Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Absence of correlation between oxysterol accumulation in lipid raft microdomains, calcium increase, and apoptosis induction on 158N murine oligodendr…

2013

There is some evidence that oxidized derivatives of cholesterol, 7-ketocholesterol (7KC) and 7β-hydroxycholesterol (7βOHC), are increased in the plasma of patients with neurodegenerative diseases associated with demyelinization of the central nervous system (CNS). It was therefore of interest to investigate the effects of these oxysterols on oligodendrocytes, the myelin-forming cells in the CNS. To this end, 158N murine oligodendrocytes were treated with 7KC or 7βOHC inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving Mcl-1, and caspase-3 activation. In contrast, under t…

Programmed cell deathOxysterolCell Survivalalpha-TocopherolApoptosisBiologyBiochemistryCell Linechemistry.chemical_compoundGlycogen Synthase Kinase 3MiceMembrane MicrodomainsAnimalsFragmentation (cell biology)Protein kinase BLipid raftKetocholesterolsCell ProliferationPharmacologyDepolarizationHydroxycholesterolsCell biologyOligodendrogliaSterolschemistryProto-Oncogene Proteins c-bcl-2ApoptosisIonomycinMyeloid Cell Leukemia Sequence 1 Proteinlipids (amino acids peptides and proteins)CalciumProto-Oncogene Proteins c-aktBiochemical pharmacology
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Phospholipidosis and down-regulation of the PI3-K/PDK-1/Akt signalling pathway are vitamin E inhibitable events associated with 7-ketocholesterol-ind…

2007

International audience; Among the oxysterols accumulating in atherosclerotic plaque, 7-ketocholesterol (7KC) is a potent apoptotic inducer, which favours myelin figure formation and polar lipid accumulation. This investigation performed on U937 cells consisted in characterizing the myelin figure formation process; determining the effects of 7KC on the PI3-K/PDK-1/Akt signalling pathway; evaluating the activities of vitamin E (Vit-E) (α-tocopherol) on the formation of myelin figures and the PI3-K/PDK-1/Akt signalling pathway and assessing the effects of PI3-K inhibitors (LY-294002, 3-methyladenine) on the activity of Vit-E on cell death and polar lipid accumulation. The ultrastructural and b…

Programmed cell deathOxysterolEndocrinology Diabetes and MetabolismClinical BiochemistryDown-RegulationApoptosisPyrimidinones[SDV.BC]Life Sciences [q-bio]/Cellular BiologyProtein Serine-Threonine KinasesBiochemistryDephosphorylationPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineMicroscopy Electron TransmissionOxazinesHumansVitamin EKetocholesterolsMolecular BiologyProtein kinase BPhospholipids030304 developmental biologyPhospholipidosis0303 health sciencesNutrition and DieteticsPhosphoinositide 3-kinasebiologyChemistryPyruvate Dehydrogenase Acetyl-Transferring KinaseU937 CellsProtein phosphatase 2Cell biology030220 oncology & carcinogenesisbiology.proteinBenzimidazolesSignal transductionProto-Oncogene Proteins c-aktSignal TransductionThe Journal of Nutritional Biochemistry
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Calcium in plant defence‐signalling pathways

2006

In plant cells, the calcium ion is a ubiquitous intracellular second messenger involved in numerous signalling pathways. Variations in the cytosolic concentration of Ca2+ ([Ca2+]cyt) couple a large array of signals and responses. Here we concentrate on calcium signalling in plant defence responses, particularly on the generation of the calcium signal and downstream calcium-dependent events participating in the establishment of defence responses with special reference to calcium-binding proteins.

Programmed cell deathPhysiologyGene Expressionchemistry.chemical_elementPlant ScienceBiologyCalciumNitric OxideCytosolPhytoalexinsCalcium-binding proteinCalcium SignalingPhosphorylationPlant DiseasesPlant ProteinsCalcium signalingCell DeathPlant ExtractsTerpenesCalcium-Binding ProteinsPlantsPlant cellElicitorCytosolchemistryBiochemistryCalciumMitogen-Activated Protein KinasesSignal transductionReactive Oxygen SpeciesSesquiterpenesNew Phytologist
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Kel1 is a phosphorylation-regulated noise suppressor of the pheromone signaling pathway.

