Search results for "kappa"

showing 10 items of 419 documents

Nuclear Translocation of Nuclear Transcription Factor-κB by α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptors Leads to Transcription of …

2003

We describe a new molecular mechanism of cell death by excitotoxicity mediated through nuclear transcription factor κB (NFκB) in rat embryonic cultures of dopaminergic neurons. Treatment of mesencephalic cultures with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) resulted in a number of changes that occurred selectively in dopaminergic neurons, including persistent elevation in intracellular Ca2+ monitored with Fura-2, and a significant increase in intramitochondrial oxidation of dihydrorhodamine 123, probably associated with transient increase of mitochondrial permeability, cytochrome c release, nuclear translocation of NFκB, and transcriptional activation of the oncogenep53.…

Programmed cell deathCell Membrane PermeabilityTime FactorsCIENCIAS MÉDICAS Y DE LA SALUDTranscription GeneticNeuriteActive Transport Cell NucleusInmunologíaExcitotoxicitymedicine.disease_causeCELL DEATHReceptors DopamineRats Sprague-DawleymedicineAnimalsReceptors AMPAalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidTranscription factorPARKINSON DISEASECaspaseNeuronsPharmacologyCell DeathNUCLEAR TRANSCRIPTIONbiologyDopaminergicNF-kappa BNFKB1Molecular biologyMitochondriaRatsCell biologyMedicina Básicabiology.proteinMolecular MedicineCalciumFemaleTumor Suppressor Protein p53Signal transductionMolecular Pharmacology
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Molecular mechanisms of rosmarinic acid from Salvia miltiorrhiza in acute lymphoblastic leukemia cells

2015

Abstract Ethnopharmacological relevance Rosmarinic acid (RA), a major hydrosoluble bioactive compound found in the Chinese medicinal herb, Salvia miltiorrhiza Bunge, which has been used in traditional Chinese medicine to treat various diseases, including cancer. However, the mechanisms have not been fully elucidated. Aim of the study Guided by microarray hybridization and Ingenuity Pathway Analysis, we identified modes of action of rosmarinic acid (RA) isolated from S. miltiorrhiza on acute lymphoblastic leukemia cells. Materials and methods Microarray data were verified by independent methods: Real-time RT-PCR (mRNA expression), resazurin assay (cytotoxicity of RA towards parental CCRF-CEM…

Programmed cell deathCell SurvivalDNA damageNecroptosisCellAntineoplastic AgentsApoptosisSalvia miltiorrhizaPharmacologyCell morphologyDepsidesSalvia miltiorrhizaCell Line TumorDrug DiscoveryCell AdhesionmedicineHumansLymphocytesCells CulturedMembrane Potential MitochondrialPharmacologybusiness.industryGene Expression ProfilingCell CycleNF-kappa BPrecursor Cell Lymphoblastic Leukemia-LymphomaCell cycleMolecular biologyDrug Resistance MultipleMolecular Docking Simulationmedicine.anatomical_structureCinnamatesDrug Resistance NeoplasmApoptosisComet AssayReactive Oxygen SpeciesbusinessDNA DamageJournal of Ethnopharmacology
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Parthenolide induces caspase-independent and AIF-mediated cell death in human osteosarcoma and melanoma cells

2013

The mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. This article shows that parthenolide stimulates in human osteosarcoma MG63 and melanoma SK-MEL-28 cells a mechanism of cell death, which is not prevented by z-VAD-fmk and other caspase inhibitors. In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. This event caused depletion of thiol groups and glutathione, NF-κB inhibition, c-Jun N-terminal kinase (JNK) activation, cell detachment from the matrix, and cellular shrinkage. The increa…

Programmed cell deathMAP Kinase Signaling SystemPhysiologyClinical BiochemistryAmino Acid Chloromethyl Ketoneschemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidePropidium iodideFragmentation (cell biology)MelanomaCaspaseOsteosarcomaCell DeathbiologyNF-kappa BApoptosis Inducing FactorNADPH OxidasesCell BiologyCaspase InhibitorsCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCell cultureCaspasesbiology.proteinApoptosis-inducing factorReactive Oxygen SpeciesSesquiterpenesParthenolide caspase-independent cell death ROS AIFJournal of Cellular Physiology
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Lovastatin attenuates ionizing radiation-induced normal tissue damage in vivo.

