Search results for "REPLICATION"

showing 10 items of 489 documents

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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Mechanisms and consequences of methylating agent-induced SCEs and chromosomal aberrations: a long road traveled and still a far way to go.

2003

Since the milestone work of Evans and Scott, demonstrating the replication dependence of alkylation-induced aberrations, and Obe and Natarajan, pointing to the critical role of DNA double-strand breaks (DSBs) as the ultimate trigger of aberrations, the field has grown extensively. A notable example is the identification of DNA methylation lesions provoking chromosome breakage (clastogenic) effects, which made it possible to model clastogenic pathways evoked by genotoxins. Experiments with repair-deficient mutants and transgenic cell lines revealed both O<sup>6</sup>-methylguanine (O<sup>6</sup>MeG) and N- methylpurines as critical lesions. For S<sub>N</sub&g…

DNA ReplicationAlkylating AgentsGuanineDNA RepairDNA damageDNA repairBase Pair MismatchApoptosisBiologyMethylationLesionAnimals Genetically ModifiedMiceO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeGeneticsmedicineAnimalsHumansPoint MutationAP siteMolecular BiologyGenetics (clinical)Chromosome AberrationsRecombination GeneticGuanosineModels GeneticCell CycleDNA replicationDNAFibroblastsMolecular biologyCell killingCell Transformation NeoplasticCancer researchDNA mismatch repairChromosome breakagemedicine.symptomSister Chromatid ExchangeDNA DamageMutagensCytogenetic and genome research
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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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Transformation of Aspergillus parasiticus using autonomously replicating plasmids from Aspergillus nidulans.

1994

A genetic transformation system for the aflatoxin-producing fungus Aspergillus parasiticus using two autonomously replicating plasmids from A. nidulans (ARp1 and pDHG25) is reported. Transformation frequencies using the plasmid pDHG25 were from 5 x 10(2) to 2.5 x 10(4) transformants per 10(6) viable protoplasts and microgram DNA. The stability of the plasmids in the transformants was also studied. This transformation system offers a new opportunity to clone genes related to aflatoxin production using appropriate aflatoxin-defective mutants.

DNA ReplicationArginine BAutonomously replicating sequenceMitosisLaboratorium voor ErfelijkheidsleerMicrobiologyAspergillus parasiticusAspergillus nidulansMicrobiologyGenetic transformationchemistry.chemical_compoundPlasmidTransformation GeneticAutonomous replicationAspergillus nidulansGeneticsDNA FungalMolecular BiologyGeneGeneticsAspergillus nidulans autonomous replicating plasmidbiologyProtoplastsfood and beveragesProtoplastbiology.organism_classificationAspergillus parasiticusTransformation (genetics)AspergilluschemistryLaboratory of GeneticsDNAPlasmidsFEMS microbiology letters
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Histone carbonylation occurs in proliferating cells

2012

12 páginas, 10 figuras (que no es encuentran en este documento, se pueden ver en: http://www.sciencedirect.com/science/article/pii/S0891584912000664)

DNA ReplicationBlotting WesternCarbonylationFree radicalsBiologyBiochemistryHistonesMicePhysiology (medical)Histone methylationHistone H2AAnimalsHistone codeEpigeneticsPhosphorylationPoly(ADP-ribosyl)ationCell proliferationEpigenomicsChromatinHistoneBiochemistryHistone methyltransferaseNIH 3T3 Cellsbiology.proteinEpigenetics
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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Fen1 is induced p53 dependently and involved in the recovery from UV-light-induced replication inhibition.

2005

Mouse embryonic fibroblasts (MEFs) that lack p53 are hypersensitive to the cytotoxic and genotoxic effect of ultraviolet (UV-C) light. They also display a defect in the recovery from UV-C-induced DNA replication inhibition. An enzyme involved in processing stalled DNA replication forks is flap endonuclease 1 (Fen1). Gene expression profiling of UV-C-irradiated MEFs revealed fen1 to be upregulated, which was confirmed by RT-PCR and Western blot experiments. Increased Fen1 levels upon UV-C exposure are due to transcriptional activation, as revealed by inhibitor studies. Fen1 induction was dose- and time-dependent; it occurred on protein level already 3 h after irradiation. Induction of Fen1 b…

DNA ReplicationCancer ResearchDNA damageDNA repairFlap EndonucleasesUltraviolet RaysMolecular Sequence DataGene ExpressionCHO CellsBiologyTransfectionchemistry.chemical_compoundMiceCricetinaeGeneticsNull cellAnimalsPromoter Regions GeneticMolecular BiologyCell ProliferationBase SequenceCell growthDNA replicationTransfection3T3 CellsDNAMolecular biologyDNA Replication InhibitionchemistryEnzyme InductionTumor Suppressor Protein p53DNAOncogene
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Determination of DNA single strand breaks and selective DNA amplification by N-nitrodimethylamine and analogs, and estimation of the indicator cells'…

1986

N-nitrodimethylamine is metabolized oxidatively to N-nitrohydroxymethylmethylamine, which decomposes to yield formaldehyde and N-nitromethylamine. All four compounds and N-nitromethylamine were tested for their ability to induce DNA single strand breaks in hepatocytes and in SV 40-transformed Chinese hamster embryo cell lines. Only the two monoalkylnitramines were positive. They induced single strand breaks in hepatocytes, but were not effective in the other cells. Formaldehyde and N-nitrohydroxymethylmethylamine were toxic to the cells. None of the compounds tested was able to induce selective DNA amplification in the two transformed cell lines. Enzymes involved in drug metabolism were ass…

DNA ReplicationCancer ResearchHamsterDNA Single-StrandedSimian virus 40BiologyChinese hamsterCell Linechemistry.chemical_compoundCricetulusCricetinaeFormaldehydeAnimalsEpoxide hydrolaseCells Culturedchemistry.chemical_classificationDose-Response Relationship DrugDNA replicationGene AmplificationGeneral Medicinebiology.organism_classificationCell Transformation ViralEmbryo MammalianRatsEnzymeOncologychemistryBiochemistryLiverCell cultureDrug metabolismDNADimethylaminesJournal of cancer research and clinical oncology
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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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On the relevance of genotoxicity for fish populations II: genotoxic effects in zebrafish (Danio rerio) exposed to 4-nitroquinoline-1-oxide in a compl…

2003

In order to characterize the impact of genotoxic potentials on populations of aquatic organisms in surface waters, zebrafish (Danio rerio) were exposed to the model genotoxicant 4-nitroquinoline-1-oxide (NQO) in a complete life-cycle test. Fish exposed to mean NQO concentrations of 0, 0.1, 0.3, 1.1, and 2.9 microg/l were examined by several genotoxicity assays with different endpoints. Assays included the unscheduled DNA synthesis (UDS) test, the comet assay, the alkaline filter elution, and the micronucleus test. The genotoxicity assays revealed an increasing genotoxicity, ranging from induction of DNA repair (even at the lowest concentration tested) to primary and secondary DNA alteration…

DNA ReplicationDNA RepairDNA repairHealth Toxicology and Mutagenesis4-Nitroquinoline 1-oxideDanioAquatic ScienceBiologymedicine.disease_causechemistry.chemical_compoundmedicineEcotoxicologyAnimalsToxicity Tests ChronicZebrafishGeneticsMicronucleus TestsDose-Response Relationship DrugMutagenicity Testsbiology.organism_classificationMolecular biology4-Nitroquinoline-1-oxideComet assaychemistryMicronucleus testToxicityComet AssayGenotoxicityMutagensAquatic toxicology (Amsterdam, Netherlands)
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