2021

Abstract Mechanisms have evolved that allow cells to detect signals and generate an appropriate response. The accuracy of these responses relies on the ability of cells to discriminate between signal and noise. How cells filter noise in signaling pathways is not well understood. We have analyzed noise suppression in the yeast pheromone signaling pathway. By combining synthetic genetic array screening, mass spectrometry and single-cell time-resolved microscopy, we discovered that the poorly characterized protein Kel1 serves as a major noise suppressor of the pathway. At the molecular level, Kel1 suppresses spontaneous activation of the pheromone response by inhibiting membrane recruitment of…

Programmed cell deathSaccharomyces cerevisiae ProteinsChemistryCellbiologiCell BiologySaccharomyces cerevisiaeSynthetic genetic arrayGeneral Biochemistry Genetics and Molecular BiologyPheromonesCell biologylaw.inventionlawFus3SuppressorPhosphorylationPheromoneSignal transductionMitogen-Activated Protein KinasesPhosphorylationNoiseSte5Adaptor Proteins Signal TransducingCyclin-Dependent Kinase Inhibitor ProteinsSignal TransductionCell reports
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Clusterin gene expression in apoptotic MDCK cells is dependent on the apoptosis-inducing stimulus

1995

Abstract Clusterin (Apolipoprotein J, complement lysis inhibitor) is a widely expressed multifunctional glycoprotein. The expression of clusterin mRNA has been reported to be elevated in a broad spectrum of apoptotic or degenerative tissues. More recently, it was shown that within these tissues clusterin is expressed in the surviving rather than in the dying cells, and that clusterin gene expression is actually down-regulated in the apoptotic cells. We have studied the expression of the clusterin gene in apoptotic MDCK cells. Cell death was initiated by three different stimuli: application of the steroid hormone antagonist RU 486, activation of protein kinase C by the application of the pho…

Programmed cell deathSteroid hormoneApolipoprotein Bmedicine.medical_treatmentCellApoptosisCell LineHormone AntagonistsProtein kinase CmedicineAnimalsRNA MessengerMolecular BiologyProtein kinase CGlycoproteinsRU 486Messenger RNAbiologyClusterinCell BiologyMolecular biologyeye diseasesMifepristoneSteroid hormoneCholesterolmedicine.anatomical_structureClusterinGene Expression RegulationApoptosisCarcinogensbiology.proteinTetradecanoylphorbol Acetatesense organsMolecular ChaperonesBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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α-Tocopherol impairs 7-ketocholesterol-induced caspase-3-dependent apoptosis involving GSK-3 activation and Mcl-1 degradation on 158N murine oligoden…

2011

Abstract In important and severe neurodegenerative pathologies, 7-ketocholesterol, mainly resulting from cholesterol autoxidation, may contribute to dys- or demyelination processes. On various cell types, 7-ketocholesterol has often been shown to induce a complex mode of cell death by apoptosis associated with phospholipidosis. On 158N murine oligodendrocytes treated with 7-ketocholesterol (20 μg/mL corresponding to 50 μM, 24–48 h), the induction of a mode of cell death by apoptosis characterised by the occurrence of cells with condensed and/or fragmented nuclei, caspase activation (including caspase-3) and internucleosomal DNA fragmentation was observed. It was associated with a loss of tr…

Programmed cell deathTime FactorsCell Survivalalpha-TocopherolApoptosisCaspase 3BiochemistryDephosphorylationGlycogen Synthase Kinase 3MiceMembrane MicrodomainsGSK-3AnimalsKetocholesterolsMolecular BiologyProtein kinase BCell ProliferationMembrane Potential MitochondrialPhospholipidosisGlycogen Synthase Kinase 3 betaCaspase 3ChemistryOrganic ChemistryCytochromes cCell BiologyCell biologyEnzyme ActivationOligodendrogliaProtein TransportProto-Oncogene Proteins c-bcl-2ApoptosisMyeloid Cell Leukemia Sequence 1 ProteinDNA fragmentationChemistry and Physics of Lipids
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Calcitonin gene-related peptide partly protects cultured smooth muscle cells from apoptosis induced by an oxidative stress via activation of ERK1/2 M…

2003

Abstract Oxidative stress induced by a glucose/glucose oxidase (G/GO) generator system dose-dependently decreased the viability of cultured vascular smooth muscle cells (VSMC) as estimated by MTT assay. Cell death was induced in 40% of cells exposed to 0.2 IU/ml of the free radical generating mixture. Annexin-V labeling, Hoechst staining together with DNA laddering demonstrated that apoptosis was responsible for this cell loss. Pretreatment of the cells with 10−8 M calcitonin gene-related peptide (CGRP) significantly attenuated the damaging effect of the oxidative stress. Indeed, cell viability was estimated to be 80% in CGRP-treated group, instead of 60% in absence of CGRP treatment. This …

Programmed cell deathVascular smooth musclep38 mitogen-activated protein kinasesCalcitonin Gene-Related PeptideMyocytes Smooth MuscleApoptosisBiologyDNA ladderingCalcitonin gene-related peptidemedicine.disease_causeProtective AgentsMuscle Smooth VascularmedicineAnimalsHumansCGRPViability assayRats WistarMolecular BiologyCells CulturedMitogen-Activated Protein Kinase 3integumentary systemSAPKCell BiologyHydrogen PeroxideMAPKMolecular biologyRatsUp-RegulationNeuropeptideOxidative StressMitogen-activated protein kinaseVascular smooth muscle cellbiology.proteinMitogen-Activated Protein KinasesOxidative stressReceptors Calcitonin Gene-Related PeptideSignal TransductionBiochimica et biophysica acta
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Docosahexaenoic acid protects human RPE cells against oxidative stress via PI3K/Akt m-TOR/p70-p85S6K pathways

