Search results for " Cholecystokinin"

showing 10 items of 12 documents

A possible association between the CCK-AR gene and persistent auditory hallucinations in schizophrenia.

2004

AbstractRecent studies have suggested that DNA variations in the CCK-AR gene might predispose individuals to schizophrenia and particularly to auditory hallucinations (AH). The aim of this study is to assess the association between AH, using a specific scale for AH in schizophrenia (PSYRATS), and the CCK-AR polymorphism at 779 in a Spanish sample. A total of 105 DSM-IV schizophrenic patients with AH and 93 unrelated controls were studied. Twenty-two patients were considered as persistent auditory hallucinators, which showed similar clinical and demographic characteristic than patients with episodic AH, but with the exception of the PSYRATS values. The persistent AH group showed an excess of…

AdultMalemedicine.medical_specialtyPsychosisPeriodicityGenotypeHallucinationsSeverity of Illness IndexGenetic determinismLinkage Disequilibrium03 medical and health sciences0302 clinical medicineGene FrequencyInternal medicineSurveys and QuestionnairesSeverity of illnessmedicineHumansAlleleSex DistributionPsychiatryAllele frequencyGenetic associationDNA PrimersDemographyAuditory hallucinationPolymorphism Geneticmedicine.diseaseIntrons030227 psychiatryReceptor Cholecystokinin ADiagnostic and Statistical Manual of Mental DisordersPsychiatry and Mental healthEndocrinologySchizophreniaSchizophreniaFemalemedicine.symptomPsychology030217 neurology & neurosurgeryEuropean psychiatry : the journal of the Association of European Psychiatrists
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Direct identification of the agonist binding site in the human brain cholecystokinin-B receptor

1999

In investigating the agonist binding site of the human brain cholecystokininB receptor (CCKBR), we employed the direct protein chemical approach using a photoreactive tritiated analogue of sulfated cholecystokinin octapeptide, which contains the p-benzoylbenzoyl moiety at the N-terminus, followed by purification of the affinity-labeled receptor to homogeneity. This probe bound specifically, saturably, and with high affinity (KD = 1.2 nM) to the CCKBR and has full agonistic activity. As the starting material for receptor purification, we used stably transfected HEK 293 cells overexpressing functional CCKBR. Covalent labeling of the WGA-lectin-enriched receptor revealed a 70-80 kDa glycoprote…

ElectrophoresisModels MolecularAgonistProtein Conformationmedicine.drug_classPeptidePhotoaffinity LabelsTritiumBiochemistryMass SpectrometrySincalidemedicineHumansBinding siteReceptorCells Culturedchemistry.chemical_classificationBinding SitesEdman degradationHEK 293 cellsBrainMolecular biologyReceptor Cholecystokinin BchemistryBiochemistryCholecystokinin B receptorChromatography GelMutagenesis Site-DirectedReceptors CholecystokininCholecystokininGlycoproteinSequence Analysis
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Inactivation of Socs3 in the Hypothalamus Enhances the Hindbrain Response to Endogenous Satiety Signals via Oxytocin Signaling.

2012

Leptin is an adipocyte-derived hormone that controls energy balance by acting primarily in the CNS, but its action is lost in common forms of obesity due to central leptin resistance. One potential mechanism for such leptin resistance is an increased hypothalamic expression of Suppressor of cytokine signaling 3 (Socs3), a feedback inhibitor of the Jak-Stat pathway that prevents Stat3 activation. Ample studies have confirmed the important role of Socs3 in leptin resistance and obesity. However, the degree to which Socs3 participates in the regulation of energy homeostasis in nonobese conditions remains largely undetermined. In this study, using adult mice maintained under standard diet, we d…

Leptinmedicine.medical_specialty[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT][SDV]Life Sciences [q-bio][ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionHypothalamusHindbrainSuppressor of Cytokine Signaling ProteinsBiologyOxytocinDevazepideSatiety ResponseEnergy homeostasis03 medical and health sciencesEatingMice0302 clinical medicineHormone AntagonistsInternal medicinemedicineAnimals[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]SOCS3[ SDV.OT ] Life Sciences [q-bio]/Other [q-bio.OT]ComputingMilieux_MISCELLANEOUS030304 developmental biology2. Zero hunger0303 health sciences[SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT]General NeuroscienceLeptindigestive oral and skin physiologyArticlesRhombencephalonEndocrinologyOxytocinHypothalamusSuppressor of Cytokine Signaling 3 Protein[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Receptors Cholecystokinin[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryHomeostasisHormonemedicine.drugSignal Transduction
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Gastric antisecretory drugs induce leukocyte-endothelial cell interactions through gastrin release and activation of CCK-2 receptors.

