Search results for "script"

showing 10 items of 5143 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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Cell death and hepatocarcinogenesis: Dysregulation of apoptosis signaling pathways

2011

Hepatocellular carcinoma (HCC) remains a disease with a poor prognosis despite recent advances in the pathophysiology and treatment. Although the disease is biologically heterogeneous, dysregulation of cellular proliferation and apoptosis both occur frequently and contribute to the malignant phenotype. Chronic liver disease is associated with intrahepatic inflammation which promotes dysregulation of cellular signaling pathways; this triggers proliferation and thus lays the ground for expansion of premalignant cells. Cancer emerges when immunological control fails and transformed cells develop resistance against cell death signaling pathways. The same mechanisms underlie the poor responsiven…

Programmed cell deathCell signalingHepatologybiologybusiness.industryGastroenterologyFas receptorCell biologyApoptosisbiology.proteinMedicineTumor necrosis factor alphaFADDSignal transductionbusinessTranscription factorJournal of Gastroenterology and Hepatology
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Trans-10, cis-12 conjugated linoleic acid induced cell death in human colon cancer cells through reactive oxygen species-mediated ER stress

2013

Dietary conjugated linoleic acids (CLA) are fatty acid isomers with anticancer activities produced naturally in ruminants or from vegetable oil processing. The anticancer effects of CLA differ upon the cancer origin and the CLA isomers. In this study, we carried out to precise the effects of CLA isomers, c9,t11 and t10,c12 CLA, on mechanisms of cell death induction in colon cancer cells. We first showed that only t10,c12 CLA treatment (25 and 50μM) for 72h triggered apoptosis in colon cancer cells without affecting viability of normal-derived colon epithelial cells. Exposure of colon cancer cells to t10,c12 CLA activated ER stress characterized by induction of eIF2α phoshorylation, splicing…

Programmed cell deathConjugated linoleic acidCHOPBiologychemistry.chemical_compoundCell Line TumormedicineHumansCytotoxic T cellLinoleic Acids ConjugatedMolecular BiologyCell ProliferationCell Deathintegumentary systemReverse Transcriptase Polymerase Chain Reactionfood and beveragesCancerCell BiologyEndoplasmic Reticulum Stressmedicine.diseaseImmunohistochemistrychemistryBiochemistryCell cultureApoptosisCancer cellCancer researchlipids (amino acids peptides and proteins)Reactive Oxygen SpeciesBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
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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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Cytotoxicity of apigenin toward multiple myeloma cell lines and suppression of iNOS and COX-2 expression in STAT1-transfected HEK293 cells.

2020

Apigenin is one of the most abundant dietary flavonoids that possesses multiple bio-functions.This study was designed to determine the influence of apigenin on gene expressions, cancer cells, as well as STAT1/COX-2/iNOS pathway mediated inflammation and tumorigenesis in HEK293-STAT1 cells. Furthermore, the cytotoxic activity toward multiple myeloma (MM) cell lines was investigated.Bioinformatic analyses were used to predict the sensitivity and resistance of tumor cells toward apigenin and to determine cellular pathways influenced by this compound. The cytotoxic and ferroptotic activity of apigenin was examined by the resazurin reduction assay. Additionally, we evaluated apoptosis, and cell …

Programmed cell deathPharmaceutical ScienceNitric Oxide Synthase Type IIApoptosis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDrug DiscoveryAntineoplastic Combined Chemotherapy ProtocolsAutophagyCytotoxic T cellHumansDAPIApigenin030304 developmental biologyCell ProliferationPharmacology0303 health sciencesDose-Response Relationship DrugChemistryCell CycleComputational BiologyCell cycleAntineoplastic Agents PhytogenicHEK293 CellsSTAT1 Transcription FactorComplementary and alternative medicineApoptosisCell cultureCyclooxygenase 2Doxorubicin030220 oncology & carcinogenesisApigeninCancer cellCancer researchMolecular MedicineMultiple MyelomaReactive Oxygen SpeciesPhytomedicine : international journal of phytotherapy and phytopharmacology
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FKBP51 Affects TNF-Related Apoptosis Inducing Ligand Response in Melanoma

2021

Melanoma is one of the most immunogenic tumors and has the highest potential to elicit specific adaptive antitumor immune responses. Immune cells induce apoptosis of cancer cells either by soluble factors or by triggering cell-death pathways. Melanoma cells exploit multiple mechanisms to escape immune system tumoricidal control. FKBP51 is a relevant pro-oncogenic factor of melanoma cells supporting NF-κB-mediated resistance and cancer stemness/invasion epigenetic programs. Herein, we show that FKBP51-silencing increases TNF-related apoptosis-inducing ligand (TRAIL)-R2 (DR5) expression and sensitizes melanoma cells to TRAIL-induced apoptosis. Consistent with the general increase in histone d…

Programmed cell deathQH301-705.5ChemistryYY1MelanomaRepressorTRAILCell Biologymedicine.diseaseYY1TRAIL melanoma cell death FKBP51 YY1Cell and Developmental Biologycell deathFKBP51Immune systemApoptosisCancer cellmelanomaCancer researchmedicineBiology (General)Transcription factorOriginal ResearchDevelopmental BiologyFrontiers in Cell and Developmental Biology
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MYC and EGR1 synergize to trigger tumor cell death by controlling NOXA and BIM transcription upon treatment with the proteasome inhibitor bortezomib

2014

The c-MYC (MYC afterward) oncogene is well known for driving numerous oncogenic programs. However, MYC can also induce apoptosis and this function of MYC warrants further clarification. We report here that a clinically relevant proteasome inhibitor significantly increases MYC protein levels and that endogenous MYC is necessary for the induction of apoptosis. This kind of MYC-induced cell death is mediated by enhanced expression of the pro-apoptotic BCL2 family members NOXA and BIM. Quantitative promoter-scanning chromatin immunoprecipitations (qChIP) further revealed binding of MYC to the promoters of NOXA and BIM upon proteasome inhibition, correlating with increased transcription. Both pr…

Programmed cell deathTranscription GeneticEGR1ApoptosisBiologyBortezomibProto-Oncogene Proteins c-mycMicehemic and lymphatic diseasesCell Line TumorProto-Oncogene ProteinsGeneticsmedicineAnimalsPromoter Regions GeneticTranscription factorCells CulturedEarly Growth Response Protein 1Zinc finger transcription factorBinding SitesOncogeneBcl-2-Like Protein 11Genes p16Gene regulation Chromatin and EpigeneticsMembrane ProteinsPromoterGenes p53Boronic AcidsChromatinddc:Gene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2PyrazinesCancer researchProteasome inhibitorApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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Peroxisome proliferator-activated receptor δ (PPARδ) activation protects H9c2 cardiomyoblasts from oxidative stress-induced apoptosis

2005

Activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma plays beneficial roles in cardiovascular disorders such as atherosclerosis and heart reperfusion. Although PPARalpha and gamma have been documented to reduce oxidative stress in the vasculature and the heart, the role of PPARdelta remains poorly studied.We focused on PPARdelta function in the regulation of oxidative stress-induced apoptosis in the rat cardiomyoblast cell line H9c2. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we showed that PPARdelta is the predominantly expressed isotype whereas PPARalpha was weakly detected. By performing cell viability assays, we …

Programmed cell deathmedicine.medical_specialtyPhysiologyBlotting WesternPeroxisome proliferator-activated receptorApoptosisCaspase 3DNA FragmentationBiologyTransfectionmedicine.disease_causeCell LineGW501516Physiology (medical)Internal medicineIn Situ Nick-End LabelingmedicineAnimalsPPAR deltaViability assayReceptorchemistry.chemical_classificationCaspase 3Reverse Transcriptase Polymerase Chain ReactionHydrogen PeroxideCatalasemedicine.diseaseRatsUp-RegulationCell biologyOxidative StressThiazolesEndocrinologychemistryApoptosisCaspasesCardiology and Cardiovascular MedicineMyoblasts CardiacOxidative stressCardiovascular Research
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Catalyzing transcriptomics research in cardiovascular disease: The CardioRNA COST action CA17129

2019

WOS: 000474931400001

Project Report0301 basic medicinemedicine.medical_specialtyBiochemistry & Molecular BiologyKnowledge managementlcsh:QH426-470BIOMARKERSbest practices and guidelines; cardiovascular disease; personalized medicine; transcriptomics; translational researchContext (language use)Translational researchDisease030204 cardiovascular system & hematologyBiologyBiochemistryLONG NONCODING RNAS03 medical and health sciencestranscriptomics0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemCIRCULATING MICRORNASTARGETScardiovascular diseaseGeneticsmedicineCost actionSet (psychology)Molecular BiologyComputingMilieux_MISCELLANEOUSGenetics & HeredityScience & Technologybusiness.industryCardiovascular system -- DiseasesPublic healthMedicine -- Research -- International cooperationpersonalized medicine3. Good healthlcsh:Genetics030104 developmental biologyAction (philosophy)PERSPECTIVEStranslational researchPersonalized medicineTranslational research biomedicalbest practices and guidelinesbusinessTranscriptomeLife Sciences & Biomedicine
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Extracorporeal shock wave-mediated changes in proliferation, differentiation, and gene expression of human osteoblasts.

2008

The goal of this study was to determine whether cell proliferation, differentiation, and gene expression of primary human osteoblasts (hOB) are influenced by shock wave application (SWA).Osteoblast cultures were isolated from cancellous bone fragments and treated with 500 impulses of energy flux densities of 0.06 mJ/mm, 0.18 mJ/mm, 0.36 mJ/mm, and 0.50 mJ/mm. Twenty-four hours and 96 hours after SWA cell proliferation, alkaline phosphatase activity, and mineralization were analyzed. The global gene expression profiling was determined 96 hours after SWA employing Affymetrix HG-U133A microarrays.After 24 hours, hOB showed a dose-dependent increase in cell proliferation from 68.7% (at 0.06 mJ/…

Proliferation differentiationGene ExpressionIn Vitro TechniquesCritical Care and Intensive Care MedicineHigh-Energy Shock WavesBone DensityGene expressionmedicineHumansHigh-Density MicroarrayOligonucleotide Array Sequence AnalysisOsteoblastsCell growthbusiness.industryReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingOsteoblastCell DifferentiationAnatomyExtracorporeal shock waveAlkaline PhosphataseCell biologyGene expression profilingmedicine.anatomical_structureSurgerybusinessCancellous boneCell DivisionThe Journal of trauma
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