Search results for "Glycosyl"

showing 7 items of 317 documents

Effects of oxidative modifications induced by the glycation of bovine serum albumin on its structure and on cultured adipose cells

2005

Non-enzymatic glycosylation (glycation) and oxidative damages represent major research areas insofar as such modifications of proteins are frequently observed in numerous states of disease. Albumin undergoes structural and functional alterations, caused by increased glycosylation during non insulin-dependent diabetes mellitus, which is closely linked with the early occurrence of vascular complications. In this work, we first characterized structural modifications induced by the glycation of bovine serum albumin (BSA). A pathophysiological effect of glycated BSA was identified in primary cultures of human adipocytes as it induces an accumulation of oxidatively modified proteins in these cell…

medicine.medical_specialtyGlycosylationIsoprostaneGlycosylationAdipose tissueIsoprostanesmedicine.disease_causeBiochemistryRAGE (receptor)chemistry.chemical_compoundGlycationInternal medicineSpectroscopy Fourier Transform InfraredAdipocytesmedicineHumansSulfhydryl CompoundsBovine serum albuminCells CulturedbiologyAlbuminSerum Albumin BovineGeneral MedicineOxidative StressEndocrinologyBiochemistrychemistrybiology.proteinOxidation-ReductionOxidative stressBiochimie
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Glucose-induced loss of glycosyl-phosphatidylinositol-anchored membrane regulators of complement activation (CD59, CD55) by in vitro cultured human u…

2000

Aims/hypothesis. This study examines whether increased glucose concentrations are responsible for a decreased expression of membrane regulators of complement activation molecules. The effect of high glucose in determining an increase in membrane attack complex deposition on endothelial cells was also investigated. Methods. Endothelial cells were isolated from umbilical cord tissue, cultured in the presence of increased concentrations of glucose, and the expression of CD46, CD55, and CD59 was detected by ELISA (enzyme-linked immunosorbent assay) and by flow cytometry. Glucose-treated endothelial cells were also incubated with antiendothelial cell antibodies and fresh complement to assess the…

medicine.medical_specialtyUmbilical VeinsEndotheliumGlycosylphosphatidylinositolsEndocrinology Diabetes and MetabolismCellCD59 AntigensCD59Complement Membrane Attack ComplexBiologyUmbilical veinMembrane Cofactor ProteinAntigens CDPregnancyInternal medicineInternal MedicinemedicineHumansComplement ActivationCells CulturedMembrane GlycoproteinsCD55 AntigensCD46Cell biologyComplement systemEndothelial stem cellEndocrinologymedicine.anatomical_structureGlucoseFemaleEndothelium VascularComplement membrane attack complexDiabetologia
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The Role of Fc Receptors on the Effectiveness of Therapeutic Monoclonal Antibodies.

2021

Since the approval of the first monoclonal antibody (mAb) in 1986, a huge effort has been made to guarantee safety and efficacy of therapeutic mAbs. As of July 2021, 118 mAbs are approved for the European market for a broad range of clinical indications. In order to ensure clinical efficacy and safety aspects, (pre-)clinical experimental approaches evaluate the respective modes of action (MoA). In addition to antigen-specificity including binding affinity and -avidity, MoA comprise Fc-mediated effector functions such as antibody dependent cellular cytotoxicity (ADCC) and the closely related antibody dependent cellular phagocytosis (ADCP). For this reason, a variety of cell-based assays have…

modes of action (MoA)GlycosylationQH301-705.5medicine.drug_classCellReceptors FcReviewBiologyMonoclonal antibodyCatalysisInorganic Chemistrychemistry.chemical_compoundMonoklonaler Antikörper ; effector function ; antibody dependent cellular phagocytosis (ADCP) ; therapeutic monoclonal antibodies (mAbs) ; Fcγ receptor (FcγR) ; modes of action (MoA) ; antibody dependent cellular cytotoxicity (ADCC)medicineAnimalsHumansAvidityClinical efficacyBiology (General)Physical and Theoretical ChemistryReceptorQD1-999Molecular BiologySpectroscopyAntibody-dependent cell-mediated cytotoxicityEffectortherapeutic monoclonal antibodies (mAbs)Organic ChemistryAntibody-Dependent Cell CytotoxicityAntibodies Monoclonalantibody dependent cellular phagocytosis (ADCP)General MedicineFcγ receptor (FcγR)Computer Science ApplicationsImmunoglobulin Fc Fragmentsantibody dependent cellular cytotoxicity (ADCC)Chemistrymedicine.anatomical_structurechemistryImmunologyImmunotherapyeffector functionInternational journal of molecular sciences
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Aberrant glycosylation of alpha-dystroglycan causes defective binding of laminin in the muscle of chicken muscular dystrophy.

