Search results for "RECEPTORS"

showing 10 items of 3254 documents

The ubiquitin-specific protease USP8 is critical for the development and homeostasis of T cells

2015

The modification of proteins by ubiquitin has a major role in cells of the immune system and is counteracted by various deubiquitinating enzymes (DUBs) with poorly defined functions. Here we identified the ubiquitin-specific protease USP8 as a regulatory component of the T cell antigen receptor (TCR) signalosome that interacted with the adaptor Gads and the regulatory molecule 14-3-3β. Caspase-dependent processing of USP8 occurred after stimulation of the TCR. T cell-specific deletion of USP8 in mice revealed that USP8 was essential for thymocyte maturation and upregulation of the gene encoding the cytokine receptor IL-7Rα mediated by the transcription factor Foxo1. Mice with T cell-specifi…

Regulatory T cellT-LymphocytesImmunologyReceptors Antigen T-Cell610 Medicine & healthBiologyCD8-Positive T-LymphocytesJurkat cellsJurkat CellsMiceddc:570EndopeptidasesmedicineImmunology and AllergyAnimalsHomeostasisHumans10239 Institute of Laboratory Animal ScienceIL-2 receptorAdaptor Proteins Signal Transducing2403 ImmunologyReceptors Interleukin-7ThymocytesEndosomal Sorting Complexes Required for TransportForkhead Box Protein O1ZAP70T-cell receptorCD28Cell DifferentiationForkhead Transcription FactorsColitisCell biologyThymocytemedicine.anatomical_structure2723 Immunology and Allergy570 Life sciences; biology590 Animals (Zoology)Ubiquitin ThiolesteraseCD8
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Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation

2009

Abstract The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of IL-6 and paucity of Th1/Th2 cytokines skewed Tregs and effector T cells into IL-17–producing T cel…

Regulatory T cellmedicine.medical_treatmentCellular differentiationImmunologyPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicMast cell; T regulatory cell; Immune responseBiologyLymphocyte ActivationT-Lymphocytes RegulatoryBiochemistryImmune toleranceMiceMice CongenicmedicineImmune ToleranceMast CellT regulatory cellImmune responseCells CulturedCell ProliferationAnimalInterleukin-6Experimental autoimmune encephalomyelitisInterleukin-17hemic and immune systemsCell DifferentiationT lymphocyteT-Lymphocytes Helper-InducerHematologyCell BiologyReceptors OX40medicine.diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structureCytokineImmunologyAnimals; Cell Differentiation; Cell Proliferation; Cells Cultured; Immune Tolerance; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mast Cells; Membrane Glycoproteins; Mice; Mice Congenic; Mice Inbred C57BL; Mice Transgenic; Receptors OX40; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Hematology; Biochemistry; Cell Biology; ImmunologyInterleukin 17Membrane GlycoproteinTumor Necrosis FactorSignal Transduction
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The putative sponge aggregation receptor. Isolation and characterization of a molecule composed of scavenger receptor cysteine-rich domains and short…

1998

Porifera (sponges) are the oldest extant metazoan phylum. Dissociated sponge cells serve as a classic system to study processes of cell reaggregation. The reaggregation of dissociated cells is mediated by an extracellularly localized aggregation factor (AF), based on heterophilic interactions of the third order; the AF bridges two cells by ligating a cell-surface-bound aggregation receptor (AR). In the present study we report cloning, expression and immunohistochemical localization of a polypeptide from the marine sponge Geodia cydonium, which very likely represents the AR. The presumed AR gene gives rise to at least three forms of alternatively spliced transcripts of 6.5, 4.9 and 3.9 kb, a…

Repetitive Sequences Amino Acidmedicine.drug_classMolecular Sequence DataReceptors Cell SurfaceCell CommunicationMonoclonal antibodyPolymerase Chain Reactionlaw.inventionAntigenlawComplementary DNAConsensus SequencemedicineAnimalsAmino Acid SequenceCloning MolecularReceptors ImmunologicReceptorCell AggregationReceptors LipoproteinRepetitive Sequences Nucleic AcidReceptors ScavengerbiologyMolecular massBase SequenceSequence Homology Amino AcidMembrane ProteinsCell BiologySequence Analysis DNAScavenger Receptors Class BMolecular biologyRecombinant ProteinsPoriferaTransmembrane domainBiochemistrybiology.proteinRecombinant DNAAntibodyProtein Binding
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Establishment of an HIV cell-cell fusion assay by using two genetically modified HeLa cell lines and reporter gene.

2003

Infection of human cells with the human immunodeficiency virus type I (HIV-1) can be mimicked by a fusion process between cells expressing the HIV envelope protein (Env) and cells expressing both human CD4 together with the appropriate human chemokine receptors. In this study, a T-tropic HIV cell-cell fusion assay was established that utilized CD4, human CXCR4 and HIV NL4-3 gp160 as fusion components and a T7 polymerase-activated luciferase as a reporter system. The HeLa T4 cells used, expressed CD4 and CXCR4, and the applied HeLa KS386 cells expressed HIV NL4-3 gp160. By combining HeLa T4 cells with HeLa KS386 cells, an approximately about 100- to 300-fold increase in luciferase activity c…

Reporter geneReceptors CXCR4Cell fusionbiologyvirusesvirus diseasesHIV envelope proteinTransfectionGp41biology.organism_classificationTransfectionMolecular biologyGiant CellsHIV Envelope Protein gp160HeLaCell FusionCell cultureGenes ReporterVirologyCD4 AntigensHIV-1HumansLuciferaseBiological AssayHeLa CellsJournal of virological methods
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The peroxisome proliferator response element (PPRE) present at positions -681/-669 in the rat liver 3-ketoacyl-CoA thiolase B gene functionally inter…

2000

Although previous data showed that the putative thiolase B PPRE located at -681/-669 bind the PPARalpha-RXRalpha heterodimer in vitro (Kliewer et al. (1992) Nature 358, 771-774), there is no evidence about the functional role of this element. By gel mobility-shift assay, we found an interaction of this PPRE with not only PPARalpha but also with HNF-4. By transfection of cells with the putative PPRE-driven luciferase reporter vector and PPARalpha, we found no significant activation of the luciferase gene expression, in contrast to the case with reporter expression driven by the PPRE of the peroxisomal bifunctional enzyme. On the other hand, HNF-4 activated the luciferase gene expression driv…

Response elementBiophysicsReceptors Cytoplasmic and NuclearBiologyTransfectionBiochemistryDNA-binding proteinPeroxisomal Bifunctional EnzymeGenes ReporterGene expressionAnimalsMolecular BiologyGeneDNA PrimersBase SequenceThiolaseCell BiologyTransfectionDNAAcetyl-CoA C-AcyltransferasePhosphoproteinsMolecular biologyRatsDNA-Binding ProteinsHepatocyte nuclear factor 4Hepatocyte Nuclear Factor 4LiverCOS CellsPeroxisome ProliferatorsTranscription FactorsBiochemical and biophysical research communications
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Cloning of a novel putative G-protein-coupled receptor (NLR) which is expressed in neuronal and lymphatic tissue.

1993

AbstractA novel G-protein-coupled receptor was isolated from mouse and rat neuronal and lymphatic tissues. The amino acid sequence of the rat receptor (rNLR) shows an overall homology of 80% to a recently cloned receptor from Burkitt's lymphoma cells (BLR1) which is exclusively expressed in lymphatic tissues [(1992) Eur. J. Immunol. 22, 2795]. Much less homology between rNLR and BLR1 was observed at the N-terminus (about 40%), whereas rNLR and the mouse homologue mNLR show 92% amino acid identity. Northern blot analysis of NLR revealed a predominant 5.5 kb mRNA species in various brain regions and neuronal cell lines, whereas in the spleen a 3 kb transcript is predominant. This distribution…

Restriction MappingInterleukin 8BiochemistryReceptors G-Protein-CoupledMiceStructural BiologyTumor Cells CulturedLymphocytesCloning MolecularReceptorPeptide sequencechemistry.chemical_classificationNeuronsGenomic LibraryBurkitt's lymphomaBrainBurkitt LymphomaPolymerase chain reactionAmino acidOligodeoxyribonucleotidesOrgan SpecificityG-protein-coupled receptorBLR1Molecular Sequence DataBiophysicsReceptors Cell SurfaceBiologyNLRGTP-Binding ProteinsComplementary DNAGeneticsmedicineAnimalsHumansNorthern blotAmino Acid SequenceRNA MessengerMolecular BiologyG protein-coupled receptorMessenger RNABase SequenceSequence Homology Amino AcidCell Biologymedicine.diseaseMolecular biologyIntronsRatsNG108-15 cellchemistryBurkitt's lymphomaFEBS letters
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A new vicious cycle involving glutamate excitotoxicity, oxidative stress and mitochondrial dynamics

2011

Glutamate excitotoxicity leads to fragmented mitochondria in neurodegenerative diseases, mediated by nitric oxide and S-nitrosylation of dynamin-related protein 1, a mitochondrial outer membrane fission protein. Optic atrophy gene 1 (OPA1) is an inner membrane protein important for mitochondrial fusion. Autosomal dominant optic atrophy (ADOA), caused by mutations in OPA1, is a neurodegenerative disease affecting mainly retinal ganglion cells (RGCs). Here, we showed that OPA1 deficiency in an ADOA model influences N-methyl-D-aspartate (NMDA) receptor expression, which is involved in glutamate excitotoxicity and oxidative stress. Opa1enu/+mice show a slow progressive loss of RGCs, activation …

