Search results for "BLAST"

showing 10 items of 2136 documents

In Vitro Biocompatibility of Several Children's Toothpastes on Human Gingival Fibroblasts

2022

The European Academy of Paediatric Dentistry has recommended fluoride toothpastes from the eruption of the first teeth in children. Toothpastes stay in the mouth in contact with human gingival fibroblasts (hGFs) for a long time. Thus, the objective of this study was to compare the cytotoxicity of five different commonly used children’s toothpastes: Oral B Kids +3 (Procter & Gamble, Alicante, Spain), Fluor Kin Calcium (Kin, Madrid, Spain), PHB Junior (PHB, Barcelona, Spain), Colgate +3 (Colgate Palmolive, Madrid, Spain) and Vitis Kids (Dentaid, Valencia, Spain) on hGFs. The children’s toothpastes were exposed to hGFs at different concentrations (1:1, 1:2, 1:4). Afterwards, several tests …

FluoridesHealth Toxicology and MutagenesisPublic Health Environmental and Occupational HealthGingivaHumansSodium FluorideDentschildren’s toothpastes; biocompatibility; SLS; fluorideFibroblastsChildOdontologiaToothpastes
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Apoptosis induced in hepatoblastoma HepG2 cells by the proteasome inhibitor MG132 is associated with hydrogen peroxide production, expression of Bcl-…

2002

This report is focused on the apoptotic effect induced by MG132, an inhibitor of 26S proteasome, in human hepatoma HepG2 cells. The results were compared with those obtained with non-transformed human Chang liver cells. MG132 reduced the viability of HepG2 cells in a time- and dose-dependent manner. The effect was in tight connection with the induction of apoptosis, as indicated by fluorescence microscopy and cytometric analysis, and was accompanied by a remarkable increase in the production of H2O2 and a reduction in mitochondrial transmembrane potential (Deltapsim). In addition cell death was prevented by antioxidants such as GSH, N-acetylcysteine or catalase. Western blot analysis showed…

G2 PhaseHepatoblastomaCancer ResearchProgrammed cell deathProteasome Endopeptidase ComplexMG132Time FactorsCell SurvivalLeupeptinsPoly ADP ribose polymeraseBlotting Westernbcl-X ProteinMitosisCaspase 3Antineoplastic AgentsApoptosismacromolecular substancesMembrane Potentialschemistry.chemical_compoundCytosolMultienzyme ComplexesMG132medicineTumor Cells CulturedHumansCaspasebiologyCaspase 3Cytochrome cCell CycleLiver NeoplasmsHydrogen PeroxideFlow CytometryMolecular biologyMitochondriaEnzyme ActivationCysteine EndopeptidasesOxidative StressOncologyBiochemistrychemistryProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinProteasome inhibitormedicine.drug
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Glutathione peroxidase 1 activity dictates the sensitivity of glioblastoma cells to oxidative stress.

2012

The high intratumoral and intertumoral heterogeneity of glioblastoma (GBM) leads to resistance to different therapies, and hence, selecting an effective therapy is very challenging. We hypothesized that the antioxidant enzyme status is a significant feature of GBM heterogeneity. The most important reactive oxygen/nitrogen species (ROS/RNS) detoxification mechanisms include superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). Expression and activity of these enzymes and the cellular response to induced oxidative stress were systematically analyzed and compared between GBM cells and nontransformed glial cells of both human and murine origin. Regardless of cell type or speci…

GPX1medicine.disease_causeSuperoxide dismutaseCellular and Molecular NeuroscienceMiceCell Line TumormedicineAnimalsHumanschemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasebiologyMicrogliaBrain NeoplasmsSuperoxide DismutaseGlutathione peroxidaseCatalaseMolecular biologyOxidative Stressmedicine.anatomical_structureNeurologychemistryCell culturebiology.proteinCancer researchNeurogliaGlioblastomaReactive Oxygen SpeciesNeurogliaOxidative stressGlia
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Roles for ELMOD2 and Rootletin in ciliogenesis.

