Search results for "HOMOLOGOUS RECOMBINATION"

showing 10 items of 39 documents

Artesunate derived from traditional Chinese medicine induces DNA damage and repair.

2008

Abstract Artesunate is a semisynthetic derivative from artemisinin, a natural product from the Chinese herb Artemisia annua L. It exerts antimalarial activity, and, additionally, artemisinin and its derivatives are active against cancer cells. The active moiety is an endoperoxide bridge. Its cleavage leads to the formation of reactive oxygen species and carbon-centered radicals. These highly reactive molecules target several proteins in Plasmodia, which is thought to result in killing of the microorganism. DNA damage induced by artemisinins has not yet been described. Here, we show that artesunate induces apoptosis and necrosis. It also induces DNA breakage in a dose-dependent manner as sho…

Cancer ResearchKu80DNA RepairDNA repairDNA damageBlotting WesternArtesunateFluorescent Antibody TechniqueApoptosisBiologyCell Linechemistry.chemical_compoundCricetulusCricetinaeAnimalsMedicine Chinese TraditionalBase excision repairDNAMolecular biologyArtemisininsComet assayOncologychemistryArtesunateCancer cellComet AssayHomologous recombinationDNA DamageCancer research
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Artesunate induces oxidative DNA damage, sustained DNA double-strand breaks, and the ATM/ATR damage response in cancer cells.

2011

Abstract Artesunate, the active agent from Artemisia annua L. used in the traditional Chinese medicine, is being applied as a first-line drug for malaria treatment, and trials are ongoing that include this drug in cancer therapy. Despite increasing interest in its therapeutic application, the mode of cell killing provoked by artesunate in human cells is unknown. Here, we show that artesunate is a powerful inducer of oxidative DNA damage, giving rise to formamidopyrimidine DNA glycosylase–sensitive sites and the formation of 8-oxoguanine and 1,N6-ethenoadenine. Oxidative DNA damage was induced in LN-229 human glioblastoma cells dose dependently and was paralleled by cell death executed by ap…

Cancer ResearchProgrammed cell deathDNA RepairRAD51Drug Evaluation PreclinicalArtesunateApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine KinasesModels Biologicalchemistry.chemical_compoundNeoplasmsTumor Cells CulturedHumansDNA Breaks Double-StrandedTumor Suppressor ProteinsMolecular biologyAntineoplastic Agents PhytogenicArtemisininsUp-RegulationNon-homologous end joiningDNA-Binding ProteinsOxidative StressCell killingOncologychemistryArtesunateApoptosisCancer cellHomologous recombinationDNA DamageMolecular cancer therapeutics
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Rad51 and BRCA2 - New Molecular Targets for Sensitizing Glioma Cells to Alkylating Anticancer Drugs

2011

First line chemotherapeutics for brain tumors (malignant gliomas) are alkylating agents such as temozolomide and nimustine. Despite growing knowledge of how these agents work, patients suffering from this malignancy still face a dismal prognosis. Alkylating agents target DNA, forming the killing lesion O(6)-alkylguanine, which is converted into DNA double-strand breaks (DSBs) that trigger apoptosis. Here we assessed whether inhibiting repair of DSBs by homologous recombination (HR) or non-homologous end joining (NHEJ) is a reasonable strategy for sensitizing glioma cells to alkylating agents. For down-regulation of HR in glioma cells, we used an interference RNA (iRNA) approach targeting Ra…

Cancer Treatmentlcsh:MedicineApoptosisToxicologyBiochemistrychemistry.chemical_compoundDrug DiscoveryRNA Small Interferinglcsh:ScienceHomologous RecombinationNeurological TumorsGene knockdownMultidisciplinaryBrain NeoplasmsGliomaFlow CytometryNon-homologous end joiningOncologyPARP inhibitorMedicinemedicine.drugResearch ArticleBiotechnologyDrugs and DevicesDrug Research and DevelopmentDNA damageMorpholinesToxic AgentsOlaparibGliomaCell Line TumormedicineHumansBiologyAntineoplastic Agents AlkylatingProtein Kinase InhibitorsBRCA2 ProteinTemozolomideBase SequenceNimustinelcsh:RCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseasechemistryMicroscopy FluorescenceChromonesCancer researchlcsh:QRad51 RecombinaseDNA DamagePLoS ONE
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Deinococcus radiodurans' SRA-HNH domain containing protein Shp (Dr1533) is involved in faithful genome inheritance maintenance following DNA damage