Retinal Ganglion CellsCancer ResearchReceptor expressionExcitotoxicityApoptosisNeurodegenerativeMitochondrionEyemedicine.disease_causeGTP PhosphohydrolasesMice0302 clinical medicineReceptorsoxidative stressPhosphorylationbcl-2-Associated X Protein0303 health sciencesbiologyGlutamate receptorMitochondriaUp-RegulationCell biologymitochondrial fusionAutosomal DominantOriginal Articlebcl-Associated Death ProteinMitochondrial fissionN-Methyl-D-AspartateBiotechnologymitochondrial fragmentationOncology and CarcinogenesisImmunologybcl-X ProteinSOD2Glutamic AcidReceptors N-Methyl-D-AspartateNMDA receptorsCell Line03 medical and health sciencesCellular and Molecular NeuroscienceBcl-2-associated X proteinOptic Atrophy Autosomal DominantmedicineAnimalsEye Disease and Disorders of Vision030304 developmental biologySuperoxide DismutaseNeurosciencesCell BiologyMolecular biologyeye diseasesOxidative StressOptic AtrophyMutationbiology.proteinOPA1 mutationBiochemistry and Cell Biologysense organsglutamate excitotoxicity030217 neurology & neurosurgeryCell Death & Disease
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Connecting temporal identity to mitosis: the regulation of Hunchback in Drosophila neuroblast lineages.

2006

Both in vertebrates and invertebrates, neural stem cells generate different cell types at different times during development. It has been suggested that this process depends on temporal identity transitions of neural progenitors, but the underlying mechanism has not been resolved, yet. Recently, Drosophila neuroblasts (NBs) have been shown to be an excellent model system to investigate this subject. Here, changes in temporal identity are regulated by sequential and transient expression of transcription factors in the NB, such as Hunchback (Hb) and Kruppel (Kr). The temporal expression profile is maintained in the progeny. Hb is expressed first and thus defines the earliest identity in a giv…

Retinal Ganglion CellsCell typeReceptors SteroidKruppel-Like Transcription FactorsDown-RegulationMitosisNerve Tissue ProteinsBiologyCell fate determinationKrüppelNeuroblastAnimalsDrosophila ProteinsNuclear export signalMolecular BiologyMitosisTranscription factorGeneticsNeuronsModels GeneticNuclear ProteinsCell DifferentiationCell BiologyNeural stem cellDNA-Binding ProteinsProtein BiosynthesisDrosophilaDevelopmental BiologyTranscription FactorsCell cycle (Georgetown, Tex.)
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Mutation Analysis Identifies GUCY2D as the Major Gene Responsible for Autosomal Dominant Progressive Cone Degeneration

2008

PURPOSE. Heterozygous mutations in the GUCY2D gene, which encodes the membrane-bound retinal guanylyl cyclase-1 protein (RetGC-1), have been shown to cause autosomal dominant inherited cone degeneration and cone–rod degeneration (adCD, adCRD). The present study was a comprehensive screening of the GUCY2D gene in 27 adCD and adCRD unrelated families of these rare disorders. METHODS. Mutation analysis was performed by direct sequencing as well as PCR and subsequent restriction length polymorphism analysis (PCR/RFLP). Haplotype analysis was performed in selected patients by using microsatellite markers. RESULTS. GUCY2D gene mutations were identified in 11 (40%) of 27 patients, and all mutation…

Retinal degenerationMaleDNA Mutational AnalysisReceptors Cell SurfaceBiologyPolymerase Chain ReactionArticlemedicineElectroretinographyMissense mutationHumansGenetic Predisposition to DiseaseCodonGeneGeneticsHaplotypeRetinal DegenerationDNAmedicine.diseasePrognosisRod Cell Outer SegmentMajor geneMolecular biologyPedigreeHaplotypesGuanylate CyclaseMutationMutation testingDisease ProgressionGUCY2DFemaleRestriction fragment length polymorphism
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The existence of FGFR1-5-HT1A receptor heterocomplexes in midbrain 5-HT neurons of the rat: relevance for neuroplasticity.

2012

The ascending midbrain 5-HT neurons to the forebrain may be dysregulated in depression and have a reduced trophic support. Within situproximity ligation assay (PLA) and supported by coimmunoprecipitation and colocation of the FGFR1 and 5-HT1A immunoreactivities in the midbrain raphe cells, evidence for the existence of FGFR1–5-HT1A receptor heterocomplexes in the dorsal and median raphe nuclei of the Sprague Dawley rat as well as in the rat medullary raphe RN33B cells has been obtained. Especially after combined FGF-2 and 8-OH-DPAT treatment, a marked and significant increase in PLA clusters was found in the RN33B cells. Similar results were reached with the FRET technique in HEK293T cells,…

Retractedmedicine.medical_specialtySerotonin receptorsEncèfalSettore BIO/11 - Biologia MolecolareBiologySettore BIO/09 - FisiologiaReceptors de serotoninaMidbrainInternal medicineRatesmedicineReceptor5-HT receptorNeuronal Plasticity Receptor Fibroblast Growth Factor Receptor Serotonin 5-HT1A Serotonergic Neurons SerotoninRapheGeneral NeuroscienceEncephalonFibroblastsRatsEndocrinologymedicine.anatomical_structurenervous systemForebrainAutoreceptor5-HT1A receptorNeuron
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