Search results for "Jurkat T-cell"

showing 3 items of 3 documents

Implication of three isoforms of PLA2in human T-cell proliferation

2002

We observed that human (Jurkat) T-cells constitutively expressed the mRNA, encoding for the four isoforms of phospholipase A(2) (PLA(2)), i.e. two secretory (type IB and type V), and two cytosolic (type IV, Ca(2+)-dependent and type VI, Ca(2+)-independent). In order to assess whether these PLA(2) isoforms are active, we labeled Jurkat T-cells with [(3)H]arachidonic acid ([(3)H]AA) and determined its release into the extracellular medium in the presence of phorbol 12-myristate 13-acetate (PMA) and ionomycin. The three PLA(2) isoforms seem functional as aristolochic acid and bromoenol lactone (BEL), the respective inhibitors of type IB/type V and type VI PLA(2)s, significantly inhibited the r…

BiophysicsAristolochic acidArachidonic AcidsPhospholipaseTritiumBiochemistryJurkat cellsGene Expression Regulation EnzymologicPhospholipases AJurkat Cellschemistry.chemical_compoundPhospholipase A2Structural BiologyGeneticsHumansPhospholipaseRNA MessengerEnzyme InhibitorsMolecular BiologyArachidonyl trifluoromethyl ketoneArachidonic AcidbiologyIonomycinCell BiologyJurkat T-cellIsoenzymesGene Expression RegulationchemistryBiochemistryIonomycinPhorbolbiology.proteinInterleukin-2Tetradecanoylphorbol AcetateCalciumlipids (amino acids peptides and proteins)Arachidonic acidCell DivisionFEBS Letters
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Thapsigargin-stimulated MAP kinase phosphorylation via CRAC channels and PLD activation: inhibitory action of docosahexaenoic acid.

2004

AbstractThis study was conducted on human Jurkat T-cells to investigate the role of depletion of intracellular Ca2+ stores in the phosphorylation of two mitogen-activated protein kinases (MAPKs), i.e. extracellular signal-regulated kinase (ERK) 1 and ERK2, and their modulation by a polyunsaturated fatty acid, docosahexaenoic acid (DHA). We observed that thapsigargin (TG) stimulated MAPK activation by store-operated calcium (SOC) influx via opening of calcium release-activated calcium (CRAC) channels as tyrphostin-A9, a CRAC channel blocker, and two SOC influx inhibitors, econazole and SKF-96365, diminished the action of the former. TG-stimulated ERK1/ERK2 phosphorylation was also diminished…

MAPK/ERK pathwayThapsigarginDocosahexaenoic AcidsBiophysicschemistry.chemical_elementCalciumBiochemistryDiglycerideschemistry.chemical_compoundJurkat CellsStructural BiologyGeneticsPhospholipase DHumansPhosphorylationMolecular BiologyProtein kinase CProtein Kinase CDiacylglycerol kinaseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phospholipase CChemistryKinasePhospholipase DRyanodine Receptor Calcium Release ChannelCell BiologyJurkat T-cellCell biologyEnzyme Activationenzymes and coenzymes (carbohydrates)Docosahexaenoic acidFatty Acids UnsaturatedThapsigarginlipids (amino acids peptides and proteins)CalciumMitogen-Activated Protein KinasesFEBS letters
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Regulation of calcium signalling by docosahexaenoic acid in human T-cells: implication of CRAC channels

2000

Abstract We elucidated the role of docosahexaenoic acid (DHA) on the increases in free intracellular calcium concentrations, [Ca2+]i, in human (Jurkat) T-cell lines. DHA evoked an increase in [Ca2+]i in a dose-dependent manner in these cells. Anti-CD3 antibody, known to stimulate increases in Ca2+ from endoplasmic reticulum (ER) via the production of inositol trisphosphate, also evoked increases in [Ca2+]i in Jurkat T-cells. We also used thapsigargin which inhibits Ca2+-ATPase of the ER and, therefore, increases Ca2+ in the cytosol. Interestingly, addition of DHA during the thapsigargin-induced peak response exerted an additive effect on the increases in [Ca2+]i in human T-cells, indicating…

ThapsigarginVoltage-dependent calcium channelEndoplasmic reticulumchemistry.chemical_elementInositol trisphosphateQD415-436Cell BiologyCalciumpolyunsaturated fatty acidCD3BiochemistryJurkat cellsJurkat T-cellsCalcium in biologyCell biologychemistry.chemical_compoundEndocrinologychemistrythapsigarginCalcium signalingJournal of Lipid Research
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