Search results for "mito"

showing 10 items of 2513 documents

FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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Dicer prevents genome instability in response to replication stress

2019

Dicer, an endoribonuclease best-known for its role in microRNA biogenesis and RNA interference pathway, has been shown to play a role in the DNA damage response and repair of double-stranded DNA breaks (DSBs) in mammalian cells. However, it remains unknown whether Dicer is also important to preserve genome integrity upon replication stress. To address this question, we focused our study on common fragile sites (CFSs), which are susceptible to breakage after replication stress. We show that inhibition of the Dicer pathway leads to an increase in CFS expression upon induction of replication stress and to an accumulation of 53BP1 nuclear bodies, indicating transmission of replication-associate…

0301 basic medicineGenome instabilityreplication stressDNA damageChromosomal fragile siteBiologygenomic instabilitycommon fragile siteCell biologySettore BIO/18 - Genetica03 medical and health sciences030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisFANCD2biology.proteinDicer PathwayMitosiscommon fragile sitesDroshaResearch PaperDicerDicerOncotarget
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Adipocytes as a Link Between Gut Microbiota-Derived Flagellin and Hepatocyte Fat Accumulation

2016

While the role of both elevated levels of circulating bacterial cell wall components and adipose tissue in hepatic fat accumulation has been recognized, it has not been considered that the bacterial components-recognizing adipose tissue receptors contribute to the hepatic fat content. In this study we found that the expression of adipose tissue bacterial flagellin (FLG)-recognizing Toll-like receptor (TLR) 5 associated with liver fat content (r = 0.699, p = 0.003) and insulin sensitivity (r = -0.529, p = 0.016) in humans (n = 23). No such associations were found for lipopolysaccharides (LPS)-recognizing TLR4. To study the underlying molecular mechanisms of these associations, human HepG2 he…

0301 basic medicineGlycerollcsh:MedicineAdipose tissueWhite adipose tissueflagellinBiochemistryImmune ReceptorsFatsEndocrinologyAnimal CellsAdipocytesMedicine and Health SciencesInsulinlcsh:ScienceToll-like ReceptorsConnective Tissue CellsMultidisciplinaryImmune System ProteinsbiologyLiver DiseasesFatty liverin kaltaiset reseptorit [toll]Lipidsadipose tissuePhysical sciencesChemistryMitochondrial respiratory chainAdipose TissueConnective Tissuebacterial componentsCellular TypesAnatomyinsuline sensitivityResearch ArticleSignal Transductionmedicine.medical_specialtyadipocytesImmunologyMonomers (Chemistry)Gastroenterology and Hepatologyta311103 medical and health sciencesInsulin resistanceInternal medicinemedicinePolymer chemistryDiabetic Endocrinologylcsh:Rta1183ta1182Biology and Life SciencesProteinsCell Biologyliver fatmedicine.diseasehepatic fatfat accumulationHormonesIRS1Fatty LiverInsulin receptor030104 developmental biologyEndocrinologyBiological TissueTLR5biology.proteinlcsh:QPLoS ONE
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Role of the DNA repair glycosylase OGG1 in the activation of murine splenocytes

2017

OGG1 (8-oxoguanine-DNA glycosylase) is the major DNA repair glycosylase removing the premutagenic DNA base modification 8-oxo-7,8-dihydroguanine (8-oxoG) from the genome of mammalian cells. In addition, there is accumulating evidence that OGG1 and its substrate 8-oxoG might function in the regulation of certain genes, which could account for an attenuated immune response observed in Ogg1-/- mice in several settings. Indications for at least two different mechanisms have been obtained. Thus, OGG1 could either act as an ancillary transcription factor cooperating with the lysine-specific demethylase LSD1 or as an activator of small GTPases. Here, we analysed the activation by lipopolysaccaride…

0301 basic medicineGuanineDNA RepairDNA repairp38 mitogen-activated protein kinasesBiologyBiochemistryDNA GlycosylasesMice03 medical and health sciencesAnimalsMolecular BiologyTranscription factorTumor Necrosis Factor-alphaKinaseActivator (genetics)MacrophagesDNACell BiologyBase excision repairMolecular biology030104 developmental biologyGene Expression RegulationDNA glycosylaseTumor necrosis factor alphaSpleenDNA DamageTranscription FactorsDNA Repair
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Mitochondrial Function in Hereditary Spastic Paraplegia: Deficits in SPG7 but Not SPAST Patient-Derived Stem Cells