2018

WOS:000452343100012; International audience; Background: Deinococcus radiodurans R1 (DR) survives conditions of extreme desiccation, irradiation and exposure to genotoxic chemicals, due to efficient DNA breaks repair, also through Mn2+ protection of DNA repair enzymes. Methods: Possible annotated domains of the DR1533 locus protein (Shp) were searched by bioinformatic analysis. The gene was cloned and expressed as fusion protein. Band-shift assays of Shp or the SRA and HNH domains were performed on oligonucleotides, genomic DNA from E. coif and DR. slip knock-out mutant was generated by homologous recombination with a kanamycin resistance cassette. Results: DR1533 contains an N-terminal SRA…

DNA RepairDNA cytosine-methylation; DNA damage; DR1533 locus; Genotoxic agents; Mn2+; SRA domain; Biophysics; Biochemistry; Molecular BiologyGenotoxic agents[SDV]Life Sciences [q-bio]DNA cytosine-methylationperspectiveSettore BIO/19 - Microbiologia GeneraleBiochemistrychemistry.chemical_compound0302 clinical medicineKanamycinCloning Molecularcytosine0303 health sciencesDR1533 locusbiologyChemistryGenotoxic agentuhrf1Mn(2+)Mn2+SRA domainDeinococcusrecognitionmanganese(ii)DNA BacterialDNA damageDNA repairoxidationUbiquitin-Protein LigasesBiophysicsSettore BIO/11 - Biologia Molecolareresistance03 medical and health sciencesBacterial ProteinsProtein DomainsDR1533 locuDrug Resistance BacterialEscherichia coliHumansfeaturesAmino Acid SequenceGeneMolecular Biology030304 developmental biologyOligonucleotideComputational BiologyDeinococcus radioduransDNA Methylationbiology.organism_classificationMolecular biologygenomic DNArepairMutationCCAAT-Enhancer-Binding ProteinsDNA damageHomologous recombination030217 neurology & neurosurgeryDNAGenome BacterialMutagens
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Gene Repair of an Usher Syndrome Causing Mutation by Zinc-Finger Nuclease Mediated Homologous Recombination

2012

PURPOSE. Human Usher syndrome (USH) is the most frequent cause of inherited deaf-blindness. It is clinically and genetically heterogeneous, assigned to three clinical types of which the most severe type is USH1. No effective treatment for the ophthalmic component of USH exists. Gene augmentation is an attractive strategy for hereditary retinal diseases. However, several USH genes, like USH1C, are expressed in various isoforms, hampering gene augmentation. As an alternative treatment strategy, we applied the zinc-finger nuclease (ZFN) technology for targeted gene repair of an USH1C, causing mutation by homologous recombination. METHODS. We designed ZFNs customized for the p.R31X nonsense mut…

Gene isoformNonsense mutationCell Cycle ProteinsBiologyRetinaCell Linechemistry.chemical_compoundHumansDNA Breaks Double-StrandedDNA CleavageHomologous RecombinationGeneAdaptor Proteins Signal TransducingZinc fingerGeneticsTargeted Gene RepairfungiZinc FingersDNAEndonucleasesZinc finger nucleaseCytoskeletal ProteinschemistryCodon NonsenseHomologous recombinationUsher SyndromesDNATargeted Gene RepairInvestigative Opthalmology & Visual Science
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Liver-specific overexpression of matrix metalloproteinase 9 (MMP-9) in transgenic mice accelerates development of hepatocellular carcinoma.

2010

Matrix metalloproteinase-9 (MMP-9) plays a central role in tumor invasion and development of metastases. Expression of MMP-9 had been shown in human hepatocellular carcinomas (HCCs). However, it remained unclear whether MMP-9 could influence development of HCC. In order to address this issue, we generated transgenic mice overexpressing MMP-9 in the liver. In order to avoid embryonic lethality a Cre-lox system was utilized for conditional overexpression of MMP-9 under control of an albumin enhancer and promoter. Induction of MMP-9 overexpression in transgenic mice was achieved by i.v. injection of an adenovirus coding for the Cre recombinase. Initiation of liver carcinogenesis was achieved b…

Genetically modified mouseCancer ResearchLiver tumorTransgeneGenetic VectorsCre recombinaseGene ExpressionMice TransgenicBiologymedicine.disease_causeMiceLiver Neoplasms ExperimentalIn vivoGene OrdermedicineAnimalsHomeostasisHumansHomologous RecombinationMolecular BiologyIntegrasesHCCSmedicine.diseaseMolecular biologyCell Transformation NeoplasticPhenotypeLiverMatrix Metalloproteinase 9Organ SpecificityHepatocellular carcinomaCarcinogenesisMolecular carcinogenesis
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Surmounting limited gene delivery into primary immune cell populations: Efficient cell type-specific adenoviral transduction by CAR.

