Search results for "DAMAGE"

showing 10 items of 1289 documents

Comparative analysis of DNA breakage, chromosomal aberrations and apoptosis induced by the anti-herpes purine nucleoside analogues aciclovir, gancicl…

2002

Nucleoside analogues have been used in antiviral therapy and suicide cancer gene therapy. Therefore, it is of importance to compare their potential cytotoxic and genotoxic action. Using metabolically competent CHO cells expressing the thymidine kinase gene of herpes simplex virus type 1 (CHO-HSVtk cells) as a model system, the induction of DNA breaks was compared with the induction of structural chromosomal aberrations and apoptosis/necrosis after exposure to the anti-herpes nucleoside analogues aciclovir (ACV), ganciclovir (GCV) and penciclovir (PCV). After continuous treatment of CHO-HSVtk cells with the drugs, LD(10) in a colony-forming assay was 50, 0.5 and 1 microM for ACV, GCV and PCV…

GanciclovirGuanineDNA damagevirusesHealth Toxicology and MutagenesisAcyclovirApoptosisCHO CellsBiologymedicine.disease_causeAntiviral AgentsThymidine KinaseChromosomesColony-Forming Units AssayNecrosisCricetulusCricetinaeGeneticsmedicineCytotoxic T cellAnimalsSimplexvirusAciclovirEnzyme InhibitorsMolecular BiologyGanciclovirChromosome AberrationsDNAMolecular biologyHerpes simplex virusApoptosisPenciclovirNucleosidemedicine.drugDNA DamageMutation research
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Young neurons from medial ganglionic eminence disperse in adult and embryonic brain.

1999

In this study, we identified neuronal precursors that can disperse through adult mammalian brain tissue. Transplanted neuronal precursors from embryonic medial ganglionic eminence (MGE), but not from lateral ganglionic eminence (LGE) or neocortex, dispersed and differentiated into neurons in multiple adult brain regions. In contrast, only LGE cells were able to migrate efficiently from the adult subventricular zone to the olfactory bulb. In embryonic brain slices, MGE cells migrated extensively toward cortex. Our results demonstrate that cells in different germinal regions have unique migratory potentials, and that adult mammalian brain can support widespread dispersion of specific populati…

Ganglionic eminenceSubventricular zoneMice Inbred StrainsNeocortexBrain damageBiologyInterneuron migrationMiceCell MovementFetal Tissue TransplantationCortex (anatomy)medicineAnimalsBrain Tissue TransplantationBrain Tissue TransplantationNeuronsNeocortexGeneral NeuroscienceMedian EminenceOlfactory BulbCorpus StriatumOlfactory bulbmedicine.anatomical_structurenervous systemLac Operonmedicine.symptomNeuroscienceStem Cell TransplantationNature neuroscience
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The “Janus” Role of C/EBPs Family Members in Cancer Progression

2020

CCAAT/enhancer-binding proteins (C/EBPs) constitute a family of transcription factors composed of six members that are critical for normal cellular differentiation in a variety of tissues. They promote the expression of genes through interaction with their promoters. Moreover, they have a key role in regulating cellular proliferation through interaction with cell cycle proteins. C/EBPs are considered to be tumor suppressor factors due to their ability to arrest cell growth (contributing to the terminal differentiation of several cell types) and for their role in cellular response to DNA damage, nutrient deprivation, hypoxia, and genotoxic agents. However, C/EBPs can elicit completely opposi…

Gene isoformCell typeDNA damagetumor suppressorCellular differentiationReviewBiologyCatalysisInorganic Chemistrylcsh:ChemistryStructure-Activity RelationshipSettore BIO/13 - Biologia ApplicataNeoplasmsAnimalsHumansProtein IsoformscancerPhysical and Theoretical ChemistryCell Cycle ProteinMolecular BiologyTranscription factorlcsh:QH301-705.5SpectroscopyCell growthOrganic Chemistrytumor promoterPromoterGeneral MedicineC/EBPComputer Science ApplicationsCell biologyGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999Multigene FamilyCCAAT-Enhancer-Binding ProteinsDisease ProgressionDisease SusceptibilityProtein BindingSignal TransductionInternational Journal of Molecular Sciences
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Progressive paraparesis in a 66-year-old man - a case study