2020

Mutations in SPG7 and SPAST are common causes of hereditary spastic paraplegia (HSP). While some SPG7 mutations cause paraplegin deficiency, other SPG7 mutations cause increased paraplegin expression. Mitochondrial function has been studied in models that are paraplegin-deficient (human, mouse, and Drosophila models with large exonic deletions, null mutations, or knockout models) but not in models of mutations that express paraplegin. Here, we evaluated mitochondrial function in olfactory neurosphere-derived cells, derived from patients with a variety of SPG7 mutations that express paraplegin and compared them to cells derived from healthy controls and HSP patients with SPAST mutations, as …

0301 basic medicineHereditary spastic paraplegiaoxidative phosphorylationOxidative phosphorylationMitochondrionmedicine.disease_causeSpastinSPG7lcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASThereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMutationparapleginParapleginGeneral NeuroscienceBrief Research Reportspastinmedicine.diseasePhenotypeCell biologymitochondria030104 developmental biology030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in Neuroscience
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DNA multigene characterization of Fasciola hepatica and Lymnaea neotropica and its fascioliasis transmission capacity in Uruguay, with historical cor…

2017

Background Fascioliasis is a pathogenic disease transmitted by lymnaeid snails and recently emerging in humans, in part due to effects of climate changes, anthropogenic environment modifications, import/export and movements of livestock. South America is the continent presenting more human fascioliasis hyperendemic areas and the highest prevalences and intensities known. These scenarios appear mainly linked to altitude areas in Andean countries, whereas lowland areas of non-Andean countries, such as Uruguay, only show sporadic human cases or outbreaks. A study including DNA marker sequencing of fasciolids and lymnaeids, an experimental study of the life cycle in Uruguay, and a review of hum…

0301 basic medicineHeredityPhysiologySnailsHelminth geneticsMoltingGeographical locationslaw.invention0302 clinical medicinelawRNA Ribosomal 16SMedicine and Health SciencesCluster AnalysisPhylogenyGalba truncatulaMammalsbiologyEcologylcsh:Public aspects of medicineAgricultureRuminants030108 mycology & parasitologyDNA HelminthGenetic MappingInfectious DiseasesTransmission (mechanics)Helminth InfectionsVertebratesResearch ArticleNeglected Tropical DiseasesMitochondrial DNAFascioliasisLivestocklcsh:Arctic medicine. Tropical medicineGenotypelcsh:RC955-962030231 tropical medicineDNA RibosomalRisk Assessment03 medical and health sciencesHepaticaBovinesAcanthaceaeDNA Ribosomal Spacerparasitic diseasesGeneticsParasitic DiseasesFasciola hepaticaAnimalsHumansHorsesSheepPublic Health Environmental and Occupational HealthOrganismsOutbreakGenetic VariationBiology and Life Scienceslcsh:RA1-1270Sequence Analysis DNAMolluscsParasitologia veterinàriaFasciola hepaticaSouth Americabiology.organism_classificationTropical DiseasesInvertebratesHaplotypesGastropodsVector (epidemiology)AmniotesUruguayCattlePeople and placesBestiarPhysiological ProcessesPLoS Neglected Tropical Diseases
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The analysis of estrogen receptor-α positive breast cancer stem-like cells unveils a high expression of the serpin proteinase inhibitor PI-9: Possibl…

2016

Abstract Breast cancer stem cells seem to play important roles in breast tumor recurrence and endocrine therapy resistance, although the underlying mechanisms have not been well established. Moreover, in some tumor systems the immunosurveillance failure against cancer cells has been related to the presence of the granzyme B inhibitor PI-9. This study explored the status of PI-9 in tumorspheres isolated from estrogen receptor-α positive (ERα+) breast cancer MCF7 cells. Studies were performed in tertiary tumorspheres which possess high levels of stemness markers (Nanog, Oct3/4 and Sox2) and self-renewal ability. The exposure to estrogens (17-β estradiol and genistein) increased the number and…

0301 basic medicineHomeobox protein NANOGReceptors CXCR4Cancer Researchmedicine.medical_specialtyEstrogen receptorBreast NeoplasmsBiologyp38 Mitogen-Activated Protein KinasesGranzymes03 medical and health sciences0302 clinical medicineBreast cancerSOX2Internal medicineserpin proteinase inhibitor 9 breast cancer stem-like cells breast cancer estrogen receptorsSettore BIO/10 - BiochimicamedicineHumansSerpinsCell ProliferationEstrogen Receptor alphaCancermedicine.diseaseGenisteinGene Expression Regulation NeoplasticImmunosurveillance030104 developmental biologyEndocrinologyOncology030220 oncology & carcinogenesisCancer cellMCF-7 CellsNeoplastic Stem CellsCancer researchFemaleNeoplasm Recurrence LocalStem cellSignal Transduction
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Tetrahydrocarbazoles decrease elevated SOCE in medium spiny neurons from transgenic YAC128 mice, a model of Huntington's disease

