Search results for " Receptors"

showing 10 items of 785 documents

Maternal effects in quail and zebra finches: behavior and hormones.

2013

8 pages; International audience; Maternal effects are influences of parents on offspring phenotype occurring through pathways other than inherited DNA. In birds, two important routes for such transmission are parental behavior and non-DNA egg constituents such as yolk hormones. Offspring traits subject to parental effects include behavior and endocrine function. Research from the Adkins-Regan lab has used three avian species to investigate maternal effects related to hormones and behavior. Experiments with chickens and Japanese quail have shown that maternal sex steroids can influence sex determination to produce biased offspring sex ratios. Because all birds have a ZZ/ZW chromosomal sex de…

0106 biological sciencesHypothalamo-Hypophyseal Systemmedicine.medical_specialtyfood.ingredientOffspringMaternal effectsPituitary-Adrenal SystemStressQuail010603 evolutionary biology01 natural sciencesBirds03 medical and health sciencesReceptors GlucocorticoidEndocrinologyfoodbiology.animalYolkInternal medicinemedicine[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisAnimalsGonadal Steroid HormonesGlucocorticoid receptorsTestosterone030304 developmental biologySteroid hormones0303 health sciences[ SDE.BE ] Environmental Sciences/Biodiversity and EcologySexual differentiationbiologyEnvironmental stressorMaternal effectSex determinationQuailEndocrinologyAnimal Science and ZoologyFinches[SDE.BE]Environmental Sciences/Biodiversity and EcologyHormone[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/Symbiosis
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The effects of nitric oxide on striatal serotoninergic transmission involve multiple targets: an in vivo microdialysis study in the awake rat

2004

Abstract The role of endogenous nitric oxide (NO) in N -methyl- d -aspartate (NMDA)-induced modulation of serotonin (5-HT) release in the striatum of freely moving rats has been studied using microdialysis technique. NMDA-induced increase in 5-HT release was significantly inhibited by selective nitric oxide synthase (nNOS) inhibitor S -methylthiocitrulline (S-Me-TC), ONOO − scavenger l -cysteine ( l -cys), and guanylate cyclase (GC) inhibitor 1 H [1,2,4]oxadiazolo[4,3- a ]quinoxalin-1-one (ODQ). These data suggest that modulation of 5-HT levels is linked to the formation of NO produced by NMDA receptor activation and that endogenously produced NO increases 5-HT concentrations both by stimul…

MaleSerotoninmedicine.medical_specialtyMicrodialysisN-MethylaspartateMicrodialysisNitric Oxide Synthase Type IPharmacologyNitric OxideSerotonergicSynaptic TransmissionNitric oxidechemistry.chemical_compoundSuperoxidesPeroxynitrous AcidInternal medicinemedicineAnimalsEnzyme InhibitorsRats WistarNeurotransmitterCyclic GMPMolecular Biologyneurotransmitters; modulators; transporters; and receptors; nitric oxide; serotonin; striatumbiologyGeneral NeuroscienceFree Radical ScavengersRatsNeostriatumNitric oxide synthasePeroxynitrous acidEndocrinologychemistryGuanylate Cyclasebiology.proteinNMDA receptorNeurology (clinical)SerotoninNitric Oxide SynthaseSignal TransductionDevelopmental Biology
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Solution and solid-state studies on the halide binding affinity of perfluorophenyl-armed uranyl–salophen receptors enhanced by anion–π Interactions

2016

The enhancement of the binding between halide anions and a Lewis acidic uranyl-salophen receptor has been achieved by the introduction of pendant electron- deficient arene units into the receptor skeleton. The association and the occurrence of the elusive anion-p interaction with halide anions (as tetrabutylammonium salts) have been demonstrated in solution and in the solid state, providing unambiguous evidence on the interplay of the concerted interactions responsible for the anion binding.

anion–π interactions; halides; host–guest systems; lewis acid–base interactions; uranyl–salophen; chemistry (all)Solid-stateHalide010402 general chemistry01 natural sciencesCatalysisIonUranyl salophenPolymer chemistryOrganic chemistryReceptorAnion bindingta116Uranyl-salphenlewis acid–base interactionsanion–π interactionsuranyl–salophen010405 organic chemistryChemistryOrganic Chemistryhost–guest systemsGeneral Chemistryinteractions0104 chemical sciencesuranyl-salophen receptorshalideschemistry (all)halide recognitionanions
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Molecular Basis for Endocrine Disruption by Pesticides Targeting Aromatase and Estrogen Receptor

