Search results for "Membrane glycoprotein"

showing 10 items of 312 documents

Expression and regulation by interferon-γ of the membrane-bound complement regulators CD46 (MCP), CD55 (DAF) and CD59 in gastrointestinal tumours

1999

The membrane-bound complement inhibitors CD46 (membrane cofactor protein), CD55 (decay-accelerating factor) and CD59 (protectin) protect tumour cells against lysis by activated complement. In this study, a total of 14 (3 gastric, 3 colonic and 8 pancreatic) gastrointestinal tumour cell lines were examined for the expression of CD46, CD55 and CD59 with respect to the regulatory efficacy of interferon-gamma (IFN-gamma). The effects of IFN-gamma on mRNA and protein expression levels of CD46, CD55 and CD59 were evaluated by Northern blot hybridisation, RT-PCR, flow cytometry and immunostaining. In unstimulated cell lines, CD46 and CD59 transcripts were expressed at comparable levels, whereas th…

Cancer Researchmedicine.medical_treatmentCD59 AntigensCD59BiologyMembrane Cofactor ProteinInterferon-gammaComplement inhibitorComplement Inactivator ProteinsAntigens CDmedicineHumansRNA MessengerNorthern blotGastrointestinal NeoplasmsComplement Inactivator ProteinsMembrane GlycoproteinsCD55 AntigensReverse Transcriptase Polymerase Chain ReactionCD46Blotting NorthernFlow CytometryBlotBlotting SouthernCytokineOncologyCancer researchImmunostainingEuropean Journal of Cancer
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Dendritic cell-tumor cell hybrids and immunotherapy: what's next?

2011

Dendritic cells (DC) are professional antigen-presenting cells currently being used as a cellular adjuvant in cancer immunotherapy strategies. Unfortunately, DC-based vaccines have not demonstrated spectacular clinical results. DC loading with tumor antigens and DC differentiation and activation still require optimization. An alternative technique for providing antigens to DC consists of the direct fusion of dendritic cells with tumor cells. These resulting hybrid cells may express both major histocompatibility complex (MHC) class I and II molecules associated with tumor antigens and the appropriate co-stimulatory molecules required for T-cell activation. Initially tested in animal models, …

Cancer Researchmedicine.medical_treatmentImmunologyAntigen-Presenting CellsHybrid CellsMajor histocompatibility complexAntigenCancer immunotherapyAntigens NeoplasmNeoplasmsmedicineImmunology and AllergyAnimalsHumansGenetics (clinical)TransplantationCell fusionMembrane GlycoproteinsbiologyHistocompatibility Antigens Class IHistocompatibility Antigens Class IICell BiologyDendritic cellImmunotherapyDendritic CellsCell biologyMembrane glycoproteinsDisease Models AnimalOncologybiology.proteinImmunotherapyAdjuvantCytotherapy
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Study of surface carbohydrates on isolated Golgi subfractions by fluorescent-lectin binding and flow cytometry

1995

The Golgi complex is a functionally heterogeneous subcellular structure that plays a key role in the synthesis, maturation, and sorting of newly synthesized glycoproteins. Fluorescent lectins have been used extensively to analyze surface glycoproteins by flow cytometry in whole cells and more recently in isolated subcellular organelles, such as mitochondria and chloroplasts. We report here the use of several fluorescein-isothiocyanate-conjugated lectins to detect and quantify specific surface sugars by flow cytometry on isolated elements from purified cis and trans-Golgi fractions from rat liver. Our results show that this approach may be useful to study Golgi composition and function, sinc…

CarbohydratesBiophysicsGolgi ApparatusPathology and Forensic MedicineFlow cytometrysymbols.namesakeEndocrinologyIsothiocyanatesLectinsOrganellemedicineAnimalsRats WistarFluorescent Dyeschemistry.chemical_classificationMembrane Glycoproteinsbiologymedicine.diagnostic_testIntracellular MembranesCell BiologyHematologyGolgi apparatusFlow CytometryWheat germ agglutininRatsChloroplastLiverBiochemistrychemistryConcanavalin Asymbolsbiology.proteinGlycoproteinFunction (biology)Protein BindingCytometry
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Protein targeting to the plasma membrane of adult skeletal muscle fiber: an organized mosaic of functional domains.

2001

The plasma membrane of differentiated skeletal muscle fibers comprises the sarcolemma, the transverse (T) tubule network, and the neuromuscular and muscle-tendon junctions. We analyzed the organization of these domains in relation to defined surface markers, beta-dystroglycan, dystrophin, and caveolin-3. These markers were shown to exhibit highly organized arrays along the length of the fiber. Caveolin-3 and beta-dystroglycan/dystrophin showed distinct, but to some extent overlapping, labeling patterns and both markers left transverse tubule openings clear. This labeling pattern revealed microdomains over the entire plasma membrane with the exception of the neuromuscular and muscle-tendon j…

Caveolin 3Muscle Fibers SkeletalNeuromuscular JunctionMuscle ProteinsProtein Sorting Signalsmedicine.disease_causeCaveolinsT-tubuleDystrophinMiceMembrane MicrodomainsViral Envelope ProteinsProtein targetingmedicineMyocyteAnimalsDystroglycansMuscle SkeletalGlycoproteinsSarcolemmaMembrane GlycoproteinsbiologyCell MembraneSkeletal muscleCell BiologyMolecular biologyTransport proteinCell biologyRatsCytoskeletal ProteinsProtein Transportmedicine.anatomical_structureTubulebiology.proteinFemaleDystrophinExperimental cell research
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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Growth control in mammalian cells by cell-cell contacts.

