Search results for "inositol 1"

showing 8 items of 8 documents

Receptor phosphorylation does not mediate cross talk between muscarinic M(3) and bradykinin B(2) receptors.

1999

This study examined cross talk between phospholipase C-coupled muscarinic M3and bradykinin B2receptors coexpressed in Chinese hamster ovary (CHO) cells. Agonists of either receptor enhanced phosphoinositide signaling (which rapidly desensitized) and caused protein kinase C (PKC)-independent, homologous receptor phosphorylation. Muscarinic M3but not bradykinin B2receptors were also phosphorylated after phorbol ester activation of PKC. Consistent with this, muscarinic M3receptors were phosphorylated in a PKC-dependent fashion after bradykinin B2receptor activation, but muscarinic M3receptor activation did not influence bradykinin B2receptor phosphorylation. Despite heterologous phosphorylatio…

Atropinemedicine.medical_specialtyReceptor Bradykinin B2PhysiologyGene ExpressionCHO CellsInositol 145-TrisphosphateMuscarinic AntagonistsBiologyMuscarinic AgonistsBradykininTransfectionTritiumInternal medicineCricetinaeMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptormedicineMuscarinic acetylcholine receptor M4AnimalsHumansBradykinin receptorPhosphorylationReceptorMethacholine ChlorideReceptor Muscarinic M3Receptors BradykininMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Cell BiologyMuscarinic acetylcholine receptor M1Receptor Cross-TalkReceptors MuscarinicRecombinant ProteinsEndocrinologyType C PhospholipasesCalciumInositolSignal TransductionThe American journal of physiology
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Inhibitory effect of nonviable preparations from human immunodeficiency virus 1 on inositol phospholipid metabolism

1989

Previously it was established [Pahwa, S., Pahwa, R., Saxinger, C., Gallo, R. C. & Good, R. A. (1985) Proc. Natl Acad. Sci. USA 82, 8198] that nonviable preparations of human immunodeficiency virus 1 (HIV-1) abolish the proliferative response of human lymphocytes to phytohemagglutinin A. Now we describe that this effect might be, at least partially, due to an impairment of the function of phospholipase C. It was found that addition of HIV-1 preparation to lymphocytes diminished the stimulation of phosphatidylinositol phosphorylation caused by phytohemagglutinin A. Moreover, this preparation completely abolished the phytohemagglutinin-A-stimulated release of inositol trisphosphate and prevent…

Inositol PhosphatesInositol 145-TrisphosphateBiologyPhospholipasePhosphatidylinositolsBiochemistrychemistry.chemical_compoundCytosolCyclic AMPPhosphatidylinositol phosphorylationHumansInositolLymphocytesPhosphorylationPhytohemagglutininsInositol phosphateProtein kinase AProtein Kinase CProtein kinase Cchemistry.chemical_classificationCell MembraneVirionBiological TransportInositol trisphosphateMolecular biologyCytosolchemistryBiochemistryType C PhospholipasesHIV-1Sugar PhosphatesCell DivisionEuropean Journal of Biochemistry
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Docosahexaenoic Acid Induces Increases in [Ca2+]ivia Inositol 1,4,5-Triphosphate Production and Activates Protein Kinase Cγ and -δ via Phosphatidylse…

2007

We investigated, in monocytic leukemia U937 cells, the effects of docosahexaenoic acid (DHA; 22:6 n-3) on calcium signaling and determined the implication of phospholipase C (PLC) and protein kinase C (PKC) in this pathway. DHA induced dose-dependent increases in [Ca2+]i, which were contributed by intracellular pool, via the production of inositol-1,4,5-triphosphate (IP3) and store-operated Ca2+ (SOC) influx, via opening of Ca2+ release-activated Ca2+ (CRAC) channels. Chemical inhibition of PLC, PKCgamma, and PKCdelta, but not of PKCbeta I/II, PKCalpha, or PKCbetaI, significantly diminished DHA-induced increases in [Ca2+]i. In vitro PKC assays revealed that DHA induced a approximately 2-fol…

Intracellular FluidDocosahexaenoic AcidsApoptosisInositol 145-TrisphosphatePhosphatidylserinesBiologyEnzyme activatorchemistry.chemical_compoundHumansCalcium SignalingPhosphatidylserine bindingProtein Kinase CProtein kinase CCalcium signalingPharmacologyBinding SitesPhospholipase CU937 CellsPhosphatidylserineMolecular biologyCell biologyEnzyme ActivationProtein Kinase C-deltachemistryDocosahexaenoic acidApoptosisMolecular Medicinelipids (amino acids peptides and proteins)Molecular Pharmacology
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Mechanisms underlying the inhibitory effects induced by pituitary adenylate cyclase-activating peptide in mouse ileum

2005

Abstract The aim of this study was to investigate the signal transduction mechanisms underlying the inhibitory effect induced by pituitary adenylate cyclase activating peptide (PACAP-27) on the spontaneous contractile activity of longitudinal muscle of mouse ileum. Mechanical activity of ileal segments was recorded isometrically in vitro. PACAP-27 produced apamin-sensitive reduction of the amplitude of the spontaneous contractions. 9-(Tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), adenylate cyclase inhibitor, or genistein and tyrphostin 25, tyrosine kinase inhibitors, had negligible effects on PACAP-27-induced inhibition. PACAP-27 effects were significantly inhibited by U-73122, phopho…