2023

The paper presents a case of progressive paraparesis in a 66-year-old man with no history of tick bite, who was finally diagnosed with neuroborreliosis on the basis of the performed tests. Proper diagnosis and introduction of causal treatment resulted in rapid improvement of the patient’s condition.

General Medicineborreliosis; damage to the nervous system; neuroborreliosisPolski Merkuriusz Lekarski
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ALS monocyte-derived microglia-like cells reveal cytoplasmic TDP-43 accumulation, DNA damage, and cell-specific impairment of phagocytosis associated…

2022

Abstract Background Amyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease characterised by the loss of upper and lower motor neurons. Increasing evidence indicates that neuroinflammation mediated by microglia contributes to ALS pathogenesis. This microglial activation is evident in post-mortem brain tissues and neuroimaging data from patients with ALS. However, the role of microglia in the pathogenesis and progression of amyotrophic lateral sclerosis remains unclear, partly due to the lack of a model system that is able to faithfully recapitulate the clinical pathology of ALS. To address this shortcoming, we describe an approach that generates monocyte-derived mi…

General NeuroscienceAmyotrophic Lateral SclerosisImmunologyNeurodegenerative DiseasesMonocytesInflammasomeDNA-Binding ProteinsCellular and Molecular NeurosciencePhagocytosisNeurologyDisease ProgressionHumansSettore MED/26 - NeurologiaMicrogliaTDP-43 inclusionsAmyotrophic lateral sclerosiDNA DamageJournal of Neuroinflammation
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Role of Gadd45a in Wip1-dependent regulation of intestinal tumorigenesis.

2012

Conversion of intestinal stem cells into tumor-initiating cells is an early step in Apc(Min)-induced polyposis. Wild-type p53-induced phosphatase 1 (Wip1)-dependent activation of a DNA damage response and p53 has a permanent role in suppression of stem cell conversion, and deletion of Wip1 lowers the tumor burden in Apc(Min) mice. Here we show that cyclin-dependent kinase inhibitor 2a, checkpoint kinase 2, and growth arrest and DNA damage gene 45a (Gadd45a) exert critical functions in the tumor-resistant phenotype of Wip1-deficient mice. We further identified Gadd45a as a haploinsufficient gene in the regulation of Wip1-dependent tumor resistance in mice. Gadd45a appears to function through…

Genes APCDNA RepairDNA repairDNA damageApoptosisCell Cycle ProteinsBiologyProtein Serine-Threonine KinasesReceptors G-Protein-CoupledMicePhosphoprotein PhosphatasesGene silencingAnimalsMolecular BiologyCheckpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p16beta CateninMice KnockoutOriginal PaperKinaseIntestinal PolyposisStem CellsJNK Mitogen-Activated Protein KinasesNuclear ProteinsCell BiologyCell biologyProtein Phosphatase 2CCheckpoint Kinase 2Cell Transformation NeoplasticCancer researchSignal transductionStem cellTumor Suppressor Protein p53GADD45ASignal TransductionCell death and differentiation
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Detection of mammalian carcinogens with an immunological DNA synthesis-inhibition test.

