Search results for "MUTATION"

showing 10 items of 2830 documents

Combining two mutations of human interleukin-6 that affect gp130 activation results in a potent interleukin-6 receptor antagonist on human myeloma ce…

1995

The pleiotropic cytokine interleukin-6 (IL-6) interacts with the specific ligand binding subunit (IL-6R alpha) of the IL-6 receptor, and this complex associates with the signal-transducing subunit gp130 (IL-6R beta). Human IL-6 acts on human and murine cells, whereas murine IL-6 is only active on murine cells. The construction of a set of chimeric human/murine IL-6 proteins has recently allowed us to define a region (residues 43-55) within the human IL-6 protein, which is important for the interaction with gp130. Subdividing this region shows that mainly residues 50-55 of the human IL-6 are necessary for this interaction. Recently, another human IL-6 double mutant (Q159E and T162P) showed r…

Protein ConformationProtein subunitmedicine.medical_treatmentMutantMolecular Sequence DataBiologyBiochemistryMiceAntigenAntigens CDmedicineCytokine Receptor gp130Tumor Cells CulturedAnimalsHumansPoint MutationInterleukin 6ReceptorMolecular BiologyMembrane GlycoproteinsBase SequenceInterleukin-6Wild typeCell BiologyReceptors InterleukinGlycoprotein 130Molecular biologyReceptors Interleukin-6CytokineOligodeoxyribonucleotidesbiology.proteinMultiple MyelomaThe Journal of biological chemistry
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Identification of Single Amino Acid Residues of Human IL-6 Involved in Receptor Binding and Signal Initiation

1996

The pleiotropic cytokine interleukin-6 (IL-6) has been predicted to be a protein with four antiparallel alpha-helices. On target cells, IL-6 interacts with a specific ligand binding receptor subunit (IL-6R), and this complex associates with the signal-transducing subunit gp130. Human IL-6 acts on human and murine cells, whereas murine IL-6 is only active on murine cells. The construction of chimeric human/murine IL-6 proteins has allowed us to define a region (residues 77-95, region 2c) within the human IL-6 protein that is important for IL-6R binding and a region (residues 50-55, region 2a2) that is important for IL-6R dependent gp130 interaction. Guided by sequence alignment and molecular…

Protein ConformationRecombinant Fusion ProteinsProtein subunitMolecular Sequence DataImmunologySequence alignmentPlasma protein bindingBiologyLigandsMiceStructure-Activity RelationshipProtein structureAntigens CDVirologyCytokine Receptor gp130AnimalsHumansPoint MutationAmino Acid SequenceAmino AcidsReceptorPeptide sequenceMembrane GlycoproteinsInterleukin-6Receptors InterleukinCell BiologyGlycoprotein 130Receptors Interleukin-6BiochemistryMutagenesis Site-DirectedSignal transductionSequence AlignmentProtein BindingSignal TransductionJournal of Interferon & Cytokine Research
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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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Refolding of the integral membrane protein light-harvesting complex II monitored by pulse EPR

2009

The major light-harvesting chlorophyll a / b complex (LHCII) of the photosynthetic apparatus in plants self-organizes in vitro. The recombinant apoprotein, denatured in dodecyl sulfate, spontaneously folds when it is mixed with its pigments, chlorophylls, and carotenoids in detergent solution, and assembles into structurally authentic LHCII in the course of several minutes. Pulse EPR techniques, specifically double-electron-electron resonance (DEER), have been used to analyze protein folding during this process. Pairs of nitroxide labels were introduced site-specifically into recombinant LHCII and shown not to affect the stability and function of the pigment-protein complex. Interspin dist…

Protein DenaturationProtein FoldingTime FactorsMultidisciplinaryPulsed EPRSuperhelixChemistryElectron Spin Resonance SpectroscopyLight-Harvesting Protein ComplexesPeasMembrane ProteinsElectronsBiological SciencesModels BiologicalProtein Structure SecondaryTransmembrane domainB vitaminsCrystallographyProtein structureMutationHelixSpin LabelsProtein foldingApoproteinsIntegral membrane proteinProceedings of the National Academy of Sciences
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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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An overview on chemical structures as ΔF508-CFTR correctors

