Search results for " glycoprotein"

showing 10 items of 430 documents

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
researchProduct

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
researchProduct

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
researchProduct

NF-κB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling

2018

NF-κB inducing kinase (NIK) is the key protein of the non-canonical NF-κB pathway and is important for the development of lymph nodes and other secondary immune organs. We elucidated the specific role of NIK in T cells using T-cell specific NIK-deficient (NIKΔT) mice. Despite showing normal development of lymphoid organs, NIKΔT mice were resistant to induction of CNS autoimmunity. T cells from NIKΔT mice were deficient in late priming, failed to up-regulate T-bet and to transmigrate into the CNS. Proteomic analysis of activated NIK-/- T cells showed de-regulated expression of proteins involved in the formation of the immunological synapse: in particular, proteins involved in cytoskeleton dy…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesT cellPrimary Cell CultureImmunologyReceptors Antigen T-CellPriming (immunology)Protein Serine-Threonine KinasesBiologyLymphocyte ActivationImmunological synapseMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsImmunology and AllergyProtein kinase BAdaptor Proteins Signal TransducingMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinasePhospholipase C gammaGene Expression ProfilingZAP70T-cell receptorMembrane ProteinsPhosphoproteinsActinsPeptide FragmentsCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisMyelin-Oligodendrocyte GlycoproteinLymph NodesSignal transductionT-Box Domain ProteinsProto-Oncogene Proteins c-aktSpleenSignal TransductionJournal of Autoimmunity
researchProduct

A critical role for the cholesterol-associated proteolipids PLP and M6B in myelination of the central nervous system.

2012

The formation of central nervous system myelin by oligodendrocytes requires sterol synthesis and is associated with a significant enrichment of cholesterol in the myelin membrane. However, it is unknown how oligodendrocytes concentrate cholesterol above the level found in nonmyelin membranes. Here, we demonstrate a critical role for proteolipids in cholesterol accumulation. Mice lacking the most abundant myelin protein, proteolipid protein (PLP), are fully myelinated, but PLP-deficient myelin exhibits a reduced cholesterol content. We therefore hypothesized that "high cholesterol" is not essential in the myelin sheath itself but is required for an earlier step of myelin biogenesis that is f…

Central Nervous SystemProteolipid protein 1Nerve Tissue ProteinsBiologyCell Line03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compoundMyelinMice0302 clinical medicineimmune system diseasesmedicineEvoked Potentials Auditory Brain StemAnimalsMyelin Proteolipid ProteinMyelin Sheath030304 developmental biology0303 health sciencesMembrane GlycoproteinsCholesterolProteolipidsLeukodystrophyPelizaeus–Merzbacher diseasemedicine.diseaseOligodendrocytenervous system diseasesMyelin proteolipid proteinmedicine.anatomical_structureCholesterolnervous systemNeurologychemistryBiochemistryEvoked Potentials Visuallipids (amino acids peptides and proteins)Vomeronasal Organ030217 neurology & neurosurgeryGlia
researchProduct

Exacerbated experimental autoimmune encephalomyelitis in mast-cell-deficient KitW-sh/W-sh mice

2011

Mast cell (MC)-deficient c-Kit mutant Kit(W/W-v) mice are protected against experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, suggesting a detrimental role for MCs in this disease. To further investigate the role of MCs in EAE, we took advantage of a recently characterized model of MC deficiency, Kit(W-sh/W-sh). Surprisingly, we observed that myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE was exacerbated in Kit(W-sh/W-sh) compared with Kit(+/+) mice. Kit(W-sh/W-sh) mice showed more inflammatory foci in the central nervous system (CNS) and increased T-cell response against myelin. To understand whether the discrepant results obtaine…

Central Nervous SystemT-LymphocytesEncephalomyelitisexperimental autoimmune encephalomyelitismast cellsInbred C57BLSeverity of Illness IndeximmunologyMiceMyelinPeptide Fragmentimmune system diseasesMast CellEncephalomyelitisMyelin SheathbiologyExperimental autoimmune encephalomyelitisMast cellProto-Oncogene Proteins c-kitPhenotypemedicine.anatomical_structuremastcell-deficient miceBone Marrow Cellgenetics/immunology/pathology/prevention /&/ controlc-kit mutationsc-kit mutations; experimental autoimmune encephalomyelitis; granulocytes; mast cellsEncephalomyelitis Autoimmune ExperimentalCentral nervous systemBone Marrow CellsPathology and Forensic MedicineMyelin oligodendrocyte glycoproteinExperimentalAnimals Antibody Formation Bone Marrow Cells; pathology Central Nervous System; pathology Encephalomyelitis; Autoimmune; Experimental; genetics/immunology/pathology/prevention /&/ control Glycoproteins; immunology Granulocytes; pathology Immunization Mast Cells; pathology Mice Mice; Inbred C57BL Mutation Myelin Sheath; immunology Myelin-Oligodendrocyte Glycoprotein Peptide Fragments; immunology Phenotype Proto-Oncogene Proteins c-kit; deficiency/genetics/metabolism Severity of Illness Index T-Lymphocytes; pathologyAntigendeficiency/genetics/metabolismmedicineAnimalsMolecular BiologyGlycoproteinsAnimalMultiple sclerosismast-cell-deficient Kit W-sh/W-sh mice.Experimental autoimmune encephalomyelitis; mast-cell-deficient Kit W-sh/W-sh mice.GranulocytegranulocytesCell Biologymedicine.diseaseEncephalomyelitiExperimental autoimmune encephalomyelitiPeptide FragmentsMice Inbred C57BLT-LymphocyteAntibody FormationMutationImmunologybiology.proteinexperimental autoimmune encephalomyelitis; mastcell-deficient mice; mast cellspathologyImmunizationMyelin-Oligodendrocyte GlycoproteinGlycoproteinAutoimmuneLaboratory Investigation
researchProduct