1992

There is a close relationship between genotoxicity, mutagenicity and carcinogenicity. But the controversy of which short-term test system best recognizes human carcinogens is still going on. Currently, the Salmonella gene mutation assay ('Ames test') is the most widely used test for the screening of mutagens. However, many in vitro tests hold unsatisfactory validity data, presumably because of the inability of present short-term tests to detect non-genotoxic carcinogens, which are increasingly being brought into focus in the discussions of genesis of cancer. One principle often neglected in this context is the property of genotoxic agents to inhibit replicative DNA synthesis in (proliferati…

GeneticsDNA ReplicationCancer ResearchDNA synthesisDNA damageCarcinogenicity TestsContext (language use)General MedicineGene mutationBiologymedicine.disease_causeAmes testImmunoenzyme TechniquesCarcinogen ScreeningmedicineCarcinogensHumansFalse Positive ReactionsCarcinogenGenotoxicityDNA DamageHeLa CellsCarcinogenesis
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Interactions between DNA damage, repair, and transcription

2010

This review addresses a variety of mechanisms by which DNA repair interacts with transcription and vice versa. Blocking of transcriptional elongation is the best studied of these mechanisms. Transcription recovery after damage therefore has often been used as a surrogate marker of DNA repair in cells. However, it has become evident that relationships between DNA damage, repair, and transcription are more complex due to various indirect effects of DNA damage on gene transcription. These include inhibition of transcription by DNA repair intermediates as well as regulation of transcription and of the epigenetic status of the genes by DNA repair-related mechanisms. In addition, since transcript…

GeneticsGenome instabilityDNA RepairTranscription GeneticbiologyDNA repairDNA damageHealth Toxicology and MutagenesisGenomic InstabilityProliferating cell nuclear antigenCell biologyHigh-mobility groupGene Expression RegulationTranscription (biology)Geneticsbiology.proteinHumansProtein–DNA interactionDNA mismatch repairMolecular BiologyDNA DamageSignal TransductionMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Fanconi anemia (FA) and crosslinker sensitivity: Re-appraising the origins of FA definition

2015

The commonly accepted definition of Fanconi anemia (FA) relying on DNA repair deficiency is submitted to a critical review starting from the early reports pointing to mitomycin C bioactivation and to the toxicity mechanisms of diepoxybutane and a group of nitrogen mustards causing DNA crosslinks in FA cells. A critical analysis of the literature prompts revisiting the FA phenotype and crosslinker sensitivity in terms of an oxidative stress (OS) background, redox-related anomalies of FA (FANC) proteins, and mitochondrial dysfunction. This re-appraisal of FA basic defect might lead to innovative approaches both in elucidating FA phenotypes and in clinical management.

Geneticsbusiness.industryDNA repairDNA damageMitomycin CDiepoxybutaneHematologymedicine.diseasemedicine.disease_causeFANC proteinschemistry.chemical_compoundOncologychemistryFanconi anemiaChromosome instabilityPediatrics Perinatology and Child HealthmedicineCancer researchbusinessOxidative stressPediatric Blood & Cancer
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Human cytochrome P450 reductase can act as a source of endogenous oxidative DNA damage and genetic instability.

2005

Studies with repair-deficient mice and other experiments suggest that oxidative DNA modifications are generated in all types of cells even under physiological conditions and that this type of endogenous DNA damage contributes to spontaneous cancer incidence. However, the cellular sources of reactive oxygen species that are relevant for nuclear oxidative DNA damage are largely unknown. Here, we report that expression of human NADPH-cytochrome P450 reductase (hOR) in cultured V79 Chinese hamster cells gives rise to elevated basal levels of oxidative purine modifications after depletion of glutathione. Also, the basal levels of micronuclei are increased in the hOR-expressing cells, and again t…

Genome instabilityAntioxidantDNA damagemedicine.medical_treatmentGlutathione reductaseEndogenyOxidative phosphorylationCHO CellsBiologyBiochemistryGenomic Instabilitychemistry.chemical_compoundPhysiology (medical)CricetinaemedicineAnimalsHumansMicronuclei Chromosome-DefectiveNADPH-Ferrihemoprotein Reductasechemistry.chemical_classificationReactive oxygen speciesGlutathioneMolecular biologyGlutathionechemistryPurinesReactive Oxygen SpeciesOxidation-ReductionDNA DamageFree radical biologymedicine
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