Search results for "RECEPTORS"

showing 10 items of 3254 documents

Dual inhibitors of histone deacetylases and other cancer-related targets: A pharmacological perspective.

2020

International audience; Epigenetic enzymes histone deacetylases (HDACs) are clinically validated anticancer drug targets which have been studied intensively in the past few decades. Although several drugs have been approved in this field, they are still limited to a subset of hematological malignancies (in particular T-cell lymphomas), with therapeutic potential not fully realized and the drug-resistance occurred after a certain period of use. To maximize the therapeutic potential of these classes of anticancer drugs, and to extend their application to solid tumors, numerous combination therapies containing an HDACi and an anticancer agent from other mechanisms are currently ongoing in clin…

0301 basic medicineDual targeting[SDV]Life Sciences [q-bio]Cancer therapyKinasesAntineoplastic AgentsBioinformaticsBiochemistryAnticancer drugsSynergistic effectsHistone Deacetylases03 medical and health sciences0302 clinical medicineDrug Delivery SystemsNeoplasmsReceptorsmedicineAnimalsHumansEpigeneticsPharmacologybiologybusiness.industryCancerDUAL (cognitive architecture)medicine.diseaseAnticancer drug3. Good healthEnzymesClinical trial[SDV] Life Sciences [q-bio]Histone Deacetylase Inhibitors030104 developmental biologyHistone030220 oncology & carcinogenesisbiology.proteinHistone deacetylases (HDACs)EpigeneticsDual inhibitorbusinessBiochemical pharmacology
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Effect of colorectal cancer-derived extracellular vesicles on the immunophenotype and cytokine secretion profile of monocytes and macrophages.

2018

Abstract. Background Macrophages are one of the most important players in the tumor microenvironment. The polarization status of tumor associated macrophages into a pro-inflammatory type M1 or anti-inflammatory type M2 may influence cancer progression and patient survival. Extracellular vesicles (EVs) are membrane-bound vesicles containing different biomolecules that are involved in cell to cell signal transfer. Accumulating evidence suggests that cancer-derived EVs are taken up by macrophages and modulate their phenotype and cytokine profile. However, the interactions of cancer-derived EVs with monocytes and macrophages at various differentiation and polarization states are poorly understo…

0301 basic medicineDynaminsLipopolysaccharidesCell SurvivalCD14Macrophage polarizationLipopolysaccharide ReceptorsShort Reportlcsh:MedicineReceptors Cell Surfacecolorectal cancerBiochemistryMonocytesImmunophenotyping03 medical and health sciencesExtracellular VesiclesInterferon-gamma0302 clinical medicineCell Line TumormedicineCXCL10MacrophageHumansendocytosisSecretionLectins C-Typelcsh:QH573-671Molecular BiologyTumor microenvironmentlcsh:CytologyChemistryMonocyteMacrophageslcsh:RCell DifferentiationCell BiologyHLA-DR AntigenscytokinesCell biology030104 developmental biologymedicine.anatomical_structureMannose-Binding Lectins030220 oncology & carcinogenesisTetradecanoylphorbol AcetateCytokine secretionChemokinesColorectal NeoplasmsMannose ReceptorCell communication and signaling : CCS
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Death Receptor 5 Displayed on Extracellular Vesicles Decreases TRAIL Sensitivity of Colon Cancer Cells

2020

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is considered to be a promising antitumor drug because of its selective proapoptotic properties on tumor cells. However, the clinical application of TRAIL is until now limited because of the resistance of several cancer cells, which can occur at various levels in the TRAIL signaling pathway. The role of decoy receptors that can side-track TRAIL, thereby preventing the formation of an activated death receptor, has been extensively studied. In this study, we have focused on extracellular vesicles (EVs) that are known to play a role in cell-to-cell communication and that can be released by donor cells into the medium transferring …

0301 basic medicineENDOCYTOSISTRAILSURFACE EXPRESSIONCell and Developmental Biology03 medical and health sciences0302 clinical medicineSecretionDR5Decoy receptorsReceptorlcsh:QH301-705.5Original Researchreceptor-ligand traffickingEXOSOMESChemistryapoptosisCell BiologyMicrovesiclesconditioned medium030104 developmental biologylcsh:Biology (General)Apoptosis030220 oncology & carcinogenesisCancer cellCancer researchTumor necrosis factor alphareceptor–ligand traffickingextracellular vesiclesDecoyDevelopmental BiologyFrontiers in Cell and Developmental Biology
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EBI2 – Sensor for dihydroxycholesterol gradients in neuroinflammation