2012

Purpose Oxidative Stress (OS) plays a critical role in the pathogenesis of age-related macular degeneration (AMD), especially by targeting the retinal pigment epithelium (RPE). Dietary habits with high consumption of docosahexaenoic acid (DHA) have been shown to prevent the development and evolution of AMD. Nevertheless, it is still unclear how DHA affects AMD. Our study aimed to investigate the involvement of the PI3K/Akt and m-TOR/p70-p85S6K pathways in human RPE cells after induction of OS, and then to assess the effect of DHA in the signaling pathways and in the protection against RPE cell death. Methods For this purpose, we used ARPE-19 cells exposed to the prooxidant agent, tert-butyl…

Programmed cell deathmacular degenerationP70-S6 Kinase 1Biologymedicine.disease_cause03 medical and health sciences0302 clinical medicine[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineoxidative stress[SDV.MHEP.OS]Life Sciences [q-bio]/Human health and pathology/Sensory OrgansProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesacide docosahexaénoiquestress oxydatifGeneral Medicinedégénérescence maculaireeye diseasesCell biologyOphthalmologyDocosahexaenoic acidBiochemistryDocosahexaenoic acidApoptosis030220 oncology & carcinogenesis[ SDV.MHEP.OS ] Life Sciences [q-bio]/Human health and pathology/Sensory OrgansPhosphorylationsense organsOxidative stress[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Fatty acids liberated from low-density lipoprotein trigger endothelial apoptosis via mitogen-activated protein kinases.

2005

Enzymatic modification of low-density lipoprotein (LDL) as it probably occurs in the arterial intima drastically increases its cytotoxicity, which could be relevant for the progression of atherosclerotic lesions. LDL was treated with a protease and cholesterylesterase to generate a derivative similar to lesional LDL, with a high content of free cholesterol and fatty acids. Exposure of endothelial cells to the enzymatically modified lipoprotein (E-LDL), but not to native or oxidized LDL, resulted in programmed cell death. Apoptosis was triggered by apoptosis signal-regulating kinase 1 dependent phosphorylation of p38. Depletion and reconstitution experiments identified free fatty acids (FFA)…

Programmed cell deathp38 mitogen-activated protein kinasesBlotting WesternApoptosisDNA FragmentationBiologyFatty Acids NonesterifiedMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundHumansPhosphorylationMolecular BiologyCells CulturedCaspase 7Cell growthKinaseCaspase 3Cell BiologyCell biologyLipoproteins LDLchemistryBiochemistryApoptosisLow-density lipoproteinCaspasesPhosphorylationlipids (amino acids peptides and proteins)Endothelium VascularLipoproteinOleic AcidCell death and differentiation
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TRAIL-R4 promotes tumor growth and resistance to apoptosis in cervical carcinoma HeLa cells through AKT.

2011

International audience; BACKGROUND: TRAIL/Apo2L is a pro-apoptotic ligand of the TNF family that engages the apoptotic machinery through two pro-apoptotic receptors, TRAIL-R1 and TRAIL-R2. This cell death program is tightly controlled by two antagonistic receptors, TRAIL-R3 and TRAIL-R4, both devoid of a functional death domain, an intracellular region of the receptor, required for the recruitment and the activation of initiator caspases. Upon TRAIL-binding, TRAIL-R4 forms a heteromeric complex with the agonistic receptor TRAIL-R2 leading to reduced caspase-8 activation and apoptosis. METHODOLOGY/PRINCIPAL FINDINGS: We provide evidence that TRAIL-R4 can also exhibit, in a ligand independent…

Proliferation indexlcsh:MedicineTNF-Related Apoptosis-Inducing LigandHeLaMicePhosphatidylinositol 3-Kinases0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchMembrane Receptor SignalingEnzyme Inhibitorslcsh:SciencePhosphoinositide-3 Kinase Inhibitors0303 health sciencesMultidisciplinaryCell Deathbiologyapoptosis3. Good healthCell biologyOncology030220 oncology & carcinogenesisMedicineFemaleSignal transductionResearch ArticleSignal TransductionProgrammed cell deathMorpholinesproliferationBlotting WesternMice Nude03 medical and health sciencesTRAIL-R4[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyBiology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologyCell growthAktCell Membranelcsh:RPTEN PhosphohydrolaseNeoplasms Experimentalbiology.organism_classificationTumor Necrosis Factor Decoy ReceptorsChromonesApoptosislcsh:QProto-Oncogene Proteins c-aktHeLa Cells
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