Search results for " Site-Directed"

showing 10 items of 132 documents

Sequence-Specific Repression of Cotranslational Translocation of the Hepatitis B Virus Envelope Proteins Coincides with Binding of Heat Shock Protein…

1997

AbstractThe large L envelope protein of the hepatitis B virus has the peculiar capacity to adopt two transmembrane topologies. The N-terminal preS domain of L initially remains in the cytosol while the S domain is cotranslationally inserted into the endoplasmic reticulum membrane. The preS region of about half of the L molecules is posttranslationally translocated to the lumenal space. We now demonstrate that the repression of cotranslational translocation of preS is conferred by a preS1-specific sequence. By analysis of L deletion mutants, the cytosolic anchorage determinant was mapped to amino acid sequence 70 to 94 of L. The intrinsic potential of this determinant to suppress cotranslati…

Hepatitis B virusHSC70 Heat-Shock ProteinsRecombinant Fusion ProteinsPlasma protein bindingBiologyGenes envCytosolViral Envelope ProteinsHeat shock proteinVirologyHumansHSP70 Heat-Shock ProteinsBinding sitePromoter Regions GeneticPeptide sequenceBinding SitesBase SequenceCell-Free SystemEndoplasmic reticulumHSC70 Heat-Shock ProteinsOligonucleotides AntisenseMolecular biologyTransmembrane proteinChaperone (protein)Protein Biosynthesisbiology.proteinMutagenesis Site-DirectedMetallothioneinCarrier ProteinsProtein BindingVirology
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Deletions in the hepatitis B virus small envelope protein: effect on assembly and secretion of surface antigen particles

1992

The small envelope S protein of hepatitis B virus carrying the surface antigen has the unique property of mobilizing cellular lipids into empty envelope particles which are secreted from mammalian cells. We studied the biogenesis of such particles using site-directed mutagenesis. In this study, we describe the effect of deletions in the N-terminal hydrophobic and hydrophilic domains of the S protein. Whereas short overlapping deletions of hydrophilic sequences flanking the first hydrophobic domain were tolerated, larger deletions of the same sequences were not. Conversely, the hydrophilic region preceding the second hydrophobic domain was not permissive for even short deletions. Deletion of…

Hepatitis B virusMolecular Sequence DataImmunologyMutantMutagenesis (molecular biology technique)Biologymedicine.disease_causeMicrobiologyViral Envelope ProteinsViral envelopeVirologymedicineInterleukin 9SecretionCloning MolecularCells CulturedSecretory pathwayMutationHepatitis B Surface AntigensBase SequenceTunicamycinEndoplasmic reticulumPrecipitin TestsMolecular biologyInsect ScienceMutagenesis Site-DirectedChromosome DeletionPlasmidsResearch ArticleJournal of Virology
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Hepatitis B virus assembly is sensitive to changes in the cytosolic S loop of the envelope proteins.

2000

Among the three related L, M, and S envelope proteins of the hepatitis B virus (HBV), the L and S polypeptides are required for virion production. Whereas the pivotal function of the pre-S region of L in nucleocapsid envelopment has been established, the contribution of its S domain and the S protein is less clear. In this study, we evaluated the role of the cytosolic S loop, common to L and S, in HBV assembly by performing mutagenesis experiments. To distinguish between the effect of the mutations on either envelope or virion formation, we investigated the ability of the mutants to assemble into secretable subviral empty envelopes and to replace the wild-type proteins in virion maturation,…

Hepatitis B virusRecombination GeneticMutationHepatitis B virusvirusesVirus AssemblyMutantMolecular Sequence DataMorphogenesisMutagenesis (molecular biology technique)Biologymedicine.disease_causeVirologyCell biologyLoop (topology)CytosolCytosolViral Envelope ProteinsSequence Analysis ProteinVirologymedicineMutagenesis Site-DirectedHumansAmino Acid SequenceFunction (biology)Virology
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The role of histones and their modifications in the informative content of chromatin

1993

It is traditionally accepted that the DNA sequence cannot by itself explain all the mechanisms necessary for the development of living beings, especially in eukaryotes. Indeed part of the information used in these processes is stored in other ways, generally called ‘epigenetic’, whose molecular mechanisms are mostly unknown. The ultimate explanation for them might reside in the non-DNA moiety of chromatin which may play an active role in heredity (‘chromatin information’). Histones are the universal structural component of chromatin. However, recent studies strongly suggest that histones, and their modifications — especially the reversible acetylation of lysines — may act as a recognition s…

Histone-modifying enzymesMolecular Sequence DataBiologymedicine.disease_causeHistonesCellular and Molecular NeuroscienceHereditymedicineAnimalsNucleosomeAmino Acid SequenceEpigeneticsMolecular BiologyPharmacologyGeneticsRegulation of gene expressionAcetylationDNACell BiologyChromatinChromatinCell biologyHistoneAcetylationMutagenesis Site-Directedbiology.proteinMolecular MedicineExperientia
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Amino acid substitutions enhancing thermostability of Bacillus polymyxa beta-glucosidase A

1996

Mutations enhancing the thermostability of β-glucosidase A of Bacillus polymyxa, a family 1 glycosyl hydrolase, have been obtained after hydroxylamine mutagenesis of a plasmid containing the bglA gene, transformation of Escherichia coli with the mutagenized plasmid, and identification of transformant colonies that showed β-glucosidase activity after a thermal treatment that inactivated the wild-type enzyme. Two additive mutations have been characterized that cause replacement of glutamate at position 96 by lysine and of methionine at position 416 by isoleucine respectively. The thermoresistant mutant enzymes showed increased resistance to other denaturing agents, such as pH and urea, while …

Hot TemperatureMutantMolecular Sequence DataBacillusHydroxylamineBiologymedicine.disease_causeHydroxylaminesBiochemistryProtein Structure Secondarychemistry.chemical_compoundHydrolaseEnzyme StabilitymedicineEscherichia coliPoint MutationAmino Acid SequenceCloning MolecularMolecular BiologyEscherichia coliThermostabilitychemistry.chemical_classificationMethionineBase Sequencebeta-GlucosidaseCell BiologyMolecular biologyRecombinant ProteinsAmino acidKineticschemistryBiochