Search results for "Instability"

showing 10 items of 724 documents

Mechanisms of human DNA repair: an update.

2003

The human genome, comprising three billion base pairs coding for 30000-40000 genes, is constantly attacked by endogenous reactive metabolites, therapeutic drugs and a plethora of environmental mutagens that impact its integrity. Thus it is obvious that the stability of the genome must be under continuous surveillance. This is accomplished by DNA repair mechanisms, which have evolved to remove or to tolerate pre-cytotoxic, pre-mutagenic and pre-clastogenic DNA lesions in an error-free, or in some cases, error-prone way. Defects in DNA repair give rise to hypersensitivity to DNA-damaging agents, accumulation of mutations in the genome and finally to the development of cancer and various metab…

Genome instabilityGeneticsDNA ReplicationDNA RepairBase pairDNA repairDNA damageBase Pair MismatchDNA replicationDNABiologyToxicologyDNA Repair ProteinAnimalsHumansHuman genomePoly(ADP-ribose) PolymerasesGeneDNA DamageToxicology
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Selection for thermostability can lead to the emergence of mutational robustness in an RNA virus

2010

Mutational robustness has important evolutionary implications, yet the mechanisms leading to its emergence remain poorly understood. One possibility is selection acting on a correlated trait, as for instance thermostability (plastogenetic congruence). Here, we examine the correlation between mutational robustness and thermostability in experimental populations of the RNA bacteriophage Qβ. Thermostable viruses evolved after only six serial passages in the presence of heat shocks, and genome sequencing suggested that thermostability can be conferred by several alternative mutations. To test whether thermostable viruses have increased mutational robustness, we performed additional passages in …

Genome instabilityGeneticsRobustness (evolution)RNARNA virusRNA PhagesBiologybiology.organism_classificationBacteriophage QβEcology Evolution Behavior and SystematicsDNA sequencingThermostabilityJournal of Evolutionary Biology
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Molecular and Cellular Insights into the Development of Uterine Fibroids

2021

Uterine leiomyomas represent the most common benign gynecologic tumor. These hormone-dependent smooth-muscle formations occur with an estimated prevalence of ~70% among women of reproductive age and cause symptoms including pain, abnormal uterine bleeding, infertility, and recurrent abortion. Despite the prevalence and public health impact of uterine leiomyomas, available treatments remain limited. Among the potential causes of leiomyomas, early hormonal exposure during periods of development may result in developmental reprogramming via epigenetic changes that persist in adulthood, leading to disease onset or progression. Recent developments in unbiased high-throughput sequencing technolog…

Genome instabilityInfertilitysteroid hormonesUterine fibroidsQH301-705.5ReviewBioinformaticsCatalysistumor-initiating cellEpigenesis GeneticInorganic Chemistrytumor bulk/single-cellsmedicineAnimalsHumansGenetic Predisposition to DiseaseEpigeneticsPhysical and Theoretical ChemistryBiology (General)Molecular BiologyQD1-999genetics/epigeneticsSpectroscopyUterine leiomyomauterine leiomyomaLeiomyomabusiness.industryOrganic ChemistryUterusMyometriumbiomarkersGeneral Medicinemedicine.diseasefemale genital diseases and pregnancy complicationsComputer Science ApplicationsGene Expression Regulation NeoplasticChemistryLeiomyomaMutationUterine Neoplasmstargetable pathwaysFemalebusinessReprogrammingInternational Journal of Molecular Sciences
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Deficiency of the Cockayne syndrome B (CSB) gene aggravates the genomic instability caused by endogenous oxidative DNA base damage in mice.

2007

The Cockayne syndrome B protein (CSB) has long been known to be involved in the repair of DNA modifications that block the RNA polymerase in transcribed DNA sequences (transcription-coupled repair). Recent evidence suggests that it also has a more general role in the repair of oxidative DNA base modifications such as 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxoG). In mammalian cells, 8-oxoG is a substrate of the repair glycosylase OGG1. Mice without this enzyme accumulate 8-oxoG in the genome and have elevated spontaneous mutation rates. To elucidate the role of CSB in the prevention of mutations by oxidative DNA base damage, we have generated mice that are deficient in Csb or Ogg1 or both ge…

Genome instabilityMaleCancer ResearchDNA repairDNA damageMice Inbred StrainsMice TransgenicBiologymedicine.disease_causeCockayne syndromeGenomic InstabilityDNA GlycosylasesMiceBacterial ProteinsGeneticsmedicineLac RepressorsAnimalsPoint MutationPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneSequence DeletionGeneticsMice KnockoutMutationPoint mutationmedicine.diseaseMolecular biologyRepressor ProteinsMutagenesis InsertionalOxidative StressDNA Repair EnzymesLiverDNA glycosylaseMutationFemaleDNA DamageOncogene
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Genomic instability in an interspecific hybrid of the genus Saccharomyces: a matter of adaptability

2020

Ancient events of polyploidy have been linked to huge evolutionary leaps in the tree of life, while increasing evidence shows that newly established polyploids have adaptive advantages in certain stress conditions compared to their relatives with a lower ploidy. The genus Saccharomyces is a good model for studying such events, as it contains an ancient whole-genome duplication event and many sequenced Saccharomyces cerevisiae are, evolutionary speaking, newly formed polyploids. Many polyploids have unstable genomes and go through large genome erosions; however, it is still unknown what mechanisms govern this reduction. Here, we sequenced and studied the natural S. cerevisiae × Saccharomyces…

Genome instabilityNuclear geneDNA Copy Number VariationsPopulationGene DosageHybridsWineGenome instabilityadaptationSaccharomyces cerevisiaeBiologyGenomeGenomic InstabilityPolyploidy03 medical and health sciencesSaccharomycesCopy-number variationAdaptationeducation030304 developmental biologyhybridsresequencing0303 health scienceseducation.field_of_study030306 microbiologyChimeraGeneral MedicineGenomicsSequence Analysis DNAbiology.organism_classificationgenome instabilityEvolutionary biologyEpistasisPloidyMicrobial evolution and epidemiology: Mechanisms of evolutionSaccharomyces kudriavzeviiGenome FungalSaccharomyces kudriavzeviiResequencingResearch ArticleMicrobial Genomics
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Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
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Molecular and physiological consequences of faulty eukaryotic ribonucleotide excision repair

2019

Abstract The duplication of the eukaryotic genome is an intricate process that has to be tightly safe‐guarded. One of the most frequently occurring errors during DNA synthesis is the mis‐insertion of a ribonucleotide instead of a deoxyribonucleotide. Ribonucleotide excision repair (RER) is initiated by RNase H2 and results in error‐free removal of such mis‐incorporated ribonucleotides. If left unrepaired, DNA‐embedded ribonucleotides result in a variety of alterations within chromosomal DNA, which ultimately lead to genome instability. Here, we review how genomic ribonucleotides lead to chromosomal aberrations and discuss how the tight regulation of RER timing may be important for preventin…

Genome instabilityRibonucleotideDNA RepairDNA repairDNA damageRibonucleotide excision repairRibonuclease HContext (language use)ReviewBiologyGenomic InstabilityGeneral Biochemistry Genetics and Molecular Biology570 Life sciences03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAnimalsHumansMolecular Biology030304 developmental biology0303 health sciencesGeneral Immunology and MicrobiologyGeneral NeuroscienceRNA–DNA hybridDNA Replication Repair & RecombinationEukaryotaDNAtopoisomerase 1ChromatinChromatinCell biologychemistryribonucleotide excision repairGenetic FitnessRNase H2030217 neurology & neurosurgeryDNA570 BiowissenschaftenThe EMBO Journal
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Checkpoint adaptation in recombination-deficient cells drives aneuploidy and resistance to genotoxic agents.

2020

Abstract Human cancers frequently harbour mutations in DNA repair genes, rendering the use of DNA damaging agents as an effective therapeutic intervention. As therapy-resistant cells often arise, it is important to better understand the molecular pathways that drive resistance in order to facilitate the eventual targeting of such processes. We employ recombination-defective diploid yeast as a model to demonstrate that, in response to genotoxic challenges, nearly all cells eventually undergo checkpoint adaptation, resulting in the generation of aneuploid cells with whole chromosome losses that have acquired resistance to the initial genotoxic challenge. We demonstrate that adaptation inhibit…

Genome instabilitySaccharomyces cerevisiae ProteinsDNA RepairDNA repairAneuploidySaccharomyces cerevisiaeBiologyBiochemistryGenomic Instabilitychemistry.chemical_compoundGene Knockout TechniquesDrug Resistance FungalmedicineCytotoxicityMolecular BiologyRecombination GeneticSirolimusCell BiologyCell Cycle Checkpointsmedicine.diseaseAneuploidyPhenotypeDiploidyCell biologyRad52 DNA Repair and Recombination ProteinchemistryAdaptationPloidyDNADNA repair
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Never cared for what they do. High structural stability of Guanine-quadruplexes in presence of strand-break damages

2021

AbstractDNA integrity is an important factor to assure genome stability and, more generally, cells and organisms’ viability. In presence of DNA damage, the normal cell cycle is perturbed while cells activate their repair processes. Although efficient, the repair system is not always able to ensure the complete restoration of gene integrity. In these cases, not only mutations may occur, but the accumulation of lesions can either lead to carcinogenesis or reach a threshold which induces apoptosis and the programmed cell death. Among the different types of DNA lesions, strand breaks produced by ionizing radiations are the most toxic, due to their inherently difficult repair, which may lead to …

Genome instabilitySenescenceProgrammed cell deathchemistry.chemical_compoundchemistryDNA damageGene expressionmedicineCarcinogenesismedicine.disease_causeGeneDNACell biology
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Long-Lasting Genomic Instability Following Arsenite Exposure inMammalian Cells: The Role of Reactive Oxygen Species

2011

Previously, we reported that the progeny of mammalian cells, which has been exposed to sodium arsenite for two cell cycles, exhibited chromosomal instability and concurrent DNA hypomethylation, when they were subsequently investigated after two months of subculturing (about 120 cell generations) in arsenite-free medium. In this work, we continued our investigations of the long-lasting arsenite-induced genomic instability by analyzing additional endpoints at several time points during the cell expanded growth. In addition to the progressive increase of aneuploid cells, we also noted micronucleated and multinucleated cells that continued to accumulate up to the 50th cell generation, as well a…

Genome instabilitySodium arseniteEpidemiologyArsenitesHealth Toxicology and MutagenesisPopulationCellarsenite; genomic instability; reactive oxygen speciesCHO CellsBiologyGenomic Instabilitychemistry.chemical_compoundMultinucleateCricetulusChromosome instabilityCricetinaemedicineAnimalseducationGenetics (clinical)Arseniteeducation.field_of_studyCell cycleDNA MethylationFlow CytometryMolecular biologyarseniteSettore BIO/18 - Geneticamedicine.anatomical_structurechemistryEnvironmental PollutantsReactive Oxygen Species
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