2018

Dihydroxycholesterols such as 7α,25-dihydroxysterols (7α,25-OHC) and 7α,27-OHC are generated from cholesterol by the enzymes CH25H, CYP7B1 and CYP27A1 in steady state but also in the context of inflammation. The G-protein coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2), also known as GPR183, senses these oxysterols and induces chemotactic migration of immune cells towards higher concentrations of these ligands. We recently showed that these ligands are upregulated in the CNS in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis and that EBI2 enhanced early infiltration of encephalitogenic T cells into the CNS. In this short-review we dis…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisInflammationContext (language use)BiochemistryReceptors G-Protein-Coupled03 medical and health sciencesImmune systemmedicineAnimalsHumansReceptorNeuroinflammationInflammationImmunity CellularChemistryChemotaxisExperimental autoimmune encephalomyelitisGPR183ChemotaxisGeneral Medicinemedicine.diseaseHydroxycholesterolsCell biologyDisease Models Animal030104 developmental biologymedicine.symptomBiochimie
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An Assay to Determine Mechanisms of Rapid Autoantibody-Induced Neurotransmitter Receptor Endocytosis and Vesicular Trafficking in Autoimmune Encephal…

2019

N-Methyl-D-aspartate (NMDA) receptors (NMDARs) are among the most important excitatory neurotransmitter receptors in the human brain. Autoantibodies to the human NMDAR cause the most frequent form of autoimmune encephalitis involving autoantibody-mediated receptor cross-linking and subsequent internalization of the antibody-receptor complex. This has been deemed to represent the predominant antibody effector mechanism depleting the NMDAR from the synaptic and extra-synaptic neuronal cell membrane. To assess in detail the molecular mechanisms of autoantibody-induced NMDAR endocytosis, vesicular trafficking, and exocytosis we transiently co-expressed rat GluN1-1a-EGFP and GluN2B-ECFP alone or…

0301 basic medicineEndosomeautoantibodiesmedia_common.quotation_subjectN-Methyl-D-aspartate receptorsEndocytosisExocytosislcsh:RC346-42903 medical and health sciences0302 clinical medicineNeurotransmitter receptorendocytosisInternalizationReceptorlcsh:Neurology. Diseases of the nervous systemmedia_commonOriginal ResearchChemistryAutoantibodyautoimmune encephalitisCell biology030104 developmental biologynervous systemNeurologyRabNeurology (clinical)exocytosisvesicular trafficking030217 neurology & neurosurgerycross-linkingFrontiers in neurology
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T cells mediate autoantibody-induced cutaneous inflammation and blistering in epidermolysis bullosa acquisita

2016

AbstractT cells are key players in autoimmune diseases by supporting the production of autoantibodies. However, their contribution to the effector phase of antibody-mediated autoimmune dermatoses, i.e., tissue injury and inflammation of the skin, has not been investigated. In this paper, we demonstrate that T cells amplify the development of autoantibody-induced tissue injury in a prototypical, organ-specific autoimmune disease, namely epidermolysis bullosa acquisita (EBA) – characterized and caused by autoantibodies targeting type VII collagen. Specifically, we show that immune complex (IC)-induced inflammation depends on the presence of T cells – a process facilitated by T cell receptor (…

0301 basic medicineEpidermolysis bullosa acquisitamedicine.medical_specialtyCollagen Type VIINeutrophilsT-LymphocytesGene ExpressionMice NudeInflammationAntigen-Antibody ComplexCell CommunicationEpidermolysis Bullosa AcquisitaArticleMice03 medical and health sciencesCricetulus0302 clinical medicinemedicineAnimalsHumansAutoantibodiesSkinAutoimmune diseaseMice Inbred BALB CMultidisciplinarybusiness.industryT-cell receptorAutoantibodyAntibodies MonoclonalReceptors Antigen T-Cell gamma-deltamedicine.diseaseNatural killer T cellDermatologyImmune complexMice Inbred C57BLDisease Models Animal030104 developmental biologyLymphatic systemImmunoglobulin GImmunologyNatural Killer T-CellsLymph NodesRabbitsmedicine.symptombusinessSpleenSignal Transduction030215 immunologyScientific Reports
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miRNA as New Regulatory Mechanism of Estrogen Vascular Action