2007

Antisecretory drugs are effective antiulcer agents, but its chronic use generates hypergastrinemia and accelerates the development of atrophic gastritis in Helicobacter pylori-positive patients. We have recently shown that gastrin exerts a proinflammatory effect in rats through CCK-2 receptor activation that contributes to the inflammation induced by H. pylori. The present study was designed to examine whether gastrin hypersecretion in response to treatment with antisecretory drugs induces an inflammatory response that could promote mucosal atrophy. The effects of omeprazole or famotidine on leukocyte/endothelial cell interactions in vivo were analyzed in rat mesenteric venules using intrav…

Malemedicine.medical_specialtyProglumidemedicine.drug_classInflammationCD18Cell CommunicationProinflammatory cytokineRats Sprague-DawleyInternal medicineGastrinsmedicineLeukocytesAnimalsOmeprazoleGastrinPharmacologyInflammationMicroscopy Videobusiness.industryEndothelial CellsProton Pump InhibitorsReceptor antagonistAnti-Ulcer AgentsFlow CytometryImmunohistochemistryReceptor Cholecystokinin BRatsFamotidineChemotaxis LeukocyteEndocrinologyGastric MucosaMolecular Medicinemedicine.symptombusinessmedicine.drugThe Journal of pharmacology and experimental therapeutics
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Cholecystokinin-8 sulfate modulates the anticonvulsant efficacy of vigabatrin in an experimental model of partial complex epilepsy in the rat.

2009

Summary Purpose:  We evaluated the possible additive effect induced by the administration of the anticonvulsant vigabatrin (VGB) and cholecystokinin-8 sulfate (CCK-8S) on an experimental model of partial complex seizures (maximal dentate gyrus activation, MDA). Moreover, the functional involvement of γ-aminobutyric acid (GABA) neurotransmission was tested by iontophoretically administering bicuculline (GABA receptor antagonist) in the dentate gyrus. Methods:  Urethane anesthetized rats were pretreated with VGB (50, 100 or 200 mg/kg, i.p.) or CCK-8S (8 nmol/kg, i.p.) alone or coadministered with VGB (50 mg/kg, i.p.). Dentate gyrus epileptic activity was obtained through the repetitive electr…

Malemedicine.medical_treatmentStimulationConvulsantsNeurotransmissionPharmacologyBicucullineRat Partial epilepsy Vigabatrin Cholecystokinin-8 sulfate ControlVigabatrinDrug Administration ScheduleSincalideVigabatrinEpilepsy Complex PartialmedicineReaction TimeAnimalsRats WistarEvoked PotentialsNootropic AgentsAnalysis of VarianceIontophoresisDose-Response Relationship DrugChemistryDentate gyrusDrug SynergismBicucullineGABA receptor antagonistElectric StimulationRatsDisease Models AnimalAnticonvulsantNeurologyAnesthesiaDentate GyrusAnticonvulsantsDrug Therapy CombinationNeurology (clinical)medicine.drugEpilepsia
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Oxytocin receptors and cholesterol: interaction and regulation.

2000

Cholesterol affects the ligand binding function of the oxytocin receptor in a highly specific manner. While the structurally-related cholecystokinin receptor shows a strong correlation between the membrane fluidity and its binding function, the oxytocin receptor behaves differently. A stringent and unique requirement of the affinity state of the oxytocin receptor for structural features of the sterol molecule has been found. The molecular requirements differ both from those postulated for sterol-phospholipid interactions and from those known to be necessary for the activity of other proteins. Employing a new detergent-free subcellular fractionation protocol, a two-fold enrichment of the oxy…