2015

Ectopic gene expression studies in primary immune cells have been notoriously difficult to perform due to the limitations in conventional transfection and viral transduction methods. Although replication-defective adenoviruses provide an attractive alternative for gene delivery, their use has been hampered by the limited susceptibility of murine leukocytes to adenoviral infection, due to insufficient expression of the human coxsackie/adenovirus receptor (CAR). In this issue of the European Journal of Immunology, Heger et al. [Eur. J. Immunol. 2015. 45: XXXX-XXXX] report the generation of transgenic mice that enable conditional Cre/loxP-mediated expression of human CAR. The authors demonstra…

Genetically modified mouseIntegrasesImmunologyCellGenetic VectorsTransfectionGene deliveryBiologyVirologyIn vitroCell biologyAdenoviridaemedicine.anatomical_structureImmune systemGenes ReporterTransduction GeneticGene TargetingmedicineImmunology and AllergyAnimalsHumansEctopic expressionReceptorHomologous RecombinationEuropean journal of immunology
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In the literature: October 2016

2016

A consortium on clinical and molecular stratification on oesophageal adenocarcinoma established in Britain has recently published in Nature Genetics , a whole-genomic sequencing analysis of more than 100 samples.1 Interestingly, they describe three distinct molecular subtypes with potential treatment relevance. This observation has also been verified in an independent validation cohort. Those three types are: (1) the ones showing homologous recombination and chromosome segregation pathways defects with enrichment of a BRCA signature. These tumours would be sensitive to DNA damaging agents, including neutron and photon irradiation with the addition of PARP inhibitors, (2) a group with high m…

GeneticsCancer ResearchChemotherapyMutationbiologymedicine.medical_treatmentliteratureImmunotherapyNewsmedicine.disease_causeGenomeOncologyGene duplicationmedicineCancer researchbiology.protein1506AntibodyHomologous recombinationCD8ESMO Open
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Horizontal gene transfer to a defensive symbiont with a reduced genome amongst a multipartite beetle microbiome

2019

ABSTRACTThe loss of functions required for independent life when living within a host gives rise to reduced genomes in obligate bacterial symbionts. Although this phenomenon can be explained by existing evolutionary models, its initiation is not well understood. Here, we describe the microbiome associated with eggs of the beetleLagria villosa, containing multiple bacterial symbionts related toBurkholderia gladioliincluding a reduced-genome symbiont thought to produce the defensive compound lagriamide. We find that the putative lagriamide producer is the only symbiont undergoing genome reduction, and that it has already lost most primary metabolism and DNA repair pathways. The horizontal acq…

GeneticsObligateHost (biology)Horizontal gene transferGene clusterMicrobiomeBiologyHomologous recombinationGenomeGene
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Hypoxia and Human Genome Stability: Downregulation of BRCA2 Expression in Breast Cancer Cell Lines

2013

Previously, it has been reported that hypoxia causes increased mutagenesis and alteration in DNA repair mechanisms. In 2005, an interesting study showed that hypoxia-induced decreases in BRCA1 expression and the consequent suppression of homologous recombination may lead to genetic instability. However, nothing is yet known about the involvement of BRCA2 in hypoxic conditions in breast cancer. Initially, a cell proliferation assay allowed us to hypothesize that hypoxia could negatively regulate the breast cancer cell growth in short term in vitro studies. Subsequently, we analyzed gene expression in breast cancer cell lines exposed to hypoxic condition by microarray analysis. Interestingly,…

Genome instabilityDNA RepairArticle SubjectDNA repairDNA damageSettore MED/06 - Oncologia MedicaDown-Regulationlcsh:MedicineBreast NeoplasmsBiologyGeneral Biochemistry Genetics and Molecular BiologyGenomic InstabilityBreast cancerCell Line TumorBreast CancermedicineHumansEnzyme Inhibitorsskin and connective tissue diseasesHypoxiaBiologyGeneral Immunology and MicrobiologyBRCA1 ProteinGenome Humanlcsh:RGenome StabilityGeneral MedicineDNA repair protein XRCC4medicine.diseaseBRCA2Cell HypoxiaAmino Acids DicarboxylicGene Expression Regulation NeoplasticCancer researchDNA mismatch repairFemaleHuman medicineHypoxia; Genome Stability; BRCA2; Breast CancerHomologous recombinationEngineering sciences. TechnologyNucleotide excision repairResearch ArticleDNA Damage
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