2018

The beneficial effects of estrogen on the cardiovascular system have been reported extensively. In fact, the incidence of cardiovascular diseases in women is lower than in age-matched men during their fertile stage of life, a benefit that disappears after menopause. These sex-related differences point to sexual hormones, mainly estrogen, as possible cardiovascular protective factors. The regulation of vascular function by estrogen is mainly related to the maintenance of normal endothelial function and is mediated by both direct and indirect gene transcription through the activity of specific estrogen receptors. Some of these mechanisms are known, but many remain to be elucidated. In recent …

0301 basic medicineEstrogen receptorReview030204 cardiovascular system & hematologyBioinformaticsEpigenesis Geneticlcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5Spectroscopyestrogen receptorsGeneral MedicineComputer Science ApplicationsMenopauseReceptors EstrogenRNA InterferenceDisease Susceptibilitymedicine.drug_classCèl·lulesBiologyepigenetic regulationCatalysisCardiovascular Physiological PhenomenaInorganic Chemistry03 medical and health sciencesestradiolmicroRNAmedicineAnimalsHumansEpigeneticsPhysical and Theoretical ChemistryMolecular BiologyGenemiRNAReceptors d'hormonesMechanism (biology)Organic ChemistryEndothelial CellsEstrogensmedicine.diseaseMicroRNAs030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Gene Expression RegulationEstrogenBlood VesselsFunction (biology)Genètica
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Prevention of an increase in cortical ligand binding to AMPA receptors may represent a novel mechanism of endogenous brain protection by G-CSF after …

2016

PURPOSE Using G-CSF deficient mice we recently demonstrated neuroprotective properties of endogenous G-CSF after ischemic stroke. The present follow-up study was designed to check, whether specific alterations in ligand binding densities of excitatory glutamate or inhibitory GABAA receptors may participate in this effect. METHODS Three groups of female mice were subjected to 45 minutes of MCAO: wildtype, G-CSF deficient and G-CSF deficient mice substituted with G-CSF. Infarct volumes were determined after 24 hours and quantitative in vitro receptor autoradiography was performed using [3H]MK-801, [3H]AMPA and [3H]muscimol for labeling of NMDA, AMPA and GABAA receptors, respectively. Ligand b…

0301 basic medicineExcitotoxicityAMPA receptorPharmacologymedicine.disease_causeReceptors N-Methyl-D-AspartateNeuroprotectionBrain IschemiaMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDevelopmental NeuroscienceGranulocyte Colony-Stimulating FactormedicineAnimalsReceptors AMPAReceptorGABAA receptorGlutamate receptorReceptors GABA-ANeuroprotectionStroke030104 developmental biologynervous systemNeurologyMuscimolchemistryAutoradiographyNMDA receptorFemaleNeurology (clinical)030217 neurology & neurosurgeryRestorative Neurology and Neuroscience
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Annexin A2-Mediated Plasminogen Activation in Endothelial Cells Contributes to the Proangiogenic Effect of Adenosine A2A Receptors

2021

Adenosine A2A receptor mediates the promotion of wound healing and revascularization of injured tissue, in healthy and animals with impaired wound healing, through a mechanism depending upon tissue plasminogen activator (tPA), a component of the fibrinolytic system. In order to evaluate the contribution of plasmin generation in the proangiogenic effect of adenosine A2A receptor activation, we determined the expression and secretion of t-PA, urokinase plasminogen activator (uPA), plasminogen activator inhibitor-1 (PAI-1) and annexin A2 by human dermal microvascular endothelial cells stimulated by the selective agonist CGS-21680. The plasmin generation was assayed through an enzymatic assay a…

0301 basic medicineFarmacologiaAngiogenesisPlasminmedicine.medical_treatmentVasodilatadorsAdenosine A2A receptorRM1-950030204 cardiovascular system & hematologyTissue plasminogen activatormicrovascular endothelial cells03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFibrinolysismedicinePharmacology (medical)urokinase plasminogen activatorPharmacologytissue plasminogen activatorChemistryBrief Research Reportannexin A2adenosine receptorsCell biology030104 developmental biologyPlasminogen activator inhibitor-1plasminogen activator inhibitor-1Therapeutics. PharmacologyPlasminogen activatorProteïnesAnnexin A2medicine.drug
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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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