstituted. These repair intermediates are harmful for DNA replication and also interfere with transcription under cell-free conditions. However, their relevance for cellular transcription has not been proved. Here we investigated the influence of uracil incorporated into a reporter vector on gene expression in human cells. The expression constructs contained a single uracil opposi…

DNA RepairTranscription GeneticGreen Fluorescent ProteinsGene ExpressionDNA and ChromosomesBiologyBiochemistryCell LineDNA Glycosylaseschemistry.chemical_compoundGenes ReporterActivation-induced (cytidine) deaminaseHumansheterocyclic compoundsProtein–DNA interactionAP siteUracilUracil-DNA GlycosidaseMolecular BiologyUracilDNACell BiologyBase excision repairMolecular biologyThymine DNA GlycosylasechemistryDNA glycosylaseGene Knockdown TechniquesUracil-DNA glycosylasebiology.proteinHeLa CellsNucleotide excision repairJournal of Biological Chemistry
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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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A microplate version of the DNA-synthesis inhibition test for rapid detection of DNA-alteration potentials.

1990

A microplate version of the DNA-synthesis inhibition test (DIT) for fast detection of DNA-alteration potentials has been developed. The DIT is based on the concept that DNA damage causes inhibition of DNA synthesis that becomes detectable some time after replicating cells have been in contact with genotoxic agents. In this test procedure human tissue culture cells (HeLa S3), prelabeled with [14C]thymidine, arfe exposed for 90 min to the substances in question. After the cells are rinsed, they are allowed to recover for 2 1/2 h in fresh culture medium, thereby unspecific interactions interfering with DNA replication are practically eliminated. Next, [3H]thymidine is added for 30 min, and the…

DNA ReplicationDNA damageBiophysicsBiologymedicine.disease_causeBiochemistryDNA Synthesis Inhibitionchemistry.chemical_compoundmedicineBenzo(a)pyreneHumansMolecular BiologyChromatographyAutoanalysisDNA synthesisMutagenicity TestsDNA replicationNitroquinolinesCell BiologyDNAMolecular biologychemistryCell cultureMutationThymidineDNAGenotoxicityDNA DamageHeLa CellsMutagensAnalytical biochemistry
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A neutralizing antibody against human DNA polymerase epsilon inhibits cellular but not SV40 DNA replication.

1999

The contribution of human DNA polymerase epsilon to nuclear DNA replication was studied. Antibody K18 that specifically inhibits DNA polymerase activity of human DNA polymerase epsilon in vitro significantly inhibits DNA synthesis both when microinjected into nuclei of exponentially growing human fibroblasts and in isolated HeLa cell nuclei. The capability of this neutralizing antibody to inhibit DNA synthesis in cells is comparable to that of monoclonal antibody SJK-132-20 against DNA polymerase alpha. Contrary to the antibody against DNA polymerase alpha, antibody K18 against DNA polymerase epsilon did not inhibit SV40 DNA replication in vitro. These results indicate that DNA polymerase e…

DNA ReplicationDNA polymeraseDNA polymerase IIDNA polymerase epsilonSimian virus 40Virus ReplicationDNA polymerase deltaAntibodiesCell LineNeutralization TestsCatalytic DomainGeneticsAnimalsHumansPolymeraseDNA clampbiologyDNA replicationDNA Polymerase IIFibroblastsMolecular biologyProliferating cell nuclear antigenBromodeoxyuridineDNA Viralbiology.proteinCattleRabbitsHeLa CellsResearch ArticleNucleic acids research
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The bacterial cytolethal distending toxin (CDT) triggers a G2 cell cycle checkpoint in mammalian cells without preliminary induction of DNA strand br…

1999

The bacterial cytolethal distending toxin (CDT) was previously shown to arrest the tumor-derived HeLa cell line in the G2-phase of the cell cycle through inactivation of CDK1, a cyclin-dependent kinase whose state of activation determines entry into mitosis. We have analysed the effects induced in HeLa cells by CDT, in comparison to those induced by etoposide, a prototype anti-tumoral agent that triggers a G2 cell cycle checkpoint by inducing DNA damage. Both CDT and etoposide inhibit cell proliferation and induces the formation of enlarged mononucleated cells blocked in G2. In both cases, CDK1 from arrested cells could be re-activated both in vitro by dephosphorylation by recombinant Cdc25…

DNA ReplicationG2 PhaseCancer ResearchCAFFEINECell cycle checkpointCytolethal distending toxinDNA damageRecombinant Fusion Proteins[SDV]Life Sciences [q-bio]Bacterial ToxinsBiologyS Phase03 medical and health sciencesCDC2 Protein KinaseGeneticsHumanscdc25 PhosphatasesCHEK1PhosphorylationMolecular BiologyMitosisEtoposide030304 developmental biology0303 health sciences030306 microbiologyCell growthDNA NeoplasmG2-M DNA damage checkpointCell cycleAntineoplastic Agents PhytogenicNeoplasm Proteins3. Good healthCell biology[SDV] Life Sciences [q-bio]BiochemistryAGENT ANTITUMEURProtein Processing Post-TranslationalCell DivisionDNA DamageHeLa Cells
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Genotoxicity of the fungicide dichlofluanid in seven assays

1991

Seven different endpoints for detection of genotoxicity have been used to demonstrate the DNA-altering properties of Dichlofluanid, a fungicide commonly used in viticulture pest control. Each endpoint (DNA synthesis inhibition test, alkaline viscosimetry, umu-test, alkaline filter elution, FADU-test, 32P-postlabeling, and electron microscopy) shows clear evidence of genotoxicity. These data indicate that application of the fungicide dichlofluanid may be mutagenic and/or carcinogenic for exposed humans.

DNA ReplicationSalmonella typhimuriumDNA AlterationEpidemiologyHealth Toxicology and MutagenesisDichlofluanidmedicine.disease_causeCell LineMicechemistry.chemical_compoundmedicineAnimalsHumansBioassayGenetics (clinical)CaptanCarcinogenAniline CompoundsMutagenicity TestsFishesDNAPesticideFungicides IndustrialFungicideBiochemistrychemistryGenotoxicityDNA DamageHeLa CellsMutagensEnvironmental and Molecular Mutagenesis
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