Search results for "recombinant protein"

showing 10 items of 707 documents

Inhibition of glycosaminoglycan modification of perlecan domain I by site-directed mutagenesis changes protease sensitivity and laminin-1 binding act…

1998

AbstractGlycosaminoglycan attachment to perlecan domain I (173 residues) was completely prevented by site-directed mutagenesis of Ser-65, Ser-71 and Ser-76 as shown by recombinant production in mammalian cells. This did not interfere with the proper folding of the domain's SEA module but enhanced its sensitivity to neutral proteases. Lack of substitution also abolished binding to the two major heparin binding sites of laminin-1.

ProteasesBasement membraneRecombinant proteinmedicine.medical_treatmentMolecular Sequence DataBiophysicsPerlecanBiochemistrySubstrate SpecificityStructural BiologyLamininEndopeptidasesGeneticsmedicineAnimalsAmino Acid SequenceBinding siteSite-directed mutagenesisMolecular BiologyGlycosaminoglycansSite-directed mutagenesisBinding SitesProteasebiologyChemistryMutagenesisCell BiologyRecombinant ProteinsBiochemistryProteoglycanProteoglycanProteolysisMutagenesis Site-Directedbiology.proteinProteoglycansHeparitin SulfateLamininHeparan Sulfate ProteoglycansProtein BindingFEBS Letters
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Pore-forming toxins trigger shedding of receptors for interleukin 6 and lipopolysaccharide.

1996

Cleavage of membrane-associated proteins with the release of biologically active macromolecules is an emerging theme in biology. However, little is known about the nature and regulation of the involved proteases or about the physiological inducers of the shedding process. We here report that rapid and massive shedding of the interleukin 6 receptor (IL-6R) and the lipopolysaccharide receptor (CD14) occurs from primary and transfected cells attacked by two prototypes of pore-forming bacterial toxins, streptolysin O and Escherichia coli hemolysin. Shedding is not induced by an streptolysin O toxin mutant which retains cell binding capacity but lacks pore-forming activity. The toxin-dependent c…

ProteasesCD14Lipopolysaccharide ReceptorsEnzyme-Linked Immunosorbent AssayBiologyTransfectionHemolysin ProteinsMonocytesCell LineHemolysin ProteinsBacterial ProteinsAntigens CDChlorocebus aethiopsEscherichia coliTumor Cells CulturedAnimalsHumansEnzyme InhibitorsReceptorCells CulturedMultidisciplinaryHaptoglobinsMacrophagesReceptors InterleukinTransfectionStaurosporineReceptors Interleukin-6Recombinant ProteinsKineticsBiochemistryStreptolysinsInterleukin-6 receptorTetradecanoylphorbol AcetateStreptolysinSignal transductionSignal TransductionResearch ArticleProceedings of the National Academy of Sciences
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The interaction of recombinant subdomains of the procollagen C-proteinase with procollagen I provides a quantitative explanation for functional diffe…

2006

The procollagen C-proteinase (PCP) is a zinc peptidase of the astacin family and the metzincin superfamily. The enzyme removes the C-terminal propeptides of fibrillar procollagens and activates other matrix proteins. Besides its catalytic protease domain, the procollagen C-proteinase contains several C-terminal CUB modules (named after complement factors C1r and C1s, the sea urchin UEGF protein, and BMP-1) and EGF-like domains. The two major splice forms of the C-proteinase differ in their overall domain composition. The longer variant, termed mammalian tolloid (mTld, i.e., PCP-2), has the protease- CUB1-CUB2-EGF1-CUB3-EGF2-CUB4-CUB5 composition, whereas the shorter form termed bone morphog…

ProteasesProtein FoldingTolloid-Like Metalloproteinasesmedicine.medical_treatmentRNA SplicingBiologyAntiparallel (biochemistry)BiochemistryBone morphogenetic protein 1law.inventionBone Morphogenetic Protein 1lawmedicineAnimalsProtein precursorDNA PrimersProteaseBase SequenceCircular DichroismMetalloendopeptidasesSurface Plasmon ResonanceRecombinant ProteinsProcollagen peptidaseSpectrometry FluorescenceBiochemistryBone Morphogenetic ProteinsRecombinant DNAMetalloproteasesElectrophoresis Polyacrylamide GelAstacinProcollagenBiochemistry
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Functional deficiencies of components of the MHC class I antigen pathway in human tumors of epithelial origin

