Search results for " cell surface"

showing 10 items of 154 documents

DOES LEPTIN PLAY A CYTOKINE-LIKE ROLE WITHIN THE AIRWAYS OF COPD PATIENTS?

2005

The leptin-leptin receptor system might be up-regulated in the airways of chronic obstructive pulmonary disease (COPD). In bronchial biopsies obtained from normal subjects and smokers, with and without COPD, the present study examined leptin and leptin-receptor expression and their co-localisation in airway and inflammatory cells. Combining immunohistochemistry with terminal deoxynucleotidyl transferase dUTP nick end-labelling techniques, apoptosis in airway and inflammatory cells and in leptin and leptin-receptor expressing cells was investigated. In the epithelial cells both leptin and leptin-receptor expression was higher in normal subjects than in smokers and COPD subjects. By contrast,…

Pulmonary and Respiratory MedicineAdultLeptinMalemedicine.medical_specialtyCopd patientsmedicine.medical_treatmentT-LymphocytesApoptosisBronchiReceptors Cell SurfaceRespiratory MucosaPulmonary Disease Chronic ObstructiveInternal medicineBiopsyMedicineHumansAgedCOPDmedicine.diagnostic_testbusiness.industryLeptindigestive oral and skin physiologyRespiratory diseaseSmokingrespiratory systemMiddle Agedmedicine.diseaseObstructive lung diseaserespiratory tract diseasesRespiratory Function TestsEndocrinologyCytokineTerminal deoxynucleotidyl transferaseCase-Control StudiesImmunologyPhysical therapyReceptors LeptinFemalebusinesshormones hormone substitutes and hormone antagonistsCD8
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EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

2005

Abstract The EBV-induced gene 3 (EBI3) is expressed in dendritic cells (DCs) and part of the cytokine IL-27 that controls Th cell development. However, its regulated expression in DCs is poorly understood. In the present study we demonstrate that EBI3 is expressed in splenic CD8−, CD8+, and plasmacytoid DC subsets and is induced upon TLR signaling. Cloning and functional analysis of the EBI3 promoter using in vivo footprinting and mutagenesis showed that stimulation via TLR2, TLR4, and TLR9 transactivated the promoter in primary DCs via NF-κB and Ets binding sites at −90 and −73 bp upstream of the transcriptional start site, respectively. Furthermore, we observed that NF-κB p50/p65 and PU.1…

RNA Capsmedicine.medical_treatmentDNA Mutational AnalysisMolecular Sequence DataImmunologyAntigen-Presenting CellsReceptors Cell SurfaceBiologyCell LineMinor Histocompatibility AntigensJurkat CellsMiceCell Line TumorGene expressionmedicineAnimalsHumansImmunology and AllergyReceptors CytokinePromoter Regions GeneticGlycoproteinsMice KnockoutMembrane GlycoproteinsInnate immune systemBase SequenceToll-Like ReceptorsHEK 293 cellsNF-kappa BTLR9hemic and immune systemsEBI3Dendritic CellsMolecular biologyToll-Like Receptor 2Up-RegulationMice Inbred C57BLToll-Like Receptor 4Protein SubunitsTLR2CytokineGene Expression RegulationToll-Like Receptor 9NIH 3T3 CellsTLR4Protein BindingSignal TransductionThe Journal of Immunology
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Endothelial cells and normal breast epithelial cells enhance invasion of breast carcinoma cells by CXCR-4-dependent up-regulation of urokinase-type p…

2008

Here we show the increase of invasion of three breast cancer cell lines (8701-BC, MDA-MB-231 and SKBR3) upon long-term co-incubation with culture medium of normal microvascular endothelial cells (MVEC) and normal breast epithelial cells (HB2). The enhancement of invasion relied on the interaction of microvascular endothelial cell and normal breast epithelial cell CXCL12 (SDF1) chemokine, whose expression by breast cancer cells was very low, with the cognate CXCR4 receptor of malignant cells, which resulted in over-expression of the urokinase-type plasminogen activator receptor (uPAR) on their surfaces. uPAR over-expression, showed by RT-PCR and Western blotting, was paralleled by increased …

Receptors CXCR4MAP Kinase Kinase 4AngiogenesisCellBreast NeoplasmsReceptors Cell SurfaceCell CommunicationBiologyCell LineReceptors Urokinase Plasminogen ActivatorPathology and Forensic MedicineMetastasisangiogenesisbreast cancerTumor Cells CulturedmedicineHumansNeoplasm InvasivenessBreastSettore BIO/06 - Anatomia Comparata E CitologiaPhosphorylationskin and connective tissue diseasesCXCR4Settore MED/04 - Patologia GeneraleNeovascularization PathologicReverse Transcriptase Polymerase Chain ReactionFibrinolysisEpithelial CellsCXCL12invasionmedicine.diseasemicroenvironmentChemokine CXCL12Neoplasm ProteinsUp-RegulationEndothelial stem cellUrokinase receptormedicine.anatomical_structureCulture Media ConditionedCancer cellCancer researchFemaleJNKEndothelium VascularBreast diseaseSDF1uPARPlasminogen activatorThe Journal of Pathology
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PAR1 signaling regulates the retention and recruitment of EPCR-expressing bone marrow hematopoietic stem cells