MaleIndolesPhosphodiesterase InhibitorsVasodilator AgentsMouse ileumStimulationSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundInositolEnzyme InhibitorsEstrenesRyanodineRyanodine receptorProtein-Tyrosine KinasesTyrphostinsGenisteinPyrrolidinonesCell biologyPituitary adenylate cyclase-activating peptideNG-Nitroarginine Methyl EsterPituitary Adenylate Cyclase-Activating PolypeptideThapsigarginSignal transductionCyclopiazonic acidhormones hormone substitutes and hormone antagonistsMuscle ContractionBoron Compoundsendocrine systemmedicine.medical_specialtyThapsigarginMuscular inhibitionCalcium-Transporting ATPasesIn Vitro TechniquesInositol 145-triphosphateBiologyPACAP-27 (pituitary adenylate cyclase activating peptide)IleumPhospholipase CInternal medicinemedicineAnimalsPharmacologyDose-Response Relationship DrugPhospholipase CAdenineMuscle SmoothMice Inbred C57BLEndocrinologyApaminchemistryAdenylyl Cyclase InhibitorsCalciumNitric Oxide SynthaseEuropean Journal of Pharmacology
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Activation of P2Y receptors by ATP and by its analogue, ADPbetaS, triggers two calcium signal pathways in the longitudinal muscle of mouse distal col…

2008

Our previous research showed that ATP and adenosine 5'-O-2-thiodiphosphate (ADPbetaS) induce contractile effects in the longitudinal muscle of mouse distal colon via activation of P2Y receptors which are not P2Y(1) or P2Y(12) subtypes. This study investigated the nature of the P2Y receptor subtype(s) and the mechanisms leading to the intracellular calcium concentration increase necessary to trigger muscular contraction. Motor responses of mouse colonic longitudinal muscle to P2Y receptor agonists were examined in vitro as changes in isometric tension. ATP or ADPbetaS induced muscular contraction, which was not affected by P2Y(11) or P2Y(13) selective antagonists. Calcium-free solution or th…

MalePurinergic P2 Receptor Agonistsmedicine.medical_specialtyP2Y receptormedicine.drug_classColonchemistry.chemical_elementCalcium channel blockerCalcium-Transporting ATPasesCalciumBiologyCholinergic AgonistsIn Vitro TechniquesCalcium in biologyMiceAdenosine TriphosphateInternal medicinemedicineAnimalsInositol 145-Trisphosphate ReceptorsCalcium SignalingEnzyme InhibitorsReceptorPharmacologyRyanodine receptorReceptors Purinergic P2Muscle SmoothRyanodine Receptor Calcium Release ChannelThionucleotidesCalcium Channel BlockersAdenosineAdenosine DiphosphateMice Inbred C57BLEndocrinologychemistryType C Phospholipasesmedicine.symptomMuscle contractionmedicine.drugMuscle ContractionEuropean journal of pharmacology
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Nuclear calcium signaling by inositol trisphosphate in GH3 pituitary cells

2008

It has been proposed that nuclear and cytosolic Ca2+ ([Ca2+]N and [Ca2+]C) may be regulated independently. We address here the issue of whether inositol trisphosphate (IP3) can, bypassing changes of [Ca2+]C, produce direct release of Ca2+ into the nucleoplasm. We have used targeted aequorins to selectively measure and compare the changes in [Ca2+]C and [Ca2+]N induced by IP3 in GH3 pituitary cells. Heparin, an IP3 inhibitor that does not permeate the nuclear pores, abolished the [Ca2+]C peaks but inhibited only partly the [Ca2+]N peaks. The permeant inhibitor 2-aminoethoxy-diphenyl-borate (2-APB) blocked both responses. Removal of ATP also inhibited more strongly the [Ca2+]C than [Ca2+]N pe…

endocrine systemCytoplasm[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]PhysiologyAequorinNucleoplasmic reticulumaequorinInositol 145-TrisphosphateCell Line03 medical and health scienceschemistry.chemical_compound0302 clinical medicinenuclear signal transductionmedicineAnimalsInositol 145-Trisphosphate Receptorsinositol trisphosphate receptorsCalcium SignalingReceptorMolecular Biology030304 developmental biologyCell Nucleus0303 health sciencesNucleoplasmbiologypituitary cellsInositol trisphosphateCell Biologyherpes simplex virusMolecular biologyRatsCytosolmedicine.anatomical_structurechemistryCytoplasmPituitary Glandbiology.proteinnucleoplasmic reticulumNucleus030217 neurology & neurosurgery
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IP 3 signalling regulates exogenous RNA i in C aenorhabditis elegans

2015

RNA interference (RNAi) is a widespread and widely exploited phenomenon. Here, we show that changing inositol 1,4,5-trisphosphate (IP3) signalling alters RNAi sensitivity in Caenorhabditis elegans. Reducing IP3 signalling enhances sensitivity to RNAi in a broad range of genes and tissues. Conversely up-regulating IP3 signalling decreases sensitivity. Tissue-specific rescue experiments suggest IP3 functions in the intestine. We also exploit IP3 signalling mutants to further enhance the sensitivity of RNAi hypersensitive strains. These results demonstrate that conserved cell signalling pathways can modify RNAi responses, implying that RNAi responses may be influenced by an animal's physiology…

inorganic chemicalscalcium signallingCell signalingMutantInositol 145-TrisphosphateBiologyModels BiologicalBiochemistryRNA interferenceRNA interferenceImage Processing Computer-AssistedGeneticsAnimalsIntestinal MucosaCaenorhabditis elegansMolecular BiologyCaenorhabditis elegansRNA Double-StrandedCalcium signalingenhanced RNAiScientific Reportsfungiinositol 145‐trisphosphateRNAbiology.organism_classificationC. elegansCell biologySignallingMicroscopy FluorescenceSignal transductionSignal TransductionEMBO reports
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