Search results for " glycoprotein"

showing 10 items of 430 documents

Regulation of T cells in asthma: implications for genetic manipulation

2004

PURPOSE OF THE REVIEW Allergic asthma is a disease characterized by airway hyperresponsiveness, inflammation and remodeling. In the past few decades it has become clear that the pathogenesis and development of this disease is controlled by cytokines released by CD4 T helper type 2 lymphocytes that develop under the influence of natural killer lymphocytes. At birth, T cell priming exhibits a T helper type 2 bias and the development of the T helper phenotype is determined in the first year of life by environmental exposure to virus or bacterial substances or environmental allergens in genetically predisposed individuals. Decreased exposure to infection in early childhood has thus been linked …

LipopolysaccharidesT-LymphocytesT cellImmunologyPriming (immunology)Receptors Cell SurfaceInflammationBiologyType 2 immune responseImmune systemAntigenHygiene hypothesismedicineHumansImmunology and AllergyGeneticsMembrane GlycoproteinsToll-Like ReceptorsT-Lymphocytes Helper-InducerEnvironmental exposureAsthmamedicine.anatomical_structureImmunologyCytokinesmedicine.symptomT-Box Domain ProteinsTranscription FactorsCurrent Opinion in Allergy and Clinical Immunology
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IL-10 down-regulates T cell activation by antigen-presenting liver sinusoidal endothelial cells through decreased antigen uptake via the mannose rece…

1998

SUMMARYOur study demonstrates that antigen-presenting liver sinusoidal endothelial cells (LSEC) induce production of interferon-gamma (IFN-γ) from cloned Th1 CD4+ T cells. We show that LSEC used the mannose receptor for antigen uptake, which further strengthened the role of LSEC as antigen-presenting cell (APC) population in the liver. The ability of LSEC to activate cloned CD4+ T cells antigen-specifically was down-regulated by exogenous prostaglandin E2 (PGE2) and by IL-10. We identify two separate mechanisms by which IL-10 down-regulated T cell activation through LSEC. IL-10 decreased the constitutive surface expression of MHC class II as well as of the accessory molecules CD80 and CD86 …

Liver cytologyT cellT-LymphocytesImmunologyAntigen presentationAntigen-Presenting CellsDown-RegulationReceptors Cell SurfaceBiologyLymphocyte ActivationDinoprostoneMiceAntigenAntigens CDmedicineImmunology and AllergyAnimalsLectins C-TypeCD86Antigen PresentationMice Inbred BALB CMembrane GlycoproteinsHistocompatibility Antigens Class IIOriginal ArticlesInterleukin-10Interleukin 10medicine.anatomical_structureMannose-Binding LectinsLiverImmunologyB7-1 AntigenCytokinesFemaleB7-2 AntigenEndothelium VascularMannoseCD80Mannose receptorMannose ReceptorClinical and experimental immunology
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Gp91phox-containing NAD(P)H oxidase increases superoxide formation by doxorubicin and NADPH

2006

Doxorubicin is a highly effective antineoplastic drug associated with a dose-dependent cardiotoxicity that may result in irreversible cardiomyopathy and heart failure. Gene variants of the superoxide-generating enzyme NAD(P)H oxidase have recently been associated with this phenotype. We investigated the mechanism of this association using lucigenin-enhanced chemiluminescence, spectrophotometry, electrochemical sensor, and electron paramagnetic resonance spectroscopy. Superoxide production was measured in female wild-type and NAD(P)H oxidase-deficient (gp91phox knockout) mice. The magnitude of the increase in superoxide production on the addition of doxorubicin was much higher in hearts of w…

LuminescenceGene ExpressionAntineoplastic AgentsPolymerase Chain ReactionBiochemistryMicechemistry.chemical_compoundSuperoxidesPhysiology (medical)medicineAnimalsDoxorubicinNADPH-Ferrihemoprotein ReductaseMice Knockoutchemistry.chemical_classificationCardiotoxicityOxidase testMembrane GlycoproteinsDose-Response Relationship DrugSuperoxideMyocardiumNADPH OxidasesMolecular biologyMice Inbred C57BLEnzymechemistryBiochemistryDoxorubicinNAD(P)H oxidaseNADPH Oxidase 2Knockout mouseNAD+ kinaseNADPmedicine.drugFree Radical Biology and Medicine
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Random, asynchronous, and asymmetric transcriptional activity of enhancer-flanking major immediate-early genes ie1/3 and ie2 during murine cytomegalo…

2001

ABSTRACT The lungs are a major organ site of cytomegalovirus (CMV) pathogenesis, latency, and recurrence. Previous work on murine CMV latency has documented a high load and an even distribution of viral genomes in the lungs after the resolution of productive infection. Initiation of the productive cycle requires expression of the ie1/3 transcription unit, which is driven by the immediate-early (IE) promoter P 1/3 and generates IE1 and IE3 transcripts by differential splicing. Latency is molecularly defined by the absence of IE3 transcripts specifying the essential transactivator protein IE3. In contrast, IE1 transcripts were found to be generated focally and randomly, reflecting sporadic P …

