Search results for "Inositol"

showing 10 items of 236 documents

Restoration of Clostridium difficile toxin-B-inhibited phospholipase D by phosphatidylinositol 4,5-bisphosphate.

1996

Receptor signalling to phospholipase D (PLD) in human embryonic kidney (HEK) cells stably expressing the m3 muscarinic acetylcholine receptor apparently involves Rho proteins. Since phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] has been recognized as an essential cofactor for PLD activity and since activated Rho proteins have been reported to stimulate the synthesis of PtdIns(4,5)P2, we studied whether in HEK cells PLD activity is regulated by PtdIns(4,5)P2 and, in particular, whether PtdIns(4,5)P2 can restore PLD activity inhibited by Clostridium difficile toxin B, which inactivates Rho proteins. Addition of MgATP to permeabilized HEK cells increased basal PLD activity and potentia…

Phosphatidylinositol 45-DiphosphateGTP'Bacterial ToxinsClostridium difficile toxin BBiologyBiochemistryCell Linechemistry.chemical_compoundBacterial ProteinsGTP-Binding ProteinsPhosphatidylcholineRhoB GTP-Binding ProteinPhospholipase DHumansPhosphatidylinositolEnzyme InhibitorsrhoB GTP-Binding ProteinPhospholipase DClostridioides difficileHEK 293 cellsCell MembraneMembrane ProteinsReceptors MuscarinicCell biologyEnzyme Activationenzymes and coenzymes (carbohydrates)chemistryPhosphatidylinositol 45-bisphosphateGuanosine 5'-O-(3-Thiotriphosphate)lipids (amino acids peptides and proteins)European journal of biochemistry
researchProduct

Pho85 and PI(4,5)P(2) regulate different lipid metabolic pathways in response to cold

2019

Lipid homeostasis allows cells to adjust membrane biophysical properties in response to changes in environmental conditions. In the yeast Saccharomyces cerevisiae, a downward shift in temperature from an optimal reduces membrane fluidity, which triggers a lipid remodeling of the plasma membrane. How changes in membrane fluidity are perceived, and how the abundance and composition of different lipid classes is properly balanced, remain largely unknown. Here, we show that the levels of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], the most abundant plasma membrane phosphoinositide, drop rapidly in response to a downward shift in temperature. This change triggers a signaling cascade trans…

Phosphatidylinositol 45-DiphosphateSaccharomyces cerevisiae ProteinsMembrane FluiditySphingoid basesAcclimatizationOrm2PhospholipidSaccharomyces cerevisiaePhosphoinositideTriacylglycerideSphingolipidArticle03 medical and health scienceschemistry.chemical_compoundGlycogen Synthase Kinase 3Gene Expression Regulation FungalMembrane fluidityLow temperatureInositolPhosphatidylinositolProtein kinase AMolecular Biology1-IP7030304 developmental biology0303 health sciencesChemistry030302 biochemistry & molecular biologyCell MembraneCell BiologyLipid MetabolismSphingolipidCyclin-Dependent KinasesCell biologyTORC2-Pkh1-Ypk1 signaling moduleCold TemperatureCytosolMetabolic pathwayPhospholipidMetabolic Networks and PathwaysSignal Transduction
researchProduct

Modulation of neuronal phospholipase D activity under depolarizing conditions

1999

Neuronal phospholipase D (PLD) activity was hypothesized to be involved in vesicle trafficking and endocytosis and, possibly, transmitter release. We here report that prolonged depolarization of rat hippocampal slices by potassium chloride (KCl) or 4-aminopyridine inhibited PLD activity. Similarly, PLD activity in rat cortical synaptosomes was significantly inhibited by depolarizing agents including veratridine and ouabain. Inhibition of calcium/calmodulin kinase II (CaMKII) which positively modulates synaptosomal PLD activity [Sarri et al. (1998) FEBS Lett. 440, 287-290] by KN-62 caused a further reduction of PLD activity in depolarized synaptosomes. Depolarization-induced inhibition of PL…