2005

Dystroglycan is a central component of dystrophin-glycoprotein complex that links extracellular matrix and cytoskeleton in skeletal muscle. Although dystrophic chicken is well established as an animal model of human muscular dystrophy, the pathomechanism leading to muscular degeneration remains unknown. We show here that glycosylation and laminin-binding activity of alpha-dystroglycan (alpha-DG) are defective in dystrophic chicken. Extensive glycan structural analysis reveals that Galbeta1-3GalNAc and GalNAc residues are increased while Siaalpha2-3Gal structure is reduced in alpha-DG of dystrophic chicken. These results implicate aberrant glycosylation of alpha-DG in the pathogenesis of mus…

musculoskeletal diseasesanimal structuresGlycosylationGlycosylationBiophysicsBiochemistryChromatography AffinityExtracellular matrixchemistry.chemical_compoundStructural BiologyLamininGeneticsDystroglycanmedicineAnimalsDystroglycanMuscular dystrophyDystrophic chickenDystroglycansMuscle SkeletalMolecular BiologybiologySkeletal muscleCell BiologyMuscular Dystrophy AnimalMuscular dystrophymedicine.diseaseMolecular biologycarbohydrates (lipids)Disease Models Animalmedicine.anatomical_structurechemistrybiology.proteinPikachurinLamininPlant LectinsITGA7ChickensProtein BindingFEBS letters
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A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA b…

2002

The Cockayne syndrome B (CSB) gene product is involved in the repair of various types of base modifications in actively transcribed DNA sequences. To investigate its significance for the repair of endogenous oxidative DNA damage, homozygous csb(-/-)/ogg1(-/-) double knockout mice were generated. These combine the deficiency of CSB with that of OGG1, a gene coding for the mammalian repair glycosylase that initiates the base excision repair of 7,8-dihydro-8-oxoguanine (8-oxoG). Compared to ogg1(-/-) mice, csb(-/-)/ogg1(-/-) mice were found to accumulate with age severalfold higher levels of oxidited purine modifications in hepatocytes, splenocytes and kidney cells. In contrast, the basal (ste…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA RepairTranscription GeneticDNA damageDNA repairBiologyGene productMicechemistry.chemical_compoundGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneDNA PrimersMice KnockoutBase SequenceHomozygoteDNA HelicasesDeoxyguanosinenutritional and metabolic diseasesBase excision repairMolecular biologyOxidative StressDNA Repair EnzymesBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineDNA glycosylaseDNADNA DamageNucleotide excision repairOncogene
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The effects of post-translational processing on dystroglycan synthesis and trafficking1

2003

Dystroglycan is a component of the dystrophin glycoprotein complex that is cleaved into two polypeptides by an unidentified protease. To determine the role of post-translational processing on dystroglycan synthesis and trafficking we expressed the dystroglycan precursor and mutants thereof in a heterologous system. A point mutant in the processing site, S655A, prevented proteolytic cleavage but had no effect upon the surface localisation of dystroglycan. Mutation of two N-linked glycosylation sites that flank the cleavage site inhibited proteolytic processing of the precursor. Furthermore, chemical inhibition of N- and O-linked glycosylation interfered with the processing of the precursor a…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesanimal structuresCOS cellsGlycosylationbiologyLactacystinBiophysicsCell Biologymusculoskeletal systemCleavage (embryo)BiochemistryDystroglycanschemistry.chemical_compoundchemistryBiochemistryStructural BiologyGeneticsbiology.proteinDystroglycanPikachurinBinding sitetissuesMolecular BiologyFEBS Letters
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Delivery of proteins into living cells by reversible membrane permeabilization with streptolysin-O

2001

The pore-forming toxin streptolysin O (SLO) can be used to reversibly permeabilize adherent and nonadherent cells, allowing delivery of molecules with up to 100 kDa mass to the cytosol. Using FITC-labeled albumin, 10 5 –10 6 molecules were estimated to be entrapped per cell. Repair of toxin lesions depended on Ca 2+ -calmodulin and on intact microtubules, but was not sensitive to actin disruption or to inhibition of protein synthesis. Resealed cells were viable for days and retained the capacity to endocytose and to proliferate. The active domains of large clostridial toxins were introduced into three different cell lines. The domains were derived from Clostridium difficile B-toxin and Clo…

rho GTP-Binding ProteinsCell Membrane PermeabilityGlycosylationCell SurvivalBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BBiologymedicine.disease_causeCell LineBacterial ProteinsAlbuminsChlorocebus aethiopsTumor Cells CulturedmedicineAnimalsHumansSecretionParticle SizeActinMultidisciplinaryDose-Response Relationship DrugSecretory VesiclesProteinsBiological TransportDextransBiological SciencesActin cytoskeletonMolecular biologyRatsCell biologyCytosolImmunoglobulin GCOS CellsStreptolysinsras ProteinsClostridium botulinumStreptolysinProceedings of the National Academy of Sciences
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