Search results for "Polymerase"

showing 10 items of 2127 documents

Parvovirus B19 nonstructural protein-induced damage of cellular DNA and resultant apoptosis.

2010

Parvovirus B19 is a widespread virus with diverse clinical presentations. The viral nonstructural protein, NS1, binds to and cleaves the viral genome, and induces apoptosis when transfected into nonpermissive cells, such as hepatocytes. We hypothesized that the cytotoxicity of NS1 in such cells results from chromosomal DNA damage caused by the DNA-nicking and DNA-attaching activities of NS1. Upon testing this hypothesis, we found that NS1 covalently binds to cellular DNA and is modified by PARP, an enzyme involved in repairing single-stranded DNA nicks. We furthermore discovered that the DNA nick repair pathway initiated by poly(ADPribose)polymerase and the DNA repair pathways initiated by …

DNA RepairDNA damageViral nonstructural proteinDNA repairPoly ADP ribose polymerasevirusesBlotting WesternParvovirus B19Viral Nonstructural ProteinsCell Linechemistry.chemical_compoundsystemic lupus erythematosusParvovirus B19 HumanHumansImmunoprecipitationPolymerasebiologyfulminant liver failureDNA damage and repairapoptosisvirus diseasesGeneral MedicineTransfectionMolecular biologyProliferating cell nuclear antigenchemistrybiology.proteinDNAautoantibodyDNA DamageResearch PaperInternational journal of medical sciences
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DNA Junction Ligands Trigger DNA Damage and Are Synthetic Lethal with DNA Repair Inhibitors in Cancer Cells.

2019

International audience; Translocation of DNA and RNA polymerases along their duplex substrates results in DNA supercoiling. This torsional stress promotes the formation of plectonemic structures, including three-way DNA junction (TWJ), which can block DNA transactions and lead to DNA damage. While cells have evolved multiple mechanisms to prevent the accumulation of such structures, stabilizing TWJ through ad hoc ligands offer an opportunity to trigger DNA damage in cells with high level of transcription and replication, such as cancer cells. Here, we develop a series of azacryptand-based TWJ ligands, we thoroughly characterize their TWJ-interacting properties in vitro and demonstrate their…

DNA RepairDNA repairDNA damage[SDV]Life Sciences [q-bio][SDV.CAN]Life Sciences [q-bio]/CancerSynthetic lethality[CHIM.THER]Chemical Sciences/Medicinal Chemistry010402 general chemistryLigands01 natural sciencesBiochemistryCatalysischemistry.chemical_compoundColloid and Surface ChemistryTranscription (biology)Cell Line TumorHumansPolymeraseCell Proliferationbiology[CHIM.ORGA]Chemical Sciences/Organic chemistryGeneral ChemistryDNA3. Good health0104 chemical sciencesCell biologychemistryCancer cellbiology.proteinMCF-7 CellsDNA supercoilNucleic Acid ConformationDNADNA DamageJournal of the American Chemical Society
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Lentiviral-Mediated Gene Therapy in Fanconi Anemia-A Mice Reveals Long-Term Engraftment and Continuous Turnover of Corrected HSCs

2015

International audience; Fanconi anemia is a DNA repair-deficiency syndrome mainly characterized by cancer predisposition and bone marrow failure. Trying to restore the hematopoietic function in these patients, lentiviral vector-mediated gene therapy trials have recently been proposed. However, because no insertional oncogenesis studies have been conducted so far in DNA repair-deficiency syndromes such as Fanconi anemia, we have carried out a genome-wide screening of lentiviral insertion sites after the gene correction of Fanca-/- hematopoietic stem cells (HSCs), using LAM-PCR and 454-pyrosequencing. Our studies first demonstrated that transduction of Fanca-/- HSCs with a lentiviral vector d…

