Search results for "phosphor"

showing 10 items of 1952 documents

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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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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Side effects of oxysterols: cytotoxicity, oxidation, inflammation, and phospholipidosis.

2008

Oxysterols are 27-carbon atom molecules resulting from autoxidation or enzymatic oxidation of cholesterol. They are present in numerous foodstuffs and have been demonstrated to be present at increased levels in the plasma of patients with cardiovascular diseases and in atherosclerotic lesions. Thus, their role in lipid disorders is widely suspected, and they might also be involved in important degenerative diseases such as Alzheimer's disease, osteoporosis, and age-related macular degeneration. Since atherosclerosis is associated with the presence of apoptotic cells and with oxidative and inflammatory processes, the ability of some oxysterols, especially 7-ketocholesterol and 7β-hydrox…

Programmed cell deathPhysiologyImmunologyBiophysicsInflammationApoptosisOxidative phosphorylationPharmacologyLipidosesBiochemistryPhospholipidosischemistry.chemical_compoundmedicinepolycyclic compoundsAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsCytotoxicitylcsh:QH301-705.5PhospholipidsPhospholipidosisInflammationlcsh:R5-920ChemistryCholesterolGeneral NeuroscienceCell BiologyGeneral MedicineOxysterolsAtherosclerosisHydroxycholesterolsBiochemistrylcsh:Biology (General)Apoptosislipids (amino acids peptides and proteins)medicine.symptomSignal transductionlcsh:Medicine (General)Oxidation-ReductionBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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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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In Vitro and in Vivo Evaluation of Water-Soluble Iminophosphorane Ruthenium(II) Compounds. A Potential Chemotherapeutic Agent for Triple Negative Bre…

2014

A series of organometallic ruthenium(II) complexes containing iminophosphorane ligands have been synthesized and characterized. Cationic compounds with chloride as counterion are soluble in water (70–100 mg/mL). Most compounds (especially highly water-soluble 2) are more cytotoxic to a number of human cancer cell lines than cisplatin. Initial mechanistic studies indicate that the cell death type for these compounds is mainly through canonical or caspase-dependent apoptosis, nondependent on p53, and that the compounds do not interact with DNA or inhibit protease cathepsin B. In vivo experiments of 2 on MDA-MB-231 xenografts in NOD.CB17-Prkdc SCID/J mice showed an impressive tumor reduction (…

Programmed cell deathStereochemistryPhosphoranesAntineoplastic AgentsTriple Negative Breast NeoplasmsMice SCIDPharmacologyIn Vitro TechniquesArticleRutheniumIn vivoCoordination ComplexesMice Inbred NODDrug DiscoverymedicineOrganometallic CompoundsCytotoxic T cellAnimalsHumansCathepsinCisplatinChemistryWaterIn vitro3. Good healthHEK293 CellsSolubilityCell cultureApoptosisMolecular MedicineFemalemedicine.drugJournal of Medicinal Chemistry
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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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7-Ketocholesterol Incorporation into Sphingolipid/Cholesterol-enriched (Lipid Raft) Domains Is Impaired by Vitamin E

2009

Cholesterol oxides, in particular 7-ketocholesterol, are proatherogenic compounds that induce cell death in the vascular wall when localized in lipid raft domains of the cell membrane. Deleterious effects of 7-ketocholesterol can be prevented by vitamin E, but the molecular mechanism involved is unclear. In this study, unlike γ-tocopherol, the α-tocopherol vitamin E form was found to prevent 7-ketocholesterol-mediated apoptosis of A7R5 smooth muscle cells. To be operative, α-tocopherol needed to be added to the cells before 7-ketocholesterol, and its anti-apoptotic effect was reduced and even suppressed when added together or after 7-ketocholesterol, respectively. Both pre- and co-treatment…

Programmed cell deathVitamin Emedicine.medical_treatmentfood and beveragesCell BiologyBiologyBiochemistrySphingolipidCell biologyCell membraneDephosphorylationchemistry.chemical_compoundmedicine.anatomical_structureBiochemistrychemistryApoptosismedicinelipids (amino acids peptides and proteins)alpha-TocopherolMolecular BiologyLipid raftJournal of Biological Chemistry
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Death of mitochondria during programmed cell death of leaf mesophyll cells

2005

The role of plant mitochondria in the programmed cell death (PCD) is widely discussed. However, spectrum and sequence of mitochondrial structural changes during different types of PCD in leaves are poorly described. Pea, cucumber and rye plants were grown under controlled growing conditions. A part of them were sprinkled with ethylene releaser to accelerate cell death. During yellowing the palisade parenchyma mitochondria were attracted to nuclear envelope. Mitochondrial matrix became electron translucent. Mitochondria entered vacuole by invagination of tonoplast and formed multivesicular bodies. Ethephon treatment increased the frequency of sticking of mitochondria to the nuclear envelope …

Programmed cell deathfood and beveragesApoptosisCell BiologyGeneral MedicineVacuoleMitochondrionPeroxisomeGolgi apparatusBiologyMitochondriaCell biologyPlant LeavesChloroplastsymbols.namesakeOrganophosphorus CompoundsPlant Growth RegulatorsApoptosissymbolsUltrastructurePlant Physiological PhenomenaCell Biology International
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How to Select a Mate: Kel1 is a Phosphorylation-Regulated Suppressor of the Pheromone Signaling Pathway

2021

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 Ste5 and…

Programmed cell deathlawChemistryFus3SuppressorPheromonePhosphorylationSignal transductionSynthetic genetic arraySte5law.inventionCell biologySSRN Electronic Journal
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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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