2019

Deletion of phenylalanine at position 508 (F508del) in the CFTR protein, is the most common mutation causing cystic fibrosis (CF). F508del causes misfolding and rapid degradation of CFTR protein a defect that can be targeted with pharmacological agents termed “correctors”. Correctors belong to various chemical classes but are generally small molecules based on nitrogen sulfur or oxygen heterocycles. The mechanism of action of correctors is generally unknown but there is experimental evidence that some of them can directly act on mutant CFTR improving folding and stability. Here we overview the characteristics of the various F508del correctors described so far to obtain indications on key ch…

Protein FoldingCystic FibrosisCFTR correctorMutantCystic Fibrosis Transmembrane Conductance RegulatorPyrimidinonesmedicine.disease_cause01 natural sciencesF508del-CFTR03 medical and health sciencesMutant proteinDrug DiscoverymedicineAnimalsHumansCFTR030304 developmental biologyPharmacology0303 health sciencesMutationCFTR correctorsbiology010405 organic chemistryChemistryOrganic ChemistryCFTR; CFTR correctors; Cystic fibrosis; Cystic fibrosis transmembrane conductance regulator; F508del-CFTR; Animals; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Humans; Mutation; Protein Folding; Pyrimidinones; ThiazolesGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaSmall moleculeCystic fibrosis transmembrane conductance regulator0104 chemical sciencesCell biologyThiazolesMechanism of actionCystic fibrosiMutationbiology.proteinmedicine.symptomProtein Aδf508 cftrEuropean Journal of Medicinal Chemistry
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Expression and glycosylation studies of human FGF receptor 4

2001

Fibroblast growth factor receptor subtype 4 (FGFR4) has been shown to have special activation properties and just one splicing form, unlike the other FGFRs. FGFR4 overexpression is correlated with breast cancer and therefore FGFR4 is a target for drug design. Our aim is to overexpress high amounts of homogeneous FGFR4 extracellular domain (FGFR4ed) for structural studies. We show that baculovirus-insect cell-expressed FGFR4ed is glycosylated on three (N88, N234, and N266) of the six possible N-glycosylation sites but is not O-glycosylated. The deglycosylated triple mutant was expressed and had binding properties similar to those of glycosylated FGFR4ed, but was still heterogeneous. Large am…

Protein FoldingGlycosylationGlycosylationBlotting WesternImmunoblottingMolecular Sequence DataProtein RenaturationBiologyFibroblast growth factorMass SpectrometryInclusion bodiesCell Line03 medical and health scienceschemistry.chemical_compoundSDG 3 - Good Health and Well-beingEscherichia coliAnimalsHumansReceptor Fibroblast Growth Factor Type 4TrypsinAmino Acid SequenceDisulfidesReceptorChromatography High Pressure Liquid030304 developmental biologyInclusion Bodies0303 health sciencesHeparin030302 biochemistry & molecular biologyFibroblast growth factor receptor 4Fibroblast growth factor receptor 3Receptors Fibroblast Growth FactorMolecular biologyRecombinant Proteins3. Good healthchemistryFibroblast growth factor receptorMutationRNA splicing/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingBaculoviridaeBiotechnology
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Missense mutations of dual oxidase 2 (DUOX2) implicated in congenital hypothyroidism have impaired trafficking in cells reconstituted with DUOX2 matu…

2007

Abstract Dual oxidase 2 (DUOX2), a reduced NAD phosphate:O2 oxidoreductase flavoprotein, is a component of the thyrocyte H2O2 generator required for hormone synthesis at the apical plasma membrane. We recently identified a specific DUOX2 maturation factor (DUOXA2) that is necessary and sufficient for expression of functional DUOX2 in mammalian cell lines. We have now used a DUOXA2 reconstituted system to provide the first characterization of natural DUOX2 missense variants (Q36H, R376W, D506N) at the molecular level, analyzing their impact on H2O2 generation, trafficking, stability, folding, and DUOXA2 interaction. The Q36H and R376W mutations completely prevent routing of DUOX2 to the cell…