Models MolecularMembrane FluidityCaveolin 1Green Fluorescent ProteinsBiologyKidneyTransfectionCholecystokinin receptorCaveolinsGenes ReportermedicineMembrane fluidityExtracellularHumansReceptorCells CulturedBinding SitesCholesterol bindingCell MembraneMembrane ProteinsGeneral MedicineOxytocin receptorRecombinant ProteinsLuminescent ProteinsMembraneCholesterolOxytocinBiochemistryReceptors OxytocinBiophysicsIndicators and ReagentsReceptors CholecystokininSteroidshormones hormone substitutes and hormone antagonistsmedicine.drugExperimental physiology
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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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Non-genomic effects of progesterone on the signaling function of G protein-coupled receptors

1999

Progesterone at concentrations between 10 microM and 200 microM affected the calcium signaling evoked by ligand stimulation of G protein-coupled receptors expressed in several cell lines. At 160 microM progesterone the signaling of all receptors was completely abolished. The effect of progesterone was fast, reversible and was not prevented by cycloheximide indicating its non-genomic nature. Overall, the action of progesterone was more cell type-specific than receptor-specific. Our results are in contrast to a recent report [Grazzini, E., Guillon, G., Mouillac, B. and Zingg, H.H. (1998) Nature 392, 509-512] in which a direct high-affinity interaction between the oxytocin receptor and progest…

Receptors Neuropeptidemedicine.medical_specialtyReceptors VasopressinTime FactorsBiophysicsStimulationCHO CellsCycloheximideBiologyNon-genomic effectCalcium signalBiochemistryCell Linechemistry.chemical_compoundStructure-Activity RelationshipSpecies SpecificityStructural BiologyInternal medicineCricetinaeProgesterone receptorGeneticsmedicineTumor Cells CulturedAnimalsHumansG protein-coupled receptorCycloheximideReceptorMolecular BiologyProgesteroneG protein-coupled receptorCalcium signalingProtein Synthesis InhibitorsDose-Response Relationship DrugCell BiologyLigand (biochemistry)Oxytocin receptorKineticsEndocrinologychemistryReceptors OxytocinAnisotropyCalciumReceptors CholecystokininSignal TransductionFEBS Letters
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Association between CCK-AR gene and schizophrenia with auditory hallucinations

2007

[Objective]: Previous studies on a possible association between CCK-AR polymorphisms and schizophrenia have been controversial. The aim of the present study was to assess a potential association between schizophrenic patients with auditory hallucinations and polymorphisms of the CCK-AR gene.

medicine.medical_specialtyGenotypeHallucinationsSingle-nucleotide polymorphismAuditory hallucinationsRegulatory Sequences Nucleic Aciddigestive systemPolymorphism Single NucleotideGene FrequencyReference ValuesInternal medicineGenotypeGene expressionGeneticsmedicineHumansSNPCCK-AR geneAllelePsychiatryGeneBiological PsychiatryGenetics (clinical)DNA Primersbusiness.industrydigestive oral and skin physiologyHaplotypeDNAmedicine.diseaseReceptor Cholecystokinin APsychiatry and Mental healthEndocrinologySchizophreniaSchizophreniaSchizophrenic Psychologybusinesshormones hormone substitutes and hormone antagonistsPsychiatric Genetics
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Gastrin: an acid-releasing, proliferative and immunomodulatory peptide?

2010

Gastrin release is affected by gastric inflammatory conditions. Antral G cells respond to inflammatory mediators by increasing gastrin secretion. Accumulating experimental evidence suggests that gastrin exerts immunomodulatory and proinflammatory effects. Gastrin could be a contributing factor to these pathologies, which may constitute a new justification for pharmacological blockade of gastrin action.

medicine.medical_specialtyInflammationdigestive systemProinflammatory cytokineGastric AcidImmunomodulationInternal medicineDrug DiscoveryGastrinsmedicineAnimalsHumansSecretionGastrin-Secreting CellsProtein PrecursorsAntrumGastrinCell ProliferationPharmacologyChemistrydigestive oral and skin physiologyGeneral MedicineBlockadeImmunomodulatory peptideEndocrinologyGastrinomaGastritisReceptors CholecystokininG cellmedicine.symptomhormones hormone substitutes and hormone antagonistsSignal TransductionMini reviews in medicinal chemistry
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