Search results for "ERK pathway"

showing 10 items of 192 documents

Impact of Glutathione Peroxidase-1 Deficiency on Macrophage Foam Cell Formation and Proliferation: Implications for Atherogenesis

2013

Clinical and experimental evidence suggests a protective role for the antioxidant enzyme glutathione peroxidase-1 (GPx-1) in the atherogenic process. GPx-1 deficiency accelerates atherosclerosis and increases lesion cellularity in ApoE(-/-) mice. However, the distribution of GPx-1 within the atherosclerotic lesion as well as the mechanisms leading to increased macrophage numbers in lesions is still unknown. Accordingly, the aims of the present study were (1) to analyze which cells express GPx-1 within atherosclerotic lesions and (2) to determine whether a lack of GPx-1 affects macrophage foam cell formation and cellular proliferation. Both in situ-hybridization and immunohistochemistry of l…

CD36 AntigensMAPK/ERK pathwayMouseMitogen-Activated Protein Kinase 3lcsh:MedicineGene ExpressionSignal transductionCardiovascularMiceMolecular cell biologyGlutathione Peroxidase GPX1lcsh:ScienceIn Situ HybridizationFoam cellMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryReverse Transcriptase Polymerase Chain ReactionKinaseSignaling cascadesScavenger Receptors Class AAnimal ModelsImmunohistochemistryLipoproteins LDLMedicineFemaleSignal transductionResearch ArticleMacrophage colony-stimulating factorMAPK signaling cascadesBlotting WesternBiologyCell GrowthModel OrganismsApolipoproteins EVascular BiologyAnimalsHumansProtein kinase ABiologyCell ProliferationGlutathione PeroxidaseMacrophage Colony-Stimulating Factorlcsh:RAtherosclerosisMolecular biologyMacrophages Peritoneallcsh:QMacrophage proliferationFoam CellsPLoS ONE
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Lovastatin causes sensitization of HeLa cells to ionizing radiation‐induced apoptosis by the abrogation of G2 blockage

2003

To investigate the effect of inhibition of Ras/Rho-regulated signalling by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) on radiation-induced cell killing and apoptosis.Different human cell lines were pretreated or not with lovastatin before exposure to gamma-rays. Afterwards, radiation-induced cell killing, formation and repair of double-strand breaks, activation of radiation-inducible signal mechanisms (i.e. p53, p21, extracellular-signal-related kinase (ERK), NF-kappaB), changes in cell cycle progression and apoptosis were analysed.As shown by a colony formation assay, lovastatin sensitized HeLa cells to gamma-radiation-induced cell killing. The lovastati…

Cyclin-Dependent Kinase Inhibitor p21G2 PhaseMAPK/ERK pathwayApoptosisBiologyHeLaCyclinspolycyclic compoundsmedicineHumansRadiology Nuclear Medicine and imagingLovastatinSensitizationRadiological and Ultrasound TechnologyKinaseNF-kappa Bnutritional and metabolic diseasesCell cyclebiology.organism_classificationCell biologyCell killingmedicine.anatomical_structureGamma RaysApoptosislipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein KinasesTumor Suppressor Protein p53DNA DamageHeLa Cellsmedicine.drugInternational Journal of Radiation Biology
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Roflumilast N-oxide reverses corticosteroid resistance in neutrophils from patients with chronic obstructive pulmonary disease

2013

Background Glucocorticoid functions are markedly impaired in patients with chronic obstructive pulmonary disease (COPD). The phosphodiesterase 4 inhibitor roflumilast N-oxide (RNO) is the active metabolite of roflumilast approved as a treatment to reduce the risk of exacerbations in patients with severe COPD. Objective We sought to characterize the differential effects of RNO versus corticosteroids and their potential additive/synergistic effect in neutrophils from patients with COPD, thus providing scientific rationale for the combination of roflumilast with corticosteroids in the clinic. Methods Peripheral blood neutrophils were isolated from patients with COPD (n = 32), smokers (n = 7), …