2020

The intensive use of pesticides has led to their increasing presence in water, soil, and agricultural products. Mounting evidence indicates that some pesticides may be endocrine disrupting chemicals (EDCs), being therefore harmful for the human health and the environment. In this study, three pesticides, glyphosate, thiacloprid, and imidacloprid, were tested for their ability to interfere with estrogen biosynthesis and/or signaling, to evaluate their potential action as EDCs. Among the tested compounds, only glyphosate inhibited aromatase activity (up to 30%) via a non-competitive inhibition or a mixed inhibition mechanism depending on the concentration applied. Then, the ability of the thr…

aromatasemedicine.drug_classHealth Toxicology and Mutagenesislcsh:MedicineEstrogen receptorMixed inhibitionEndocrine Disruptors010501 environmental sciencesPharmacology01 natural sciencesArticle03 medical and health scienceschemistry.chemical_compoundImidaclopridReceptorsmedicineHumansAromataseestrogenic activity030304 developmental biology0105 earth and related environmental sciences0303 health sciencesAromatase inhibitorendocrine disrupting chemicalbiologyAromatase Inhibitorslcsh:RPublic Health Environmental and Occupational HealthEstrogenspesticidesPesticideThiaclopridEstrogenmolecular dynamicsReceptors EstrogenchemistryEstrogenMELN allosteric inhibitionbiology.proteingene reporter assayAromatase; Endocrine disrupting chemical; Estrogen receptor; Estrogenic activity; Gene reporter assay; MELN allosteric inhibition; Molecular dynamics; Neonicotinoids; Pesticides; Aromatase; Aromatase Inhibitors; Estrogens; Humans; Receptors Estrogen; Endocrine Disruptors; Pesticidesneonicotinoidsestrogen receptorInternational Journal of Environmental Research and Public Health
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AN IL-6/IL-6 SOLUBLE RECEPTOR (IL-6R) HYBRID PROTEIN (H-IL-6) INDUCES EPO-INDEPENDENT ERYTHROID DIFFERENTIATION IN HUMAN CD34+CELLS

2000

H-IL-6 is a hybrid protein constructed to contain IL-6 and its soluble receptor linked by a flexible peptide chain. Here we show that H-IL-6 strongly enhances proliferation of human CD34(+)cells in serum-free liquid culture, and that the majority of the cells generated belong to the erythroid lineage, being positive for the marker Glycophorin A. Conversely, H-IL-6 does not increase the number of myeloid, CD13-positive cells. Comparable effects are observed on progenitors from cord blood and adult peripheral blood. Therefore, H-IL-6 triggers an erythroid-inducing signal in haematopoietic progenitor cells, independently from erythropoietin (EPO).

ErythrocytesTime FactorsMyeloidCellular differentiationInterleukin 6Antigens CD34BiochemistryCulture Media Serum-FreeSerum-Freehemic and lymphatic diseasesReceptorsLeukocytesImmunology and AllergyErythropoiesisGlycophorinsStem Cell FactorbiologyChemistryCord bloodCell DifferentiationHematologyFetal BloodFlow CytometryEndothelial stem cellHaematopoiesismedicine.anatomical_structureGlycophorinCD34+medicine.drugRecombinant Fusion ProteinsMononuclearImmunologyCD13 AntigensmedicineHumansGlycophorinAntigensProgenitor cellErythropoietinMolecular BiologyInterleukin 3Interleukin-6CD34+; Cord blood; Erythropoiesis; Interleukin 6; Stem cell factor; Antigens CD34; CD13 Antigens; Cell Differentiation; Culture Media Serum-Free; Erythrocytes; Erythropoietin; Fetal Blood; Flow Cytometry; Glycophorin; Hematopoietic Stem Cells; Humans; Interleukin-6; Leukocytes Mononuclear; Peptides; Receptors Interleukin-6; Recombinant Fusion Proteins; Stem Cell Factor; Time Factors; Immunology and Allergy; Immunology; Biochemistry; Hematology; Molecular BiologyHematopoietic Stem CellsReceptors Interleukin-6Molecular biologyCulture MediaErythropoietinLeukocytes Mononuclearbiology.proteinCD34PeptidesCytokine
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CD14+CD16+ monocytes in coronary artery disease and their relationship to serum TNF-α levels

2004

SummaryMonocytes play a central role in the inflammatory disease atherosclerosis. CD14+CD16+ monocytes are considered proinflammatory monocytes, as they have an increased capacity to produce proinflammatory cytokines, such as TNF-α, and are elevated in various inflammatory diseases. We hypothesized that patients with coronary artery disease (CAD) have increased levels of CD14+CD16+ monocytes, and that CD14+CD16+ monocytes are associated with inflammation markers. We investigated CD14+CD16+ monocytes in 247 patients with CAD and 61 control subjects using flow cytometry. In addition serum concentrations of TNF-α, IL-6, and Hs-CRP were assessed. Patients with CAD had higher levels of CD14+CD16…

MaleArteriosclerosismedicine.medical_treatmentCD14Lipopolysaccharide ReceptorsInflammationCell SeparationCoronary Artery DiseaseCD16MonocytesBody Mass IndexProinflammatory cytokineCoronary artery diseaseRisk FactorsOdds RatioHumansMedicineAgedInflammationAnalysis of VarianceInterleukin-6Tumor Necrosis Factor-alphabusiness.industryMonocyteReceptors IgGAntibodies MonoclonalHematologyMiddle AgedFlow Cytometrymedicine.diseaseLogistic ModelsCytokinemedicine.anatomical_structureCase-Control StudiesImmunologyFemaleTumor necrosis factor alphamedicine.symptombusinessThrombosis and Haemostasis
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Subcellular targeting of multiligand-binding protein gC1qR.

1999

Abstract gC1q receptor, a protein originally described as the cell surface receptor for the globular heads of complement factor C1q, has been found to bind human H-kininogen with high affinity and specificity. Therefore, gC1qR has been considered candidate kininogen docking site on the surfaces of platelets, neutrophils and endothelial cells. Recent work demonstrating that gC1qR is an intracellular protein that is tightly associated with mitochondria rather than targeted to the cell surface has challenged this view. To further probe cellular trafficking routes of gC1qR, we overexpressed human gC1qR in a mammalian cell and monitored cell surface exposure of recombinant gC1qR by virtue of its…

CellComplement factor IBiologyLigandsMitochondrial ProteinsCell surface receptormedicineAnimalsHumansBinding siteReceptorPharmacologyBinding SitesMembrane GlycoproteinsBinding proteinComplement C1qBiological TransportTransfectionMolecular biologyCell biologyReceptors Complementmedicine.anatomical_structureHyaluronan ReceptorsCell cultureCOS CellsCarrier ProteinsProtein Processing Post-Translationalcirculatory and respiratory physiologySubcellular FractionsImmunopharmacology
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CXCR7 Reactivates ERK Signaling to Promote Resistance to EGFR Kinase Inhibitors in NSCLC

2019

Abstract Although EGFR mutant–selective tyrosine kinase inhibitors (TKI) are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical G protein-coupled receptor, activates the MAPK–ERK pathway via β-arrestin. Depletion of CXCR7 inhibited the MAPK pathway, significantly attenuated EGFR TKI resistance, and resulted in mesenchymal-to-epithelial transition. CXCR7 overexpression was essential in reactivation of ERK1/2 for the generation of EGFR TKI–resistant persister cells. Many patients with non–small cell lung cancer (NSCLC) harboring an EGFR kinase domain mutatio…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsDrug ResistanceDrug resistanceTransgenicMiceChemokine receptor0302 clinical medicineNeoplasmsCarcinoma Non-Small-Cell LungReceptorsMedicineNon-Small-Cell LungCXCRReceptorLungbeta-ArrestinsCancerEGFR inhibitorsTumorKinaseLung CancerErbB ReceptorsOncology5.1 Pharmaceuticals030220 oncology & carcinogenesisDevelopment of treatments and therapeutic interventionsTyrosine kinaseEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemOncology and CarcinogenesisMice TransgenicArticleCell LineExperimental03 medical and health sciencesClinical ResearchCell Line TumorAnimalsHumansOncology & CarcinogenesisProtein Kinase InhibitorsReceptors CXCRbusiness.industryCarcinomaNeoplasms Experimentalrespiratory tract diseases030104 developmental biologyProtein kinase domainDrug Resistance NeoplasmMutationCancer researchNeoplasmbusinessCancer Research
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FGFR a promising druggable target in cancer: Molecular biology and new drugs.

2017

Abstract: Introduction: The Fibroblast Growth Factor Receptor (FGFR) family consists of Tyrosine Kinase Receptors (TKR) involved in several biological functions. Recently, alterations of FGFR have been reported to be important for progression and development of several cancers. In this setting, different studies are trying to evaluate the efficacy of different therapies targeting FGFR. Areas Covered: This review summarizes the current status of treatments targeting FGFR, focusing on the trials that are evaluating the FGFR profile as inclusion criteria: Multi-Target, Pan-FGFR Inhibitors and anti-FGF (Fibroblast Growth Factor)/FGFR Monoclonal Antibodies. Expert opinion: Most of the TKR share …

0301 basic medicineFibroblast Growth FactorDruggabilityFibroblast growth factorTyrosine-kinase inhibitorReceptor tyrosine kinase0302 clinical medicineNeoplasmsFGFR inhibitorsFGFMolecular Targeted TherapyCancerCancer; FGF; FGFR; FGFR inhibitors; Drug Resistance Neoplasm; Fibroblast Growth Factors; Gene Fusion; Humans; Molecular Targeted Therapy; Mutation; Neoplasms; Protein Kinase Inhibitors; Receptors Fibroblast Growth Factor; Signal Transduction; Hematology; Oncology; Geriatrics and GerontologybiologyFGFRHematologyFGFR inhibitorOncologyFibroblast growth factor receptor030220 oncology & carcinogenesisembryonic structuresSignal transductionbiological phenomena cell phenomena and immunityGene FusionHumanSignal Transductionmusculoskeletal diseasesanimal structuresmedicine.drug_classProtein Kinase Inhibitor03 medical and health sciencesmedicineHumansProtein Kinase InhibitorsCancer; FGF; FGFR; FGFR inhibitorsbusiness.industryCancermedicine.diseaseMolecular biologyReceptors Fibroblast Growth FactorFibroblast Growth Factors030104 developmental biologyDrug Resistance NeoplasmCancer cellMutationbiology.proteinNeoplasmHuman medicineGeriatrics and GerontologybusinessCritical reviews in oncology/hematology
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Synthesis and evaluation of (S)-2-(2-[18F]fluoroethoxy)-4-([3-methyl-1-(2-piperidin-1-yl-phenyl)-butyl-carbamoyl]-methyl)-benzoic acid ([18F]repaglin…

2004

18F-labeled non-sulfonylurea hypoglycemic agent (S)-2-(2-[(18)F]fluoroethoxy)-4-((3-methyl-1-(2-piperidin-1-yl-phenyl)-butylcarbamoyl)-methyl)-benzoic acid ([(18)F]repaglinide), a derivative of the sulfonylurea-receptor (SUR) ligand repaglinide, was synthesized as a potential tracer for the non-invasive investigation of the sulfonylurea 1 receptor status of pancreatic beta-cells by positron emission tomography (PET) in the context of type 1 and type 2 diabetes. [(18)F]Repaglinide could be obtained in an overall radiochemical yield (RCY) of 20% after 135 min with a radiochemical purity higher than 98% applying the secondary labeling precursor 2-[(18)F]fluoroethyltosylate. Specific activity w…

Fluorine RadioisotopesCancer ResearchBiodistributionMetabolic Clearance RateReceptors DrugContext (language use)Sulfonylurea ReceptorsRats Sprague-DawleyIslets of Langerhanschemistry.chemical_compoundPiperidinesmedicineRadioligandAnimalsTissue DistributionRadiology Nuclear Medicine and imagingPotassium Channels Inwardly RectifyingBenzoic acidChemistryBiological activityLigand (biochemistry)RepaglinideRatsDissociation constantBiochemistryOrgan SpecificityRats Inbred LewIsotope LabelingPositron-Emission TomographyFeasibility StudiesMolecular MedicineATP-Binding Cassette TransportersCarbamatesMultidrug Resistance-Associated ProteinsRadiopharmaceuticalsNuclear chemistrymedicine.drugNuclear Medicine and Biology
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