DNA RepairDNA repair[SDV]Life Sciences [q-bio]Genetic enhancementGenetic VectorsBiologymedicine.disease_causePolymerase Chain ReactionViral vectorCell LineMiceFanconi anemiaTransduction Genetichemic and lymphatic diseasesDrug DiscoveryGeneticsmedicineAnimalsMolecular BiologyGenetics (clinical)Mice KnockoutFanconi Anemia Complementation Group A ProteinLentivirusBone marrow failureGenetic Therapymedicine.diseaseHematopoietic Stem CellsFANCA3. Good health[SDV] Life Sciences [q-bio]Fanconi AnemiaCancer researchMolecular MedicineStem cellCarcinogenesis
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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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Thoughts on What Chemists Can Contribute to Fighting SARS-CoV-2 - A Short Note on Hand Sanitizers, Drug Candidates and Outreach.

2020

Abstract The SARS‐CoV‐2 outbreak causing the respiratory disease COVID‐19 has left many chemists in academia without an obvious option to contribute to fighting the pandemic. Some of our recent experiences indicate that there are ways to overcome this dilemma. A three‐pronged approach is proposed.

DNA Replication2019-20 coronavirus outbreakCoronavirus disease 2019 (COVID-19)Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Hand SanitizersPneumonia Viral010402 general chemistry01 natural sciencesAntiviral AgentsCatalysisalcohols2-PropanolBetacoronavirusViewpointantiviralsPolitical sciencePandemicHumansPandemicshealth care economics and organizationsEthanol010405 organic chemistrybusiness.industrySARS-CoV-2pandemicCOVID-19General MedicineGeneral ChemistryDNA-Directed RNA PolymerasesPublic relations0104 chemical sciencesDilemmaOutreachViewpointsChemists in the CommunitybusinessCoronavirus InfectionsdisinfectantsCoronavirus InfectionsAngewandte Chemie (International ed. in English)
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Late activation of stress kinases (SAPK/JNK) by genotoxins requires the DNA repair proteins DNA-PKcs and CSB.

2005

Although genotoxic agents are powerful inducers of stress kinases (SAPK/JNK), the contribution of DNA damage itself to this response is unknown. Therefore, SAPK/JNK activation of cells harboring specific defects in DNA damage-recognition mechanisms was studied. Dual phosphorylation of SAPK/JNK by the genotoxin methyl methanesulfonate (MMS) occurred in two waves. The early response (≤2 h after exposure) was similar in cells knockout for ATM, PARP, p53, and CSB or defective in DNA-PKcscompared with wild-type cells. The late response however (≥4 h), was drastically reduced in DNA-PKcsand Cockayne's syndrome B (CSB)-deficient cells. Similar results were obtained with human cells lacking DNA-PKc…

DNA ReplicationAlkylationDNA RepairDNA damageDNA repairPoly ADP ribose polymeraseDNA-Activated Protein KinaseBiologyModels Biologicalchemistry.chemical_compoundMiceAnimalsHumansPhosphorylationPoly-ADP-Ribose Binding ProteinsMolecular BiologyDNA-PKcsCells CulturedKinaseDNA HelicasesJNK Mitogen-Activated Protein KinasesNuclear ProteinsCell BiologyBase excision repairDNAArticlesMethyl MethanesulfonateMolecular biologyMethyl methanesulfonateDNA-Binding ProteinsEnzyme Activationenzymes and coenzymes (carbohydrates)DNA Repair EnzymeschemistryPhosphorylationProtein Processing Post-TranslationalDNA DamageMutagensSignal TransductionMolecular biology of the cell
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Lovastatin protects human endothelial cells from the genotoxic and cytotoxic effects of the anticancer drugs doxorubicin and etoposide

2006

Background and purpose: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they exert pleiotropic effects on cellular stress responses and death. Here, we analysed whether lovastatin affects the sensitivity of primary human endothelial cells (HUVEC) to the anticancer drug doxorubicin. Experimental approach: We investigated whether pretreatment of HUVEC with low dose of lovastatin influences the cellular sensitivity to doxorubicin. To this end, cell viability, proliferation and apoptosis as well as DNA damage-triggered stress response were analysed. Key results: Lovastatin reduced the cytotoxic potency of doxorub…