Lung DiseasesMuromegalovirusTranscription GeneticvirusesImmunologyReplicationEnhancer RNAsBiologyMicrobiologyImmediate early proteinImmediate-Early ProteinsTransactivationMiceViral ProteinsViral Envelope ProteinsTranscription (biology)VirologyVirus latencymedicineAnimalsEnhancerTranscription factorGenes Immediate-EarlyLungGeneticsMice Inbred BALB CMembrane Glycoproteinsvirus diseasesHerpesviridae Infectionsmedicine.diseaseUpstream EnhancerVirus LatencyEnhancer Elements GeneticInsect ScienceTrans-ActivatorsFemaleJournal of virology
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Targeted Repolarization of Tumor‐Associated Macrophages via Imidazoquinoline‐Linked Nanobodies

2021

Abstract Tumor‐associated macrophages (TAMs) promote the immune suppressive microenvironment inside tumors and are, therefore, considered as a promising target for the next generation of cancer immunotherapies. To repolarize their phenotype into a tumoricidal state, the Toll‐like receptor 7/8 agonist imidazoquinoline IMDQ is site‐specifically and quantitatively coupled to single chain antibody fragments, so‐called nanobodies, targeting the macrophage mannose receptor (MMR) on TAMs. Intravenous injection of these conjugates result in a tumor‐ and cell‐specific delivery of IMDQ into MMRhigh TAMs, causing a significant decline in tumor growth. This is accompanied by a repolarization of TAMs to…

Lung NeoplasmsGeneral Chemical Engineeringmedicine.medical_treatmentGeneral Physics and AstronomyMedicine (miscellaneous)TLR 7/8 agonist02 engineering and technology01 natural scienceschemistry.chemical_compoundCancer immunotherapyTumor-Associated MacrophagesTumor MicroenvironmentMacrophageM2 macrophagesGeneral Materials ScienceReceptorResearch ArticlesMice KnockoutMembrane GlycoproteinsChemistrytumor associated macrophagesQGeneral EngineeringImidazoles021001 nanoscience & nanotechnologynanobodiesmedicine.anatomical_structureDrug deliveryQuinolines0210 nano-technologyMannose ReceptorResearch ArticleT cellScience010402 general chemistryBiochemistry Genetics and Molecular Biology (miscellaneous)Immune systemmedicineAnimalsrepolarizationcancer immunotherapyCancerSingle-Domain Antibodiesmedicine.disease0104 chemical sciencesImidazoquinolineMice Inbred C57BLDisease Models AnimalToll-Like Receptor 6Toll-Like Receptor 7drug deliveryCancer research
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Measles virus enhances the expression of cellular immediate-early genes and DNA-binding of transcription factor AP-1 in lung epithelial A549 cells.

2002

In this work we investigated the effect of measles virus (MV) infection on the expression of immediate-early genes junB, c-jun and c-fos mRNA as well as AP-1 DNA-binding activity in the lung epithelial-like adenocarcinoma cell line A549. The transcription factor AP-1, which is a group of dimeric complexes of the Fos and Jun family proteins, is an important regulator in many cellular responses to different extracellular stimuli. Membrane cofactor protein CD46, which acts as a receptor for laboratory-adapted and vaccine strains of MV, has been reported to associate with beta1 integrin molecules, which are known to trigger signaling events and activate immediate-early genes. The expression of …

Lung NeoplasmsJUNBBiologyMeasles virusMembrane Cofactor Protein03 medical and health sciencesAntigens CDVirologyGene expressionTumor Cells CulturedHumansMononegaviralesTranscription factorGenes Immediate-Early030304 developmental biologyA549 cell0303 health sciencesMembrane GlycoproteinsCD46Interleukin-6030302 biochemistry & molecular biologyGeneral MedicineDNAbiology.organism_classificationVirology3. Good healthTranscription Factor AP-1Gene Expression RegulationMeasles virusImmediate early geneArchives of virology
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Down-regulation of human CYP3A4 by the inflammatory signal interleukin-6: molecular mechanism and transcription factors involved.