2009

Abstract Background and purpose HMG-CoA-reductase inhibitors (statins) are widely used lipid-lowering drugs. Moreover, they have pleiotropic effects on cellular stress responses, proliferation and apoptosis in vitro . Here, we investigated whether lovastatin attenuates acute and subchronic ionizing radiation-induced normal tissue toxicity in vivo . Materials and methods Four hours to 24h after total body irradiation (6Gy) of Balb/c mice, acute pro-inflammatory and pro-fibrotic responses were analyzed. To comprise subchronic radiation toxicity, mice were irradiated twice with 2.5Gy and analyses were performed 3weeks after the first radiation treatment. Molecular markers of inflammation and f…

Programmed cell deathPathologymedicine.medical_specialtyStatinmedicine.drug_classCell SurvivalPharmacologyRadiation DosageMiceRandom AllocationIn vivoFibrosisReference ValuesRadiation IonizingmedicineAnimalsHumansRadiology Nuclear Medicine and imagingLovastatinRNA MessengerRadiation InjuriesLungProbabilityMice Inbred BALB CChemistryTumor Necrosis Factor-alphaNF-kappa BDose-Response Relationship RadiationHematologymedicine.diseaseCTGFIntestinesDisease Models AnimalRadiation Injuries ExperimentalOncologyLiverApoptosisToxicitylipids (amino acids peptides and proteins)FemaleLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsInflammation Mediatorsmedicine.drugDNA DamageRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
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Dexamethasone treatment of naïve organ of Corti explants alters the expression pattern of apoptosis-related genes.

2009

Dexamethasone treatment of organ of Corti explants challenged with an ototoxic level of an inflammatory cytokine modulates NFkappaB signaling and the expression levels of both pro-and anti-apoptosis-related genes. It is not known if naïve organ of Corti explants will respond in a similar manner to treatment with a corticosteroid. This study examines the response of naïve organ of Corti explants to treatment with dexamethasone.Three-day-old rat organ of Corti explants were cultured for 1, 2, or 4 days. Four-day in vitro cultures were fixed, stained with FITC-phalloidin and hair cells were counted. ELISA was performed on 2-day cultures to determine the levels of phosphorylated nuclear factor …

Programmed cell deathPathologymedicine.medical_specialtyTime Factorsmedicine.medical_treatmentAnti-Inflammatory Agentsbcl-X ProteinGene ExpressionApoptosisCell CountEnzyme-Linked Immunosorbent AssayBiologyDexamethasoneStatistics NonparametricAndrologyRats Sprague-DawleyOrgan Culture TechniquesGene expressionmedicineAnimalsInner earPhosphorylationMolecular BiologyOrgan of CortiDexamethasonebcl-2-Associated X ProteinAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceNF-kappa BRatsCytokinemedicine.anatomical_structureAnimals NewbornProto-Oncogene Proteins c-bcl-2Organ of CortiApoptosisReceptors Tumor Necrosis Factor Type Isense organsNeurology (clinical)Hair cellDevelopmental Biologymedicine.drugBrain research
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Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress.

2012

7-Ketocholesterol (7-KC)-induced apoptosis of macrophages is considered a key event in the development of human atheromas. In the present study, the effect of indicaxanthin (Ind), a bioactive pigment from cactus pear fruit, on 7-KC-induced apoptosis of human monocyte/macrophage THP-1 cells was investigated. A pathophysiological condition was simulated by using amounts of 7-KC that can be reached in human atheromatous plaque. Ind was assayed within a micromolar concentration range, consistent with its plasma level after dietary supplementation with cactus pear fruit. Pro-apoptotic effects of 7-KC were assessed by cell cycle arrest, exposure of phosphatidylserine at the plasma membrane, varia…

Programmed cell deathPyridinesCellMedicine (miscellaneous)Apoptosismedicine.disease_causeMonocytesCell Linechemistry.chemical_compoundCytosolmedicineHumansSulfhydryl CompoundsKetocholesterolsNutrition and DieteticsChemistryPlant ExtractsMonocyteMacrophagesNF-kappa BNADPH OxidasesOpuntiaPhosphatidylserineAtherosclerosisPlaque AtheroscleroticCell biologyBetaxanthinsMitochondriaCytosolOxidative Stressmedicine.anatomical_structureApoptosisNADPH Oxidase 4FruitDietary SupplementsCalciumReactive Oxygen SpeciesIndicaxanthinOxidative stressPhytotherapyThe British journal of nutrition
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Combined inhibition of Bcl-2 and NFκB synergistically induces cell death in cutaneous T-cell lymphoma.

2019

Abstract Therapeutic options for cutaneous T-cell lymphoma (CTCL) are limited and curative treatment regimens are not available. Thus, new targeted and well-tolerated therapeutic approaches are urgently needed. In this respect, we have recently shown that dimethyl fumerate (DMF) inhibits NF-κB acting as a survival factor in CTCL. Similarly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been shown to induce cell death in CTCL especially when combined with histone deacetylase inhibitors. Therefore, we hypothesized that inhibition of Bcl-2 should potentiate NF-κB inhibition in a novel combination treatment of CTCL. We show that, in vitro, the Bcl-2 inhibitors ABT-199 an…