2021

AbstractELMOD2 is a GTPase activating protein (GAP) with uniquely broad specificity for ARF family GTPases. We previously showed that it acts with ARL2 in mitochondrial fusion and microtubule stability and with ARF6 during cytokinesis. Mouse embryonic fibroblasts deleted for ELMOD2 also displayed changes in cilia related processes including increased ciliation, multiciliation, ciliary morphology, ciliary signaling, centrin accumulation inside cilia, and loss of rootlets at centrosomes with loss of centrosome cohesion. Increasing ARL2 activity or overexpressing Rootletin reversed these defects, revealing close functional links between the three proteins. This was further supported by the fin…

GTPase-activating proteinBiologyMicrotubulesMitochondrial DynamicsCell Line03 medical and health sciencesMice0302 clinical medicineMicrotubuleGTP-Binding ProteinsCiliogenesisAnimalsHumansCiliaMolecular Biology030304 developmental biologyCytokinesisCentrosome0303 health sciencesADP-Ribosylation FactorsCiliumGTPase-Activating ProteinsCell BiologyArticlesFibroblastsCell biologyMitochondriaCytoskeletal Proteinsmitochondrial fusionCentrosomeCentrinRootletin030217 neurology & neurosurgeryCytokinesisSignal TransductionMolecular biology of the cell
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MRI-Visible Poly(ε-caprolactone) with Controlled Contrast Agent Ratios for Enhanced Visualization in Temporary Imaging Applications

2013

International audience; Hydrophobic macromolecular contrast agents (MMCAs) are highly desirable to provide safe and efficient magnetic resonance (MR) visibility to implantable medical devices. In this study, we report on the synthesis and evaluation of novel biodegradable poly(ε-caprolactone)-based MMCAs. Poly(α-propargyl-ε-caprolactone-co-ε-caprolactone)s containing 2, 5, and 10 mol % of propargyl groups have been prepared by ring-opening copolymerization of ε-caprolactone and the corresponding propargylated lactone. In parallel, a diazido derivative of the clinically used diethylenetriaminepentaacetic acid (DTPA)/Gd3+ complex has been synthesized. Finally, MRI-visible poly(ε-caprolactone)…

Gadolinium DTPAPolymers and PlasticsMacromolecular SubstancesPolyestersContrast MediaBiocompatible MaterialsBioengineering02 engineering and technology010402 general chemistrybiomedical01 natural sciencesImagingBiomaterialsMicechemistry.chemical_compoundPoly(ε-caprolactone)Polymer chemistryMaterials ChemistryCopolymerAnimalsmacromolecularCell Proliferationchemistry.chemical_classificationMolecular Structure[CHIM.ORGA]Chemical Sciences/Organic chemistryMRI; Poly(ε-caprolactone); ImagingSpin–lattice relaxationFibroblastsHydrophobic[CHIM.ORGA] Chemical Sciences/Organic chemistry021001 nanoscience & nanotechnologyGraftingMagnetic Resonance ImagingvisibleCycloaddition0104 chemical sciencescopolymerizationchemistryPropargylDTPA0210 nano-technologyCaprolactoneLactoneMacromoleculeMRI
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Galectin-3 Impairment of MYCN-Dependent Apoptosis-Sensitive Phenotype Is Antagonized by Nutlin-3 in Neuroblastoma Cells

2012

MYCN amplification occurs in about 20-25% of human neuroblastomas and characterizes the majority of the high-risk cases, which display less than 50% prolonged survival rate despite intense multimodal treatment. Somehow paradoxically, MYCN also sensitizes neuroblastoma cells to apoptosis, understanding the molecular mechanisms of which might be relevant for the therapy of MYCN amplified neuroblastoma. We recently reported that the apoptosis-sensitive phenotype induced by MYCN is linked to stabilization of p53 and its proapoptotic kinase HIPK2. In MYCN primed neuroblastoma cells, further activation of both HIPK2 and p53 by Nutlin-3 leads to massive apoptosis in vitro and to tumor shrinkage an…