Anandamide-induced apoptosis in Chang liver cells involves ceramide and JNK/AP-1 pathway

2006

In the present study we demonstrate that anandamide, the most important endogenous cannabinoid, markedly induced apoptosis in Chang liver cells, an immortalized non-tumor cell line derived from normal liver tissue, while it induced only modest effects in a number of hepatoma cell lines. The apoptotic effect was reduced by methyl-beta-cyclodextrin, a membrane cholesterol depletor, suggesting an interaction between anandamide and the membrane microdomains named lipid rafts. Anandamide effects were mediated by the production of ceramide, as demonstrated by experiments performed with the sphingomyelinase inhibitor, desipramine, or with the sphingomyelinase activator, melittin. This conclusion w…

CeramideProgrammed cell deathFas Ligand ProteinCell SurvivalPolyunsaturated AlkamidesLiver cytologyp38 mitogen-activated protein kinasesBlotting WesternApoptosisArachidonic AcidsBiologyCeramidesCell LineMembrane Potentialschemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsGeneticsHumansEnzyme InhibitorsMembrane GlycoproteinsBcl-2-Like Protein 11Dose-Response Relationship DrugDesipramineJNK Mitogen-Activated Protein KinasesMembrane ProteinsFree Radical ScavengersGeneral MedicineAnandamideEndocannabinoid systemAcetylcysteineCell biologyEnzyme ActivationTranscription Factor AP-1cannabinoids apoptosis tumor cells JNK/AP1LiverchemistryApoptosisCaspasesMitochondrial MembranesTumor Necrosis FactorsApoptosis Regulatory ProteinsSphingomyelinEndocannabinoidsSignal TransductionInternational Journal of Molecular Medicine
researchProduct

Cascades of transcriptional induction during dendritic cell maturation revealed by genome-wide expression analysis.

2003

Dendritic cells (DC) are central regulators of immunity. Signal-induced maturation of DCs is assumed to be the starting point for specific immune responses. To further understand this process, we analyzed the alteration of transcript profiles along the time course of CD40 ligand-induced maturation of human myeloid DCs by Affymetrix GeneChip microarrays covering >6800 genes. Besides rediscovery of genes already described as associated with DC maturation proving reliability of the methods used, we identified clusterin as novel maturation marker. Looking across the time course, we observed synchronized kinetics of distinct functional groups of molecules whose temporal coregulation underscores …

ChemokineTime FactorsMicroarrayTranscription GeneticCell Survivalmedicine.medical_treatmentImmunoglobulinsBiochemistryMiceAntigens CDGeneticsmedicineAnimalsHumansMolecular BiologyGeneCells CulturedOligonucleotide Array Sequence AnalysisMembrane GlycoproteinsClusterinbiologyGenome HumanReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingDendritic cell3T3 CellsDendritic CellsFlow CytometryMolecular biologyCell biologyGene expression profilingCytokinebiology.proteinB7-1 AntigenRNAB7-2 AntigenDNA microarrayBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
researchProduct

Toll-like receptor 2 is dispensable for acquired host immune resistance to Candida albicans in a murine model of disseminated candidiasis

2004

Previous work by our group showed that Toll-like receptor 2 (TLR2) is essential for activation of innate immunity, playing a major role in the response of macrophages to Candida albicans, triggering cytokine and chemokine expression, and therefore TLR2 -/- mice are more susceptible to systemic primary candidiasis. In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the…

Chemokinemedicine.medical_treatmentImmunologyReceptors Cell SurfaceMicrobiologyMicrobiologyInterferon-gammaMiceCandida albicansmedicineAnimalsCandida albicansAntibodies FungalMice KnockoutToll-like receptorMembrane GlycoproteinsInnate immune systembiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisbiology.organism_classificationDisseminated CandidiasisInterleukin-12Immunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLTLR2Infectious DiseasesCytokineImmunoglobulin GImmunologybiology.proteinCytokinesMicrobes and Infection
researchProduct

Toll-like receptor-2 is essential in murine defenses against Candida albicans infections

2004

In this work, we studied the role of toll-like receptor-2 (TLR2) in murine defenses against Candida albicans. TLR2-deficient mice experimentally infected intraperitoneally (i.p.) or intravenously (i.v.) in vivo had very significant impaired survival compared with that of control mice. In vitro production of TNF-alpha and macrophage inhibitory protein-2 (MIP-2) by macrophages from TLR2-/- mice in response to yeasts and hyphae of C. albicans were significantly lower (80% and 40%, respectively; P <0.05) than production by macrophages from wild-type mice. This impaired production of TNF-alpha and MIP-2 probably contributed to the 41% decreased recruitment of neutrophils to the peritoneal cavity…

Chemokinemedicine.medical_treatmentPhagocytosisChemokine CXCL2ImmunologyHyphaeCell CountReceptors Cell SurfaceMicrobiologyMicrobiologyMicePhagocytosisIn vivoCandida albicansmedicineAnimalsMacrophageCandida albicansCells CulturedMice KnockoutToll-like receptorMembrane GlycoproteinsbiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisFlow Cytometrybiology.organism_classificationImmunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLDisease Models AnimalInfectious DiseasesCytokineMacrophages Peritonealbiology.proteinChemokinesReactive Oxygen SpeciesMicrobes and Infection
researchProduct