2002

The hepatic drug-metabolizing cytochrome P-450 (CYP) enzymes are down-regulated during inflammation. In vitro studies with hepatocytes have shown that the cytokines released during inflammatory responses are largely responsible for this CYP repression. However, the signaling pathways and the cytokine-activated factors involved remain to be properly identified. Our research has focused on the negative regulation of CYP3A4 (the major drug-metabolizing human CYP) by interleukin 6 (IL-6) (the principal regulator of the hepatic acute-phase response). CYP3A4 down-regulation by IL-6 requires activation of the glycoprotein receptor gp130; however, it does not proceed through the JAK/STAT pathway, a…

MAPK/ERK pathwaySTAT3 Transcription FactorMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesDown-RegulationBiologyBiochemistryTransactivationCytochrome P-450 Enzyme SystemAntigens CDGeneticsCCAAT-Enhancer-Binding Protein-alphaCytokine Receptor gp130Tumor Cells CulturedCytochrome P-450 CYP3AHumansRNA MessengerSTAT3Molecular BiologyTranscription factorCells CulturedMembrane GlycoproteinsDose-Response Relationship DrugInterleukin-6Reverse Transcriptase Polymerase Chain ReactionCCAAT-Enhancer-Binding Protein-betaJAK-STAT signaling pathwayProtein-Tyrosine KinasesGlycoprotein 130Molecular biologyDNA-Binding ProteinsGene Expression Regulationbiology.proteinHepatocytesTrans-ActivatorsSignal transductionBiotechnologyAcute-Phase ProteinsSignal TransductionTranscription FactorsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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Caspartin and calprismin, two proteins of the shell calcitic prisms of the Mediterranean fan mussel Pinna nobilis.

2005

We used the combination of preparative electrophoresis and immunological detection to isolate two new proteins from the shell calcitic prisms of Pinna nobilis, the Mediterranean fan mussel. The amino acid composition of these proteins was determined. Both proteins are soluble, intracrystalline, and acidic. The 38-kDa protein is glycosylated; the 17-kDa one is not. Ala, Asx, Thr, and Pro represent the dominant residues of the 38-kDa protein, named calprismin. An N-terminal sequence was obtained from calprismin. This sequence, which comprises a pattern of 4 cysteine residues, is not related to any known protein. The second protein, named caspartin, exhibits an unusual amino acid composition, …

MESH : Molecular Sequence DataMESH : Calcium CarbonateMESH: BivalviaMESH: ElectrophoresisMESH: Amino Acid Sequence01 natural sciencesBiochemistrychemistry.chemical_compoundMESH : BivalviaMESH: AnimalsMESH: CrystallizationCalciteImmunoassay0303 health sciencesbiologyMESH : Amino Acid SequenceImmunogold labellingMESH : ImmunoassayBiochemistryMESH: Calcium CarbonateMESH : CrystallizationCrystallizationMESH: ImmunoassayElectrophoresisAmino Acid Sequence;Animals;Bivalvia;Calcium Carbonate;Crystallization;Electrophoresis;Glycoproteins;Immunoassay;Molecular Sequence DataMolecular Sequence DataMESH: Glycoproteins010402 general chemistryCalcium CarbonateBiomaterials03 medical and health sciencesAnimalsAmino Acid Sequence[SDV.IB.BIO]Life Sciences [q-bio]/Bioengineering/BiomaterialsMolecular Biology030304 developmental biologyGlycoproteinsAntiserumMESH: Molecular Sequence DataMESH : ElectrophoresisCell BiologyMussel[ SDV.IB.BIO ] Life Sciences [q-bio]/Bioengineering/Biomaterialsbiology.organism_classificationMESH : Glycoproteins0104 chemical sciencesBivalvia[SDV.IB.BIO] Life Sciences [q-bio]/Bioengineering/BiomaterialsCalcium carbonatechemistryPolyclonal antibodiesbiology.proteinBiomatériauxMESH : AnimalsPinna nobilisCysteine
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Podoplanin serum and urine concentration in transitional bladder cancer

2016

Background Podoplanin (PDP) is a mucin - a type of transmembrane protein expressed in numerous tissues during ontogeny and in adult animals, including the brain, heart, kidney, osteoblasts and lymphoid organs. Objective The aim of this study was to determine podoplanin concentration in the blood serum and urine of patients with bladder cancer. Quantifying podoplanin concentration and its correlation with various clinicopathological parameters may be useful for more accurate predictions and identifying high-risk patients. Methods The present study included 82 patients with bladder cancer confirmed by transurethral resection or cystectomy and 27 healthy volunteers. The Surface Plasmon Resonan…

Male0301 basic medicineCancer ResearchPathologymedicine.medical_specialtymedicine.medical_treatmentUrineCystectomy03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBlood serumBiomarkers TumorGeneticsmedicineHumansAgedNeoplasm StagingCarcinoma Transitional CellKidneyCreatinineMembrane GlycoproteinsBladder cancerbusiness.industryGeneral MedicineMiddle AgedSurface Plasmon Resonancemedicine.disease030104 developmental biologymedicine.anatomical_structureTransitional cell carcinomaUrinary Bladder NeoplasmsOncologyPodoplaninchemistryCreatinine030220 oncology & carcinogenesisFemalebusinessCancer Biomarkers
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