Phosphatidylinositol 45-DiphosphateTime FactorsBiophysicschemistry.chemical_elementCalciumHippocampusBiochemistryOuabainMembrane PotentialsPotassium Chloridechemistry.chemical_compoundStructural BiologyCa2+/calmodulin-dependent protein kinaseSynaptosomeElectrochemistryPhospholipase DGeneticsmedicineAnimalsPhospholipase D activityEnzyme InhibitorsRats WistarMolecular BiologyProtein Kinase CProtein Synthesis InhibitorsSynaptosomePhospholipase DCalcium/calmodulin-dependent protein kinase IINeomycinDepolarizationPhosphatidylinositol-45-bisphosphateCell BiologyRatsCell biologyenzymes and coenzymes (carbohydrates)chemistryCalcium-Calmodulin-Dependent Protein KinasesDepolarizationlipids (amino acids peptides and proteins)VeratridineSynaptosomesmedicine.drugFEBS Letters
researchProduct

Control of cellular phosphatidylinositol 4,5-bisphosphate levels by adhesion signals and Rho GTPases in NIH 3T3 fibroblasts

2000

The involvement of small GTPases of the Rho family in the control of phosphoinositide metabolism by adhesion signals was examined in NIH 3T3 fibroblasts. Abrogation of adhesion signals by detachment of cells from their substratum resulted in a time-dependent decrease in the cellular level of PtdIns(4,5)P2 by approximately 50%. This effect could be mimicked by treatment of adherent cells with Clostridium difficile toxin B and toxin B-1470, which inhibit specific subsets of Rho and Ras GTPases. Detachment of cells that had been pretreated with the clostridial toxins did not cause a further reduction in PtdIns(4,5)P2 levels, suggesting that the target GTPases are integrated into the control of…

Phosphatidylinositol 45-Diphosphaterac1 GTP-Binding Proteinrho GTP-Binding ProteinsBacterial ToxinsCellClostridium difficile toxin BRAC1GTPasePhospholipaseBiologyTransfectionBiochemistryMicechemistry.chemical_compoundPhosphoinositide Phospholipase CBacterial ProteinsCell AdhesionmedicineAnimalsPhosphorylationInositol phosphatechemistry.chemical_classificationPhospholipase CCytotoxinsPhosphoric Diester Hydrolases3T3 CellsMolecular biologyRecombinant ProteinsCell biologyKineticsPhosphotransferases (Alcohol Group Acceptor)medicine.anatomical_structurechemistryPhosphatidylinositol 45-bisphosphateType C PhospholipasesCalciumSignal TransductionEuropean Journal of Biochemistry
researchProduct

Phosphatidylinositol-3-kinase activity during in vitro dendritic cell generation determines suppressive or stimulatory capacity.

2011

Modulating PI3K at different stages of dendritic cells (DC) generation could be a novel means to balance the generation of immunosuppressive versus immunostimulatory DC. We show that PI3K inhibition during mouse DC generation in vitro results in cells that are potently immunosuppressive and characteristic of CD8alpha- CD11c+ CD11b+ DC. These DC exhibited low surface class I and class II MHC, CD40, and CD86 and did not produce TNF-alpha. In allogeneic MLR, these DC were suppressive. Although in these mixed cultures, there was no increase in the frequency of CD4+ CD25+ Foxp3+ cells, the Foxp3 content on a per cell basis was significantly increased. Sustained TLR9 signaling in the presence of …

Phosphatidylinositol-3-kinaseSignaling.TLROligonucleotidesImmunoregulationDendritic cells
researchProduct

Activation of alpha-1A adrenoceptors mobilizes calcium from the intracellular stores in myocytes from rat portal vein.