2000

An association between oncogenic transformation and repression of different components of the MHC class I antigen processing machinery (APM) have been described in murine model systems. In order to discover whether a similar correlation exists, human tumor cell lines of distinct histology with altered ras protein were analyzed for the expression of APM components utilizing RT-PCR and Western blot analyses. A heterogeneous expression pattern of MHC class I antigens, TAP peptide transporter, proteasome subunits, proteasome activator PA28 and the chaperones calnexin, calreticulin as well as tapasin was displayed by these tumor cell lines. Single or combined deficiencies in the expression and/o…

Proteasome Endopeptidase ComplexGene ExpressionInterferon-gammaMiceTapasinATP Binding Cassette Transporter Subfamily B Member 3Multienzyme ComplexesCalnexinGene expressionMHC class ITumor Cells CulturedAnimalsHumansNeoplasms Glandular and EpithelialATP Binding Cassette Transporter Subfamily B Member 2DNA PrimersAntigen PresentationTransplantationBase SequencebiologyAntigen processingMHC class I antigenHistocompatibility Antigens Class IProteinsHematologyTransporter associated with antigen processingRecombinant ProteinsCell biologyCysteine EndopeptidasesGenes rasMutationCancer researchbiology.proteinATP-Binding Cassette TransportersCalreticulinBone Marrow Transplantation
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Quantitative Analysis of Prion-Protein Degradation by Constitutive and Immuno-20S Proteasomes Indicates Differences Correlated with Disease Susceptib…

2004

Abstract The main part of cytosolic protein degradation depends on the ubiquitin-proteasome system. Proteasomes degrade their substrates into small peptide fragments, some of which are translocated into the endoplasmatic reticulum and loaded onto MHC class I molecules, which are then transported to the cell surface for inspection by CTL. A reliable prediction of proteasomal cleavages in a given protein for the identification of CTL epitopes would benefit immensely from additional cleavage data for the training of prediction algorithms. To increase the knowledge about proteasomal specificity and to gain more insight into the relation of proteasomal activity and susceptibility to prion diseas…

Proteasome Endopeptidase ComplexPrionsMolecular Sequence DataImmunologyCellProtein degradationPeptide MappingMultienzyme ComplexesMHC class ImedicineAnimalsHumansImmunology and AllergyAmino Acid SequencePeptide sequenceAllelesCell Line TransformedSheepbiologyHydrolysisMolecular biologyPeptide FragmentsRecombinant ProteinsCell biologyCysteine EndopeptidasesKineticsCytosolCTL*medicine.anatomical_structureProteasomeCell culturebiology.proteinDisease SusceptibilityThe Journal of Immunology
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Kinetic analysis and molecular modeling of the inhibition mechanism of roneparstat (SST0001) on human heparanase

2016

Heparanase is a β-d-glucuronidase which cleaves heparan sulfate chains in the extracellular matrix and on cellular membranes. A dysregulated heparanase activity is intimately associated with cell invasion, tumor metastasis and angiogenesis, making heparanase an attractive target for the development of anticancer therapies. SST0001 (roneparstat; Sigma-Tau Research Switzerland S.A.) is a non-anticoagulant 100% N-acetylated and glycol-split heparin acting as a potent heparanase inhibitor, currently in phase I in advanced multiple myeloma. Herein, the kinetics of heparanase inhibition by roneparstat is reported. The analysis of dose-inhibition curves confirmed the high potency of roneparstat (I…

Protein Conformation alpha-Helical0301 basic medicineSST0001Molecular modelhomology modelingAmino Acid MotifsPlasma protein bindingMolecular Dynamics SimulationBiochemistryMolecular Docking SimulationheparanaseSubstrate Specificity03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePolysaccharidesHumansProtein Interaction Domains and MotifsHeparanaseHomology modelingEnzyme InhibitorsGlucuronidaseBinding Siteskinetic inhibition analysisHeparinComputational BiologyHeparan sulfateRecombinant ProteinsAcidobacteriaMolecular Docking SimulationEnzyme bindingKinetics030104 developmental biologyCarbohydrate SequenceFondaparinuxchemistryBiochemistryStructural Homology ProteinDocking (molecular)030220 oncology & carcinogenesisBiophysicsroneparstatThermodynamicsProtein Conformation beta-StrandORIGINAL ARTICLESProtein BindingGlycobiology
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Crystal structure of bacteriophage fr capsids at 3.5 A resolution.

1994

The structure of recombinant capsids of the bacterial virus fr has been determined by X-ray crystallography at 3.5 A resolution. The capsids were produced by expressing the fr coat protein in Escherichia coli, the natural host of the virus, and are probably essentially identical to the protein shell of the native virus. The structure was determined using molecular replacement with the protein shell of the related MS2 virus, and refined to a crystallographic R-factor of 0.228. A comparison of the protein shells of the viruses shows that they are very similar, and indicates that they may have a similar regulation of the assembly of the quasi-symmetrical protein shell.