2017

AbstractHuntington's disease (HD) is a hereditary neurodegenerative disease caused by a polyglutamine expansion within the huntingtin (HTT) gene. One of the cellular functions that is dysregulated in HD is store-operated calcium entry (SOCE), a process in which the depletion of Ca2+ from the endoplasmic reticulum (ER) induces Ca2+ influx from the extracellular space. We detected an enhanced activity of SOC channels in medium spiny neurons (MSNs) from YAC128 mice, a transgenic model of HD, and investigated whether this could be reverted by tetrahydrocarbazoles. The compound 6-bromo-N-(2-phenylethyl)-2,3,4,9-tetrahydro-1H-carbazol-1-amine hydrochloride was indeed able to restore the disturbed…

0301 basic medicineHuntingtinTransgeneCarbazolesBiophysicsMice TransgenicBiologyEndoplasmic ReticulumMedium spiny neuronYAC128BiochemistryMice03 medical and health sciences0302 clinical medicineHuntington's diseaseTetrahydrocarbazolesmedicineAnimalsHomeostasisHuntingtinMolecular BiologyCells CulturedMembrane Potential MitochondrialNeuronsSOC channelsMedium spiny neuronsIon TransportEndoplasmic reticulumHuntington's diseaseStore-operated calcium entryCell Biologymedicine.diseaseStore-operated calcium entryCulture MediaCell biology030104 developmental biologyBiochemistryCalcium030217 neurology & neurosurgeryHomeostasisBiochemical and Biophysical Research Communications
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Enhanced Antibacterial Activity of Repurposed Mitomycin C and Imipenem in Combination with the Lytic Phage vB_KpnM-VAC13 against Clinical Isolates of…

2021

Study Group on Mechanisms of Action and Resistance to Antimicrobials (GEMARA) on behalf of the Spanish Society of Infectious Diseases and Clinical Microbiology (SEIMC).

0301 basic medicineImipenemKlebsiella pneumoniaemedicine.drug_classMitomycin030106 microbiologyAntibioticsResistanceDrug repurposingMicrobial Sensitivity TestsBacteriophage therapybeta-LactamasesMicrobiologyPersistence03 medical and health sciencesMechanisms of Resistancemedicinepolycyclic compoundsHumansPharmacology (medical)BacteriophagesPathogenhealth care economics and organizationsPharmacologybiologyMitomycin CBroth microdilutionbiochemical phenomena metabolism and nutritionbiology.organism_classificationAntimicrobialhumanitiesAnti-Bacterial AgentsKlebsiella InfectionsSynergyImipenemKlebsiella pneumoniae030104 developmental biologyInfectious DiseasesLytic cyclemedicine.drugAntimicrobial agents and chemotherapy
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N-(2-methyl-indol-1H-5-yl)-1-naphthalenesulfonamide : a novel reversible antimitotic agent inhibiting cancer cell motility

2016

Este es el post-print que se ha publicado de forma definitiva en: https://www.sciencedirect.com/science/article/abs/pii/S0006295216301423 A series of compounds containing the sulfonamide scaffold were synthesized and screened for their in vitro anticancer activity against a representative panel of human cancer cell lines, leading to the identification of N-(2-methyl-1H-indol-5-yl)-1-naphthalenesulfonamide (8e) as a compound showing a remarkable activity across the panel, with IC50 values in the nanomolar-to-low micromolar range. Cell cycle distribution analysis revealed that 8e promoted a severe G2/M arrest, which was followed by cellular senescence as indicated by the detection of senescen…

0301 basic medicineIndolesSulfonamides - Therapeutic use.MotilityApoptosisAntimitotic AgentsMicrotubulesBiochemistryJurkat Cells03 medical and health sciences0302 clinical medicineCell MovementTubulinMicrotubuleCélulas cancerosas - Motilidad.Apoptosis.HumansSulfamidas - Uso terapéutico.MitosisCell ProliferationPharmacologySulfonamidesMolecular StructurebiologyCancer cells - Motility.Cell cycleCell biologyMitosis.030104 developmental biologyTubulinCell cultureApoptosis030220 oncology & carcinogenesisCancer cellMCF-7 Cellsbiology.proteinDrug Screening Assays AntitumorDNA Damage
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