1990

Growth of normal diploid mammalian cells in vitro is strongly regulated by the actual cell density. Cell-cell contacts via specific plasma membrane glycoproteins whose glycan moieties interact with specific receptors has been found to be a main growth regulatory principle. Malignant growth is suggested to result from impaired function of these receptors.

Cell signalingGlycanbiologyCell divisionContact InhibitionHealth Toxicology and MutagenesisPublic Health Environmental and Occupational HealthContact inhibitionCell CommunicationPlatelet Membrane GlycoproteinsCell aggregationCell biologyMembrane glycoproteinsCell surface receptorbiology.proteinCell AdhesionHumansCell adhesionCell DivisionCell AggregationResearch ArticleEnvironmental health perspectives
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Distinct Signaling Cascades of TREM-1, TLR and NLR in Neutrophils and Monocytic Cells

2013

Triggering receptor expressed on myeloid cells 1 (TREM-1) is an important mediator of innate inflammatory responses in microbial infections and sepsis. TREM-1 ligation on neutrophils (PMN) or monocytes results in the production of proinflammatory cytokines. Engagement of TREM-1 induces the activation of MAP kinases as well as rapid Ca<sup>2+</sup> mobilization. However, a detailed understanding of TREM-1 signaling pathways is currently lacking. We evaluated the TREM-1 signaling hierarchy in monocytic cells and found that the acute myeloid leukemia cell line MUTZ-3 expresses TREM-1 in a natural and functional manner. We compared essential signaling molecules of the TREM-1, TLR an…

Cell signalingMyeloidNeutrophilsp38 Mitogen-Activated Protein KinasesMonocytesProinflammatory cytokinePhosphatidylinositol 3-KinasesCell Line TumormedicineHumansImmunology and AllergyCalcium SignalingReceptors ImmunologicExtracellular Signal-Regulated MAP KinasesPI3K/AKT/mTOR pathwayCalcium signalingMembrane GlycoproteinsChemistryToll-Like ReceptorsMyeloid leukemiaImmunity InnateTriggering Receptor Expressed on Myeloid Cells-1Cell biologyLeukemia Myeloid Acutemedicine.anatomical_structureOrgan SpecificityCell cultureImmunologyCytokinesInflammation MediatorsSignal transductionResearch ArticleJournal of Innate Immunity
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Regulation of the type II oncostatin M receptor expression in lung-derived epithelial cells

1998

AbstractOncostatin M (OSM) is a potent modulator of human lung-derived epithelial cell function. This cytokine binds two distinct receptor complexes: type I OSM receptor which is also a functional receptor for leukemia inhibitory factor (LIF), and type II OSM-specific receptor. The role of these two distinct receptors in mediating the response of individual cell types to OSM has not been delineated. In contrast to LIF, OSM induces synthesis of α1-antichymotrypsin and α1-antiproteinase inhibitor in lung-derived epithelial cells. The differential responsiveness to LIF and OSM suggested that the response of lung epithelial cells to OSM may be mediated by the OSM-specific receptor. Therefore, w…

Cell typemedicine.medical_treatmentTransforming growth factor β1Respiratory SystemBronchial epitheliumBiophysicsBronchiOncostatin MInterleukin 1 receptor type IILeukemia Inhibitory FactorBiochemistryDexamethasoneAntigens CDStructural BiologyCytokine Receptor gp130GeneticsmedicineHumansReceptors CytokineReceptorLungMolecular BiologyLymphokinesMembrane GlycoproteinsbiologyInterleukin-6ChemistryfungiOncostatin MOncostatin M receptorEpithelial CellsReceptors Oncostatin MCell BiologyGrowth InhibitorsCell biologyInterleukin 31CytokineGene Expression Regulationbiology.proteinCancer researchCytokinesInflammation MediatorsPeptidesLeukemia inhibitory factorFEBS Letters
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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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Extramedullary Expansion of Hematopoietic Progenitor Cells in Interleukin (IL)-6–sIL-6R Double Transgenic Mice

1997

Soluble cytokine receptors modulate the activity of their cognate ligands. Interleukin (IL)-6 in association with the soluble IL-6 receptor (sIL-6R) can activate cells expressing the gp130 signal transducer lacking the specific IL-6R. To investigate the function of the IL-6–sIL-6R complex in vivo and to discriminate the function of the IL-6–sIL-6R complex from the function of IL-6 alone, we have established a transgenic mouse model. Double-transgenic mice coexpressing IL-6 and sIL-6R were generated and compared with IL-6 and sIL-6R single-transgenic mice. The main phenotype found in IL-6–sIL-6R mice was a dramatic increase of extramedullary hematopoietic progenitor cells in liver and spleen…

Cellular differentiationmedicine.medical_treatmentImmunologyMice TransgenicCell SeparationBiologyArticleMiceAntigens CDCytokine Receptor gp130medicineAnimalsHumansImmunology and AllergyPeripheral blood cellInterleukin 6Interleukin 3Membrane GlycoproteinsInterleukin-6Body WeightInterleukinCell DifferentiationArticlesOrgan SizeFlow CytometryHematopoietic Stem CellsGlycoprotein 130ImmunohistochemistryMolecular biologyCell biologymedicine.anatomical_structureCytokineLiverbiology.proteinBone marrowCell DivisionSpleenSignal TransductionJournal of Experimental Medicine
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