1994

International audience; Intracellular free Ca++ concentration ([Ca++]i) was monitored using the fluorescence from the dye fura-2-acetoxymethylester in single myocytes from rat portal vein. In the presence of oxodipine (a L-type Ca++ channel inhibitor), norepinephrine (10 microM) evoked transient increases in [Ca++]i which were related to release of Ca++ from intracellular stores. The alpha-1 adrenoceptors mediating intracellular Ca++ release and inositol phosphate accumulation were identified by using subtype-selective agonists and antagonists. Pretreatment with chloroethylclonidine had little effect on the norepinephrine-induced increase in [Ca++]i and inositol phosphate accumulation. In c…

Portal VeinInositol Phosphates[SDV]Life Sciences [q-bio]Molecular Sequence Data[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]In Vitro TechniquesAntibodiesMuscle Smooth VascularRats[SDV] Life Sciences [q-bio]NorepinephrineChloride ChannelsReceptors Adrenergic alpha-1[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]AnimalsCalciumAmino Acid SequenceRats Wistar[SDV.BC] Life Sciences [q-bio]/Cellular BiologyAdrenergic alpha-AntagonistsCells CulturedSignal Transduction
researchProduct

Targeting Bcl-2 family proteins modulates the sensitivity of B-cell lymphoma to rituximab-induced apoptosis.

2008

The chimeric monoclonal antibody rituximab is the standard of care for patients with B-cell non-Hodgkin lymphoma (B-NHL). Rituximab mediates complementdependent cytotoxicity and antibodydependent cellular cytotoxicity of CD20-positive human B cells. In addition, rituximab sensitizes B-NHL cells to cytotoxic chemotherapy and has direct apoptotic and antiproliferative effects. Whereas expression of the CD20 antigen is a natural prerequisite for rituximab sensitivity, cell-autonomous factors determining the response of B-NHL to rituximab are less defined. To this end, we have studied rituximab-induced apoptosis in human B-NHL models. We find that rituximab directly triggers apoptosis via the m…

Programmed cell deathLymphoma B-CellImmunologyMedizinAntineoplastic AgentsApoptosisMice SCIDBiochemistryPiperazinesNitrophenolsAntibodies Monoclonal Murine-DerivedMicePhosphatidylinositol 3-Kinasesimmune system diseaseshemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansB-cell lymphomaCD20SulfonamidesbiologyBcl-2 familyBiphenyl CompoundsAntibodies MonoclonalCell BiologyHematologymedicine.diseaseAntigens CD20LymphomaGene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2Apoptosisbiology.proteinCancer researchMyeloid Cell Leukemia Sequence 1 ProteinRituximabSignal transductionRituximabNeoplasm Transplantationmedicine.drugSignal TransductionBlood
researchProduct

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
researchProduct

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
researchProduct

Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast can…

2010

Introduction Accumulating evidence suggests that both levels and activity of the estrogen receptor (ER) and the progesterone receptor (PR) are dramatically influenced by growth-factor receptor (GFR) signaling pathways, and that this crosstalk is a major determinant of both breast cancer progression and response to therapy. The phosphatidylinositol 3-kinase (PI3K) pathway, a key mediator of GFR signaling, is one of the most altered pathways in breast cancer. We thus examined whether deregulated PI3K signaling in luminal ER+ breast tumors is associated with ER level and activity and intrinsic molecular subtype. Methods We defined two independent molecular signatures of the PI3K pathway: a pro…

ProteomeMessengerEstrogen receptorPhosphatidylinositol 3-Kinases0302 clinical medicineReceptorsTumor Cells CulturedInsulin-Like Growth Factor IReceptorCancerOligonucleotide Array Sequence AnalysisMedicine(all)0303 health sciencesCulturedTumorBlottingReverse Transcriptase Polymerase Chain ReactionPrognosis3. Good healthTumor CellsGene Expression Regulation NeoplasticReceptors Estrogen030220 oncology & carcinogenesisFemaleSignal transductionWesternmedicine.drugBiotechnologySignal TransductionResearch Articlemedicine.medical_specialtyBlotting WesternOncology and CarcinogenesisBreast NeoplasmsBiology03 medical and health sciencesInternal medicineProgesterone receptorBreast CancerBiomarkers TumormedicineGeneticsHumansRNA MessengerOncology & CarcinogenesisPI3K/AKT/mTOR pathway030304 developmental biologyCell ProliferationNeoplasticCell growthGene Expression ProfilingEstrogenGene expression profilingEndocrinologyGene Expression RegulationCancer researchRNAProto-Oncogene Proteins c-aktTamoxifenBiomarkersBreast Cancer Research : BCR
researchProduct