Protein FoldingMutantMutation MissenseBiologyEndoplasmic ReticulumCell membranesymbols.namesakeEndocrinologyMutant proteinPolysaccharidesCalnexinmedicineCongenital HypothyroidismAnimalsHumansMolecular BiologyCells CulturedFlavoproteinsOxidative foldingEndoplasmic reticulumCell MembraneMembrane ProteinsNADPH OxidasesDual oxidase 2General MedicineHydrogen PeroxideGolgi apparatusDual OxidasesRatsProtein Transportmedicine.anatomical_structureMannosyl-Glycoprotein Endo-beta-N-AcetylglucosaminidaseBiochemistrysymbolsOxidation-ReductionMolecular endocrinology (Baltimore, Md.)
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Influence of hydrophobic matching on association of model transmembrane fragments containing a minimised glycophorin A dimerisation motif

2005

AbstractThe principles that govern the folding and packing of membrane proteins are still not completely understood. In the present work, we have revisited the glycophorin A (GpA) dimerisation motif that mediates transmembrane (TM) helix association, one of the best-suited models of membrane protein oligomerisation. By using artificial polyleucine TM segments we have demonstrated in this study that a pattern of only five amino acids (GVxxGVxxT) promotes specific dimerisation. Further, we have used this minimised GpA motif to assess the influence of hydrophobic matching on the TM helix packing process in detergent micelles and found that this factor modulates helix–helix association and/or d…

Protein FoldingRecombinant Fusion ProteinsAmino Acid MotifsMolecular Sequence DataBiophysicsBiochemistryMicelleHydrophobic mismatchHydrophobic mismatchStructural BiologyLeucineHelix packingGeneticsGlycophorinAnimalsHumansAmino Acid SequenceGlycophorinsMolecular BiologyPolyacrylamide gel electrophoresischemistry.chemical_classificationbiologyChemistryGlycophorin AProteïnes de membranaMembrane ProteinsMembrane protein associationCell BiologyTransmembrane proteinAmino acidTransmembrane domainBiochemistryMembrane proteinMutationTransmembrane helixBiophysicsbiology.proteinPeptidesDimerizationHydrophobic and Hydrophilic Interactions
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BAG3 mediates chaperone-based aggresome-targeting and selective autophagy of misfolded proteins.

2010

Increasing evidence indicates the existence of selective autophagy pathways, but the manner in which substrates are recognized and targeted to the autophagy system is poorly understood. One strategy is transport of a particular substrate to the aggresome, a perinuclear compartment with high autophagic activity. In this paper, we identify a new cellular pathway that uses the specificity of heat-shock protein 70 (Hsp70) to misfolded proteins as the basis for aggresome-targeting and autophagic degradation. This pathway is regulated by the stress-induced co-chaperone Bcl-2-associated athanogene 3 (BAG3), which interacts with the microtubule-motor dynein and selectively directs Hsp70 substrates …

Protein FoldingRecombinant Fusion ProteinsDyneinGreen Fluorescent ProteinsAggrephagyMice TransgenicBAG3BiochemistryMiceJUNQ and IPODChlorocebus aethiopsGeneticsAutophagyAnimalsHumansPoint MutationHSP70 Heat-Shock ProteinsMolecular BiologyAdaptor Proteins Signal TransducingSequence DeletionInclusion BodiesMotor NeuronsbiologySuperoxide DismutaseAutophagyScientific ReportsDyneinsTransport proteinCell biologyProtein TransportAggresomeHEK293 CellsSpinal CordChaperone (protein)COS Cellsbiology.proteinApoptosis Regulatory ProteinsProteasome InhibitorsEMBO reports
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