Programmed cell deathT cellImmunologyAntineoplastic AgentsApoptosisBiochemistryMicehemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansRNA Small InterferingCell ProliferationNeoplasm StagingCell DeathDose-Response Relationship Drugbusiness.industryCutaneous T-cell lymphomaNF-kappa BDrug SynergismCell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysLymphomaLymphoma T-Cell CutaneousHistone Deacetylase InhibitorsDisease Models Animalmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCancer researchRNA InterferenceHistone deacetylaseSignal transductionbusinessProtein BindingBlood
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NF-κB Inhibition Restores Sensitivity to Fas-Mediated Apoptosis in Lymphoma Cell Lines

2003

Failure to perform the Fas-related apoptosis pathway can account for tumor resistance both to chemotherapeutic agents and to immunological effectors. We studied the role of NK-kappaB in Fas-resistance, employing the Fas-sensitive human T-lymphoma HuT78 cell line and its Fas-resistant variants HuT78B1 and HuT78G9. All these cell lines expressed high levels of constitutively activated NF-kappaB. Pretreatment of cells with NF-kappaB inhibitors (PDTC, MG132, or SN50) strongly enhanced CH11-induced apoptosis in HuT78 and Hut78G9 cells, while only MG132 showed a similar potentiating effect in HuT78B1. The described synergism was significantly inhibited by pretreatment with the anti-Fas-blocking a…

ProlineLeupeptinsT cellAntineoplastic AgentsApoptosisBiologyLymphoma T-CellGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundHistory and Philosophy of ScienceThiocarbamatesCell Line TumorMG132medicineHumansfas Receptorapoptosis NF-KappaB MG132 Fas/FasL systemEffectorGeneral NeuroscienceNF-kappa BNF-κBmedicine.diseaseMolecular biologyLymphomamedicine.anatomical_structurechemistryApoptosisCell culturebiology.proteinAntibodyPeptidesAnnals of the New York Academy of Sciences
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The apoptotic effects and synergistic interaction of sodium butyrate and MG132 in human retinoblastoma Y79 cells

1999

This study deals with the apoptotic effect exerted on human retinoblastoma Y79 cells by both sodium butyrate and an inhibitor of 26S proteasome [z-Leu-Leu-Leu-CHO (MG132)] and their synergistic effect. Exposure to sodium butyrate (1-4 mM) induced an accumulation of cells in the G2-M phase that was already visible after 24 h of treatment, when morphological and biochemical signs of apoptosis appeared only in a small number of cells (5-10%). Thereafter, the apoptotic effects increased progressively with slow kinetics, reaching a maximum after 72 h of exposure, when they concerned a large fraction of cells (>75% with 4 mM sodium butyrate). Sodium butyrate stimulated the conversion of procaspas…

Proteasome Endopeptidase ComplexTime FactorsLeupeptinsApoptosisCytochrome c GroupCysteine Proteinase InhibitorsProto-Oncogene Proteins c-mycTumor Cells CulturedHumanssodium butyrateLamin Type BCaspase 3Cell CycleNF-kappa BRetinoblastomaNuclear ProteinsFlow CytometryLaminsMitochondriaButyratesKineticsCaspasesI-kappa B ProteinsPoly(ADP-ribose) PolymerasesTumor Suppressor Protein p53Peptide Hydrolases
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Activation of the p75 neurotrophin receptor through conformational rearrangement of disulphide-linked receptor dimers.

2009

Ligand-mediated dimerization has emerged as a universal mechanism of growth factor receptor activation. Recent structural studies have shown that neurotrophins interact with dimers of the p75 neurotrophin receptor (p75NTR), but the actual mechanism of receptor activation has remained elusive. Here we show that p75NTR forms disulphide-linked dimers independently of neurotrophin binding through the highly conserved Cys257 in its transmembrane domain. Mutation of Cys257 abolished neurotrophin-dependent receptor activity but did not affect downstream signaling by the p75NTR/NgR/Lingo-1 complex in response to MAG, indicating the existence of distinct, ligand-specific activation mechanisms for p7…

Protein ConformationMutantNeuronesReceptor Nerve Growth FactorMiceProtein structureChlorocebus aethiopsNerve Growth FactorLow-affinity nerve growth factor receptorRNA Small InterferingReceptorskin and connective tissue diseasesReceptors neuralsCells CulturedNeuronsCell DeathGeneral NeuroscienceNF-kappa BCell biologyTransmembrane domainSIGNALINGOligopeptidesNeurotrophinProtein BindingSignal Transductionmusculoskeletal diseasesPROTEINSNeuroscience(all)Green Fluorescent ProteinsNerve Tissue ProteinsReceptors Nerve Growth FactorSuperior Cervical GanglionBiologyTransfectionMOLNEUROArticleGrowth factor receptorAnimalsHumansProtein Interaction Domains and MotifsReceptors Growth FactorCysteineBinding SitesMembrane Proteinsbiological factorsRatsnervous systemAnimals NewbornNeurotrophin bindingMutationbiology.proteinsense organsProtein MultimerizationrhoA GTP-Binding ProteinProteïnesNeuron
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