Search results for "glycoproteins"

showing 10 items of 496 documents

[Post-translational regulation of N-glycosylated proteins expression in human intestinal cells in culture].

1991

International audience; HT-29 cells derived from a human colonic adenocarcinoma, can express a typical intestinal differentiation. Undifferentiated HT-29 cells accumulate N-linked glycoproteins substituted with unprocessed carbohydrate chains before to degrade them. Conversely, carbohydrate chains of N-linked glycoproteins are classically processed in differentiated HT-29 cells. The instability of N-linked glycoproteins in undifferentiated HT-29 cells is due to their rapid delivery from the endoplasmic reticulum to a compartment with lysosomal characteristics. This catabolitic pathway involves a bypass of the Golgi apparatus.

Cell Transformation NeoplasticDrug StabilityLeupeptinsPolysaccharides[ CHIM.ORGA ] Chemical Sciences/Organic chemistry[CHIM.ORGA]Chemical Sciences/Organic chemistryColonic NeoplasmsTumor Cells CulturedHumansAdenocarcinoma[CHIM.ORGA] Chemical Sciences/Organic chemistryProtein Processing Post-TranslationalGlycoproteins
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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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Differential regulation of the clusterin gene by Ha-ras and c-myc oncogenes and during apoptosis

1998

Clusterin (ApoJ) is an extracellular glycoprotein expressed during processes of tissue differentiation and regression that involve programmed cell death (apoptosis). Increased clusterin expression has also been found in tumors, however, the mechanism underlying this induction is not known. Apoptotic processes in tumors could be responsible for clusterin gene activation. Alternatively, oncogenic mutations could modulate signal transduction, thereby inducing the gene. We examined the response of the rat clusterin gene to two oncogenes, Ha-ras and c-myc, in transfected Rat1 fibroblasts. While c-myc overexpression did not modify clusterin gene activity, the Ha-ras oncogene produced a seven to t…

Cell signalingProgrammed cell deathUltraviolet RaysPhysiologyRecombinant Fusion ProteinsClinical BiochemistryGenes mycApoptosisDNA FragmentationBiologyTransfectionProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)AnimalsRNA MessengerCell Line TransformedGlycoproteinsOncogeneClusterinCell CycleCell BiologyTransfectionFibroblastsCell cycleeye diseasesRatsClusterinGenes rasApoptosisMutationCancer researchbiology.proteinsense organsSignal transductionMolecular ChaperonesSignal TransductionJournal of Cellular Physiology
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Immunohistochemical location of HPL, SP1 and β-HCG in normal placentas of varying gestational age

1986

Sixty-four placentas at various gestational ages were examined by immunohistochemical stains for HPL, SP1 and beta-HCG according to a modified PAP method (Sternberger 1970). Syncytiotrophoblast cell layer was identified as the main site of synthesis. Extravillous immunohistochemical reactions for HPL and SP1 (but not for beta-HCG) were found in X-cells of the basal plate and in the intervillous trophoblast islands. These cell types would thus seem to be derived from trophoblast. Hofbauer-cells of villous connective tissue stained specifically for beta-HCG apparently because of HCG phagocytosis. The intensity of staining for HPL, SP1 and beta-HCG was evaluated semiquantitatively in the syncy…

Cell typeTime FactorsPlacentaBasal plate (neural tube)Connective tissuePregnancy ProteinsBiologyChorionic GonadotropinImmunoenzyme TechniquesAndrologySyncytiotrophoblastPregnancymedicineHumansreproductive and urinary physiologyStaining and LabelingHistocytochemistryPregnancy-Specific beta 1-GlycoproteinsObstetrics and GynecologyGestational ageTrophoblastGeneral MedicinePlacental Lactogenfemale genital diseases and pregnancy complicationsTrophoblastsStainingmedicine.anatomical_structureembryonic structuresImmunologyImmunohistochemistryFemaleChorionic VilliArchives of Gynecology
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Multiple signal transduction pathways regulate clusterin (gp 80) gene expression in MDCK cells

1996

ABSTRACT Clusterin (gp 80, apolipoprotein J, TRPM-2) is a widely expressed multifunctional glycoprotein. Its demonstrated and proposed functions include the transport of lipids and membrane fragments, the inhibition of the cytolytic action of the terminal complement complex and the modulation of cell—cell interactions. The expression of the gene is enhanced during tissue injury and remodelling and by hormone-withdrawal-induced apoptosis of prostate and mammary cells. We show here that, in the kidney-derived epithelial cell line MDCK, clusterin mRNA is repressed by glucocorticoids and by progesterone. Treatment with epidermal growth factor also represses clusterin gene expression in MDCK cel…

Cell typeTranscription GeneticKidneyDexamethasoneEpitheliumCell LineAlkaloidsDogsEndocrinologyEpidermal growth factor1-Methyl-3-isobutylxanthineGene expressionCyclic AMPAnimalsRNA MessengerEnzyme InhibitorsAldosteroneMolecular BiologyProgesteroneProtein Kinase CProtein kinase CGlycoproteinsBenzophenanthridinesMessenger RNAEpidermal Growth FactorClusterinbiologyChemistryMolecular biologyeye diseasesPhenanthridinesCell biologyKineticsClusterinCell culturebiology.proteinTetradecanoylphorbol Acetatesense organsSignal transductionMolecular ChaperonesSignal TransductionJournal of Molecular Endocrinology
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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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