Galectin 3Cancer TreatmentGene Dosagelcsh:MedicineApoptosisProtein-Serine-Threonine KinaseBiochemistryPiperazineschemistry.chemical_compoundNeuroblastoma0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchSignaling in Cellular Processeslcsh:ScienceEnergy-Producing OrganellesApoptotic SignalingNuclear ProteinOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinMultidisciplinaryCell DeathImidazolesOncogene ProteinNuclear ProteinsTransfectionNutlin3. Good healthGene Expression Regulation NeoplasticProtein TransportCell killingPhenotypeOncologyGalectin-3030220 oncology & carcinogenesisGene Knockdown TechniquesMedicineResearch ArticleSignal TransductionHumanBiologyBioenergeticsProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinModels Biological03 medical and health sciencesNeuroblastomaCell Line TumormedicineHumansBiologyImidazolePiperazineneoplasms030304 developmental biologylcsh:RGene AmplificationChemotherapy and Drug Treatmentmedicine.diseasechemistryCell cultureApoptosisPediatric OncologyCytoprotectionGene Knockdown TechniqueCancer researchlcsh:QTumor Suppressor Protein p53Carrier ProteinsCarrier ProteinDNA Damage
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Astacins: proteases in development and tissue differentiation

2013

Capítulo en: Stöker, Walter; Brix, Klaudia (eds.). Proteases: structure and function. Wien: Springer, 2013

GastrulationProteasesanimal structuresOntogenyExtracellular matrix assemblyembryonic structuresBiophysicsAstacinBiologyBlastulaPolyspermyEmbryonic stem cellCell biology
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Influence ofKi-ras-driven oncogenic transformation on the protein network of murine fibroblasts

2007

Ki-ras gene mutations that specifically occur in codons 12, 13 and 61 are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, stable transfectants of NIH3T3 cells carrying different Ki-ras4B gene mutations were generated. Wild type Ki-ras transformants, mock transfectants and parental cells served as controls. These in vitro model systems were systematically analyzed for their protein expression pattern using two-dimensional gel electrophoresis followed by mass spectrometry and/or protein sequencing. Using this approach, a number of target molecules that are differentially but coordi…

Gel electrophoresismedicine.diagnostic_testWild typeFibroblastsBiologyGene mutationTransfectionmedicine.disease_causeProteomicsBiochemistryMolecular biologyMiceCell Transformation NeoplasticWestern blotHeat shock proteinNIH 3T3 Cellsras ProteinsmedicineAnimalsMitogen-Activated Protein KinasesCarcinogenesisMolecular BiologyGeneSignal TransductionPROTEOMICS
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Expresión inmunohistoquímica de la proteína mycN y el estado del gen MYCN en tumores neuroblásticos

2007

Antecedentes: Los tumores neuroblásticos son de los tumores pediátricos más frecuentes. A pesar de su gran variedad genética, clínica e histopatológica, la amplificación del gen MYCN es siempre un indicador de mal pronóstico. Este oncogen codifica una proteína nuclear que se une al ADN y activa la transcripción de sus genes diana. Un aumento en el número de copias del gen no se corresponde siempre con sobreexpresión de su proteína. El valor pronóstico de la detección de la proteína es controvertido. Métodos: Se han analizado 220 muestras de NB. Mediante la técnica de FISH se ha establecido el estado del gen, mientras que la inmunohistoquímica ha permitido el estudio de la expresión de la pr…

Gen MYCNjjjkkkNeuroblastomaProteína mycNUNESCO::CIENCIAS MÉDICAS ::Patología::OncologíaUNESCO::CIENCIAS MÉDICASBiology:CIENCIAS MÉDICAS [UNESCO]:CIENCIAS MÉDICAS ::Patología::Oncología [UNESCO]Neuroblastoma ; Proteína mycN ; Gen MYCNjjjkkkMolecular biologyPathology and Forensic Medicine
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Anaplastic lymphoma kinase expression in neuroblastomas and its relationship with genetic, prognostic, and predictive factors

2011

Gene DosageReceptor Protein-Tyrosine KinasesProtein-Tyrosine KinasesBiologyPrognosisPathology and Forensic MedicineCohort StudiesSurvival RateNeuroblastomaExpression (architecture)Cancer researchHumansAnaplastic lymphoma kinaseAnaplastic Lymphoma KinaseChromosome DeletionIn Situ Hybridization FluorescenceNeoplasm StagingHuman Pathology
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