2015

Retention of long-term repopulating hematopoietic stem cells (LT-HSCs) in the bone marrow is essential for hematopoiesis and for protection from myelotoxic injury. We report that signaling cascades that are traditionally viewed as coagulation related also control retention of endothelial protein C receptor-positive (EPCR(+)) LT-HSCs in the bone marrow and their recruitment to the blood via two pathways mediated by protease activated receptor 1 (PAR1). Thrombin-PAR1 signaling induces nitric oxide (NO) production, leading to EPCR shedding mediated by tumor necrosis factor-α-converting enzyme (TACE), enhanced CXCL12-CXCR4-induced motility and rapid stem and progenitor cell mobilization. Conver…

Receptors CXCR4Receptors Cell SurfaceADAM17 ProteinIntegrin alpha4beta1BiologyNitric OxideArticleGeneral Biochemistry Genetics and Molecular BiologyMiceBone MarrowCell MovementCell AdhesionmedicineAnimalsReceptor PAR-1Progenitor cellcdc42 GTP-Binding ProteinCell adhesionEndothelial protein C receptorThrombinEndothelial Protein C ReceptorGeneral MedicineHematopoietic Stem CellsChemokine CXCL12Cell biologyMice Inbred C57BLTransplantationADAM ProteinsHaematopoiesismedicine.anatomical_structureCdc42 GTP-Binding ProteinImmunologyBone marrowStem cellProtein CSignal TransductionNature Medicine
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Alcadein cleavages by amyloid beta-precursor protein (APP) alpha- and gamma-secretases generate small peptides, p3-Alcs, indicating Alzheimer disease…

2009

Alcadeins (Alcs) constitute a family of neuronal type I membrane proteins, designated Alc(alpha), Alc(beta), and Alc(gamma). The Alcs express in neurons dominantly and largely colocalize with the Alzheimer amyloid precursor protein (APP) in the brain. Alcs and APP show an identical function as a cargo receptor of kinesin-1. Moreover, proteolytic processing of Alc proteins appears highly similar to that of APP. We found that APP alpha-secretases ADAM 10 and ADAM 17 primarily cleave Alc proteins and trigger the subsequent secondary intramembranous cleavage of Alc C-terminal fragments by a presenilin-dependent gamma-secretase complex, thereby generating "APP p3-like" and non-aggregative Alc pe…

Receptors Cell SurfaceADAM17 ProteinBiochemistryPresenilinCell LineADAM10 ProteinAmyloid beta-Protein PrecursorMiceAlzheimer Diseasemental disordersAmyloid precursor proteinmedicineAnimalsHumansReceptorMolecular BiologyPeptide sequencechemistry.chemical_classificationbiologyProtein Synthesis Post-Translational Modification and DegradationCalcium-Binding ProteinsMembrane ProteinsCell Biologymedicine.diseaseMolecular biologyAmino acidProtease NexinsADAM ProteinsMembrane proteinchemistrybiology.proteinAlzheimer's diseaseAmyloid Precursor Protein SecretasesPeptidesAmyloid precursor protein secretaseThe Journal of biological chemistry
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Inhibition of GABA and benzodiazepine receptor binding by penicillins.

1980

Penicillins are thought to be GABA receptor antagonists. In order to determine the affinities of various penicillin derivatives for the GABA receptor, their potencies as inhibitors of specific [3H]GABA binding to rat brain membranes were investigated. All investigated penicillins inhibit specific [3H]GABA binding, with IC50 values ranging from 2 to 60 mM. The results are consistent with the assumption that penicillins are weak GABA receptor antagonists.

Receptors Cell SurfaceFlunitrazepamPenicillinsPharmacologygamma-Aminobutyric acidBenzodiazepinesStructure-Activity RelationshipGABA receptorpolycyclic compoundsmedicineStructure–activity relationshipAnimalsgamma-Aminobutyric AcidBenzodiazepine receptor bindingChemistryGeneral NeuroscienceBrainGABA receptor antagonistReceptors GABA-AAffinitiesRatsPenicillinnervous systemBiochemistryFlunitrazepammedicine.drugNeuroscience letters
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Adhesion of 8701-BC breast cancer cells to type V collagen and 67 kDa receptor

1992

Ductal infiltration carcinomas (d.i.c.) of the breast are potentially highly metastatic tumours, associated with drastic alterations of the architecture and molecular composition of the extracellular matrix at the tumour-host interface. 8701-BC, a recently characterized cell line, isolated from primary d.i.c., was used to study different aspects of tumor cell-substratum interactions. Since type V collagen deposition is augmented in d.i.c. we have examined the ability of 8701-BC cells to interact with this collagen species. We have found that cell binding to type V collagen was mediated by protein homologous to the 67 kDa laminin receptor (67-R). This conclusion is substantiated by the follo…

Receptors CollagenbiologyIntegrinMammary Neoplasms ExperimentalLactoseReceptors Cell SurfaceCell BiologyMolecular biologyChromatography AffinityCollagen receptorExtracellular matrixCollagen type I alpha 167 kDa Laminin ReceptorMembrane proteinCell AdhesionTumor Cells Culturedbiology.proteinAnimalsCollagenCell adhesionReceptorJournal of Cell Science
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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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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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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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