CyclopropanesLipopolysaccharidesMaleMAPK/ERK pathwaymedicine.medical_specialtyNeutrophilsPrimary Cell CultureImmunologyDrug ResistanceAminopyridinesGene ExpressionComplex MixturesDexamethasoneHistone DeacetylasesPhosphatidylinositol 3-KinasesPulmonary Disease Chronic ObstructiveGlucocorticoid receptorAdrenal Cortex HormonesInternal medicineTobaccomedicineHumansImmunology and AllergyMacrophage Migration-Inhibitory FactorsDexamethasoneActive metaboliteRoflumilastAgedCOPDbusiness.industryInterleukin-8Drug SynergismMiddle Agedmedicine.diseaseIntramolecular OxidoreductasesEndocrinologyMatrix Metalloproteinase 9BenzamidesMitogen-Activated Protein Kinase PhosphatasesFemaleMacrophage migration inhibitory factorPhosphodiesterase 4 InhibitorsbusinessBiomarkersGlucocorticoidmedicine.drugJournal of Allergy and Clinical Immunology
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“Cysteinyl leukotriene-1 receptor activation in a human bronchial epithelial cell line leads to signal transducer and activator of transcription 1-me…

2008

Abstract We studied the effect of leukotriene D(4) (LTD(4)) on a human bronchial epithelial cell line (16HBE) overexpressing the cysteinyl leukotriene (CysLT) (1) receptor (HBECysLT(1)R), looking at the associated signal transduction mechanisms as well as at effects on inflammatory cell adhesion. The results obtained showed that LTD(4) increases the phosphorylation of extracellular signal-regulated protein kinase (ERK) 1/2 and of the signal transducer and activator of transcription 1 (STAT-1) in serine 727 (STAT-1Ser727), resulting in increased eosinophil adhesion to HBECysLT(1)R, associated with enhanced surface expression of intercellular adhesion molecule (ICAM) 1. Pretreatment with a Cy…

CyclopropanesMAPK/ERK pathwayIndolesBronchiAcetatesSulfidesBiologyCysteinyl leukotriene-1cysteinyl leukotrieneCell LineLeukotriene D4MaleimidesInterferon-gammaCell AdhesionHumansProtein kinase ACells CulturedProtein kinase CReceptors LeukotrienePharmacologyKinaseMEK inhibitorMembrane ProteinsEpithelial CellsIntercellular Adhesion Molecule-1Intercellular adhesion moleculeCell biologyEosinophilsSTAT1 Transcription FactorQuinolinesLeukotriene AntagonistsMolecular MedicinePhosphorylationMitogen-Activated Protein KinasesSignal transduction
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How DNA lesions are turned into powerful killing structures: Insights from UV-induced apoptosis

2008

Mammalian cells treated with ultraviolet (UV) light provide one of the best-known experimental systems for depicting the biological consequences of DNA damage. UV irradiation induces the formation of DNA photoproducts, mainly cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts [(6-4)PPs], that drastically impairs DNA metabolism, culminating in the induction of cell death by apoptosis. While CPDs are the most important apoptosis-inducing lesions in DNA repair proficient cells, recent data indicates that (6-4)PPs also signals for apoptosis in DNA repair deficient cells. The toxic effects of these unrepaired DNA lesions are commonly associated with transcription …

DNA ReplicationMAPK/ERK pathwayProgrammed cell deathBase SequenceTranscription GeneticUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisMolecular Sequence DataApoptosisPyrimidine dimerBiologyCell biologychemistry.chemical_compoundchemistryBiochemistryApoptosisAutophagyGeneticsUltraviolet lightAnimalsHumansDNADNA DamageMutation Research/Reviews in Mutation Research
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Polycystin-1 downregulation induces ERK-dependent mTOR pathway activation in a cellular model of psoriasis