DNA ReplicationCell SurvivalDNA damageApoptosisBiologyPharmacologypolycyclic compoundsmedicineHumansTopoisomerase II InhibitorsDoxorubicinLovastatinEtoposideEtoposideFluorescent DyesPharmacologyAntibiotics AntineoplasticReverse Transcriptase Polymerase Chain ReactionTopoisomeraseCell CycleEndothelial Cellsnutritional and metabolic diseasesAntimutagenic AgentsFibroblastsCell cycleResearch PapersAntineoplastic Agents PhytogenicDoxorubicinDrug Resistance NeoplasmHMG-CoA reductasebiology.proteinlipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsTopoisomerase-II InhibitorReactive Oxygen SpeciesFluorescein-5-isothiocyanateDNA Damagemedicine.drugBritish Journal of Pharmacology
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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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DNA polymeraseθ up-regulation is associated with poor survival in breast cancer, perturbs DNA replication, and promotes genetic instability

2010

“Replicative stress” is one of the main factors underlying neoplasia from its early stages. Genes involved in DNA synthesis may therefore represent an underexplored source of potential prognostic markers for cancer. To this aim, we generated gene expression profiles from two independent cohorts (France,n= 206; United Kingdom,n= 117) of patients with previously untreated primary breast cancers. We report here that among the 13 human nuclear DNA polymerase genes, DNA Polymerase θ (POLQ) is the only one significantly up-regulated in breast cancer compared with normal breast tissues. Importantly,POLQup-regulation significantly correlates with poor clinical outcome (4.3-fold increased risk of de…

DNA ReplicationGenome instabilityDNA damageDNA polymerase[SDV]Life Sciences [q-bio]DNA Polymerase ThetaBreast NeoplasmsDNA-Directed DNA PolymeraseKaplan-Meier Estimatemedicine.disease_causeBioinformaticsGenomic InstabilityCell LineCohort Studies03 medical and health sciences0302 clinical medicineBreast cancerCell Line TumorChromosome instabilityCyclin EmedicineHumansComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesMultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCancerMiddle AgedBiological SciencesPrognosismedicine.diseaseUnited KingdomUp-RegulationGene Expression Regulation Neoplastic030220 oncology & carcinogenesisCancer researchbiology.proteinFemaleRNA InterferenceFranceCarcinogenesisDNA DamageProceedings of the National Academy of Sciences
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Are the leukocyte telomere length attrition and telomerase activity alteration potential predictor biomarkers for sporadic TAA in aged individuals?

2014

A large variability in occurrence, complications, and age/gender manifestations characterizes individual susceptibility of sporadic thoracic aortic aneurysms (TAA), even in subjects with the same risk factor profiles. The reasons are poorly understood. On the other hand, TAA pathophysiology mechanisms remain unclear than those involved in abdominal aorta aneurysms. However, recent evidence is suggesting a crucial role of biological ageing in inter-individual risk variation of cardiovascular diseases, including sporadic TAA. Biological age rather than chronological age is a better predictor of vascular risk. Relevant assumptions support this concept. In confirming this evidence and our preli…

DNA ReplicationMaleTelomerasePathologymedicine.medical_specialtyAgingGenotypeEnzyme-Linked Immunosorbent AssayBiologyPolymerase Chain ReactionArticleAortic aneurysmRisk FactorsGenotypemedicineIn Situ Nick-End LabelingLeukocytesSporadic TAA. Biological ageing . Leukocyte telomere length attrition . Telomere activity alteration . Predictor TAAbiomarkersSettore MED/05 - Patologia ClinicaHumansGenetic Predisposition to DiseaseRisk factorTelomere ShorteningSettore MED/04 - Patologia GeneraleAortic Aneurysm ThoracicSettore MED/23 - Chirurgia CardiacaGeneral MedicineDNAMiddle AgedTelomeremedicine.diseaseMolecular medicineImmunohistochemistryPathophysiologyTelomereAgeingImmunologyFemaleGeriatrics and GerontologyBiomarkersAge (Dordrecht, Netherlands)
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