Protein ConformationvirusesMolecular Sequence DataRNA PhagesBiologymedicine.disease_causeCrystallography X-RayViruslaw.inventionBacteriophageCapsidStructural BiologylawmedicineComputer GraphicsEscherichia coliMolecular replacementAmino Acid SequenceMolecular BiologyEscherichia coliConserved SequenceLevivirusResolution (electron density)biology.organism_classificationRecombinant ProteinsCrystallographyCapsidMutationBiophysicsRecombinant DNABacterial virusSequence AlignmentJournal of molecular biology
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Production of biologically active recombinant avidin in baculovirus-infected insect cells

1997

Abstract An efficient lepidopteran insect cell system was established for the expression of a recombinant form of chicken egg-white avidin. The gene product was obtained in both secreted and intracellular forms, and biologically active recombinant avidin was isolated using affinity chromatography on an iminobiotin–agarose column. Similar to the known quaternary structure of the native egg-white protein, the purified recombinant protein was glycosylated and assembled mainly into tetramers. Like native avidin, the recombinant tetramer also exhibited a high level of thermostability, and was further stabilized upon binding biotin. The biotin-binding and structural properties of the recombinant …

Protein DenaturationGlycosylationProtein ConformationGenetic VectorsBiotinEnzyme-Linked Immunosorbent AssaySpodopteraChromatography Affinitylaw.inventionchemistry.chemical_compoundAffinity chromatographyBiotinTetramerlawAnimalsbiologySepharoseAvidinFusion proteinRecombinant ProteinsBiochemistrychemistryBiotinylationRecombinant DNAbiology.proteinProtein quaternary structureBaculoviridaeChickensBiotechnologyAvidinProtein Expression and Purification
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Expression and renaturation of the N-terminal extracellular domain of torpedo nicotinic acetylcholine receptor alpha-subunit.

1998

The N-terminal extracellular region (amino acids 1-209) of the alpha-subunit of the nicotinic acetylcholine receptor (nAChR) from Torpedo marmorata electric tissue was expressed as inclusion bodies in Escherichia coli using the pET 3a vector. Employing a novel protocol of unfolding and refolding, in the absence of detergent, a water-soluble globular protein of 25 kDa was obtained displaying approximately 15% alpha-helical and 45% beta-structure. The fragment bound alpha-[3H]bungarotoxin in 1:1 stoichiometry with a KD value of 0.5 nM as determined from kinetic measurements (4 nM from equilibrium binding). The kinetics of association of toxin and fragment were of second order, with a similar …

Protein DenaturationProtein FoldingMolecular Sequence DataReceptors NicotinicTorpedoBiochemistrylaw.inventionchemistry.chemical_compoundGanglion type nicotinic receptorlawExtracellularmedicineEscherichia coliAnimalsAmino Acid SequenceCloning MolecularMolecular BiologyMethyllycaconitineCell BiologyBungarotoxinBungarotoxinsRecombinant ProteinsNicotinic acetylcholine receptorBiochemistrychemistryAlpha-4 beta-2 nicotinic receptorTorpedoAcetylcholinemedicine.drugProtein BindingThe Journal of biological chemistry
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The protease domain of procollagen C-proteinase (BMP1) lacks substrate selectivity, which is conferred by non-proteolytic domains.

2007

Abstract Procollagen C-proteinase (PCP) removes the C-terminal pro-peptides of procollagens and also processes other matrix proteins. The major splice form of the PCP is termed BMP1 (bone morphogenetic protein 1). Active BMP1 is composed of an astacin-like protease domain, three CUB (complement, sea urchin Uegf, BMP1) domains and one EGF-like domain. Here we compare the recombinant human full-length BMP1 with its isolated proteolytic domain to further unravel the functional influence of the CUB and EGF domains. We show that the protease domain alone cleaves truncated procollagen VII within the short telopeptide region into fragments of similar size as the full-length enzyme does. However, u…

Protein FoldingCollagen Type VIIDNA Complementarymedicine.medical_treatmentClinical BiochemistryAmino Acid MotifsGene ExpressionGlutamic AcidBiochemistryBone morphogenetic protein 1Mass SpectrometryBone Morphogenetic Protein 1Cell LineSubstrate SpecificityProtein structuremedicineEscherichia coliAnimalsHumansCysteineDisulfidesMolecular BiologyInclusion BodiesMetalloproteinaseProteasebiologyChemistryMetalloendopeptidasesRecombinant ProteinsProtein Structure TertiaryFibronectinProcollagen peptidaseDrosophila melanogasterBiochemistryBone Morphogenetic ProteinsMutationbiology.proteinProtein foldingAstacinBiological chemistry
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