2018

Psoriatic plaques tend to localize to the knees and elbows, areas that are particularly subject to mechanical stress resulting from bending and friction. Moreover, plaques often develop at sites of mechanical trauma or injury (Koebner phenomenon). Nevertheless, mechanotransduction has never been linked to psoriasis. Polycystins (polycystin-1, PC1; polycystin-2, PC2) are mechanosensitive molecules that function as key regulators of cellular mechanosensitivity and mechanotransduction. The aim of this in vitro study was to investigate the role of polycystins in the development of psoriasis. We showed that PC1 knockdown in HaCaT cells led to an elevated mRNA expression of psoriasis-related biom…

Genetic Markers0301 basic medicineMAPK/ERK pathwayendocrine systemTRPP Cation ChannelsMAP Kinase Signaling SystemDown-RegulationModels BiologicalCell Line03 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementPsoriasismedicineHumansPsoriasisMechanotransductionMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationGene knockdownCell growthChemistryTOR Serine-Threonine Kinasesmedicine.diseaseCell biologyHaCaT030104 developmental biologyGene Knockdown Techniques030220 oncology & carcinogenesisMolecular MedicineBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Non-small cell lung cancer (NSCLC), EGFR downstream pathway activation and TKI targeted therapies sensitivity: Effect of the plasma membrane-associat…

2017

Adenocarcinoma of Non-Small Cell Lung Cancer (NSCLC) is a severe disease. Patients carrying EGFR mutations may benefit from EGFR targeted therapies (e.g.: gefitinib). Recently, it has been shown that sialidase NEU3 directly interacts and regulates EGFR. In this work, we investigate the effect of sialidase NEU3 overexpression on EGFR pathways activation and EGFR targeted therapies sensitivity, in a series of lung cancer cell lines. NEU3 overexpression, forced after transfection, does not affect NSCLC cell viability. We demonstrate that NEU3 overexpression stimulates the ERK pathway but this activation is completely abolished by gefitinib treatment. The Akt pathway is also hyper-activated upo…

Genetics and Molecular Biology (all)0301 basic medicineOncologyMAPK/ERK pathwayLung NeoplasmsColorectal cancerCell Membraneslcsh:Medicinenon-small cell lung cancer (NSCLC)BiochemistryLung and Intrathoracic TumorsAntineoplastic Agent0302 clinical medicineProtein-Tyrosine KinaseCarcinoma Non-Small-Cell LungMedicine and Health SciencesPost-Translational ModificationPhosphorylationNon-Small-Cell Lunglcsh:ScienceTumorMultidisciplinaryBlottingGefitinibTransfectionProtein-Tyrosine KinasesBIO/10 - BIOCHIMICAErbB ReceptorsOncology030220 oncology & carcinogenesisAdenocarcinomaPhosphorylationHyperexpression TechniquesElectrophoresis Polyacrylamide GelCellular Structures and OrganellesWesternReceptorHumanmedicine.drugSignal TransductionResearch ArticleElectrophoresismedicine.medical_specialtyBlotting WesternNeuraminidaseAntineoplastic AgentsReal-Time Polymerase Chain ReactionTransfectionResearch and Analysis MethodsCell Line03 medical and health sciencesGefitinibInternal medicineCell Line TumormedicineGeneticsGene Expression and Vector TechniquesHumansPoint MutationMolecular Biology TechniquesMolecular BiologyPI3K/AKT/mTOR pathwayColorectal CancerMolecular Biology Assays and Analysis TechniquesPolyacrylamide GelBiochemistry Genetics and Molecular Biology (all)Epidermal Growth Factorbusiness.industryCarcinomalcsh:RCell MembraneQuinazolineCancers and NeoplasmsBiology and Life SciencesProteinsCell Biologymedicine.diseaserespiratory tract diseasesNon-Small Cell Lung CancerLung Neoplasm030104 developmental biologyAgricultural and Biological Sciences (all)MutationQuinazolineslcsh:QReceptor Epidermal Growth FactorAntineoplastic Agents; Blotting Western; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Cell Membrane; Electrophoresis Polyacrylamide Gel; Humans; Lung Neoplasms; Neuraminidase; Protein-Tyrosine Kinases; Quinazolines; Real-Time Polymerase Chain Reaction; Receptor Epidermal Growth Factor; Signal Transduction; Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)businessPloS one
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The Ras/Raf-1/MEK1/ERK Signaling Pathway Coupled to Integrin Expression Mediates Cholinergic Regulation of Keratinocyte Directional Migration

2005

The physiologic mechanisms that determine directionality of lateral migration are a subject of intense research. Galvanotropism in a direct current (DC) electric field represents a natural model of cell re-orientation toward the direction of future migration. Keratinocyte migration is regulated through both the nicotinic and muscarinic classes of acetylcholine (ACh) receptors. We sought to identify the signaling pathway mediating the cholinergic regulation of chemotaxis and galvanotropism. The pharmacologic and molecular modifiers of the Ras/Raf-1/MEK1/ERK signaling pathway altered both chemotaxis toward choline and galvanotropism toward the cathode in a similar way, indicating that the sam…

KeratinocytesMAPK/ERK pathwayIntegrinsalpha7 Nicotinic Acetylcholine ReceptorMAP Kinase Signaling SystemIntegrinMAP Kinase Kinase 1Receptors NicotinicBiologyTransfectionBiochemistryMuscarinic acetylcholine receptormedicineHumansRNA Small InterferingKeratinocyte migrationExtracellular Signal-Regulated MAP KinasesMolecular BiologyCells CulturedChemotaxisReceptor Muscarinic M1ChemotaxisCell BiologyAcetylcholineUp-RegulationCell biologyElectrophysiologyras Proteinsbiology.proteinraf KinasesLamellipodiumSignal transductionAcetylcholineSignal Transductionmedicine.drugJournal of Biological Chemistry
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MEK1 Required for Invasive Growth of mIMCD3 renal Cells in a 3D Collagen Matrix

2004

Branching morphogenesis is an essential process during kidney development: This process controls epithelialization of the metanephric mesenchyme during the induction of branching structures and in this way determines the number of nephrons. Various grow factors, such HGF, have been implicated in branching morphogenesis in renal cells, including mIMCD3 ( murine inner medullary collecting duct) and MDCK cells. Growth factors which induce branching morphogenesis in renal cells also activate the MEK1/ERK pathway. The authors analyzed the potential role that this pathway might play in branching morphogenesis. The authors show that PD98059, a specific inhibitor of MEK1,inhibits branching of mIMCD…

Kidney development branching morphogenesis in renal cells MEK1/ERK pathway
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Severe metabolic alterations in liver cancer lead to ERK pathway activation and drug resistance

2020

Background: The extracellular signal-regulated kinase (ERK) pathway regulates cell growth, and is hyper-activated and associated with drug resistance in hepatocellular carcinoma (HCC). Metabolic pathways are profoundly dysregulated in HCC. Whether an altered metabolic state is linked to activated ERK pathway and drug response in HCC is unaddressed. Methods: We deprived HCC cells of glutamine to induce metabolic alterations and performed various assays, including metabolomics (with 13C-glucose isotope tracing), microarray analysis, and cell proliferation assays. Glutamine-deprived cells were also treated with kinase inhibitors (e.g. Sorafenib, Erlotinib, U0126 amongst other MEK inhibitors). …

Life sciences; biology0301 basic medicineSorafenibMAPK/ERK pathwayCarcinoma HepatocellularResearch paperMAP Kinase Signaling SystemGlutamineProliferationlcsh:MedicineAntineoplastic AgentsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineDownregulation and upregulationddc:570medicineSerineHumansHCCProtein Kinase InhibitorsCell Proliferationlcsh:R5-920Cell growthChemistryKinaseMicroarray analysis techniquesLiver Neoplasmslcsh:RGeneral MedicineHep G2 Cellsdigestive system diseasesMetabolic pathway030104 developmental biologyAnaerobic glycolysisDrug Resistance NeoplasmKinase inhibitors030220 oncology & carcinogenesisCancer researchMetabolomeMetabolic stateAerobic glycolysisTranscriptomelcsh:Medicine (General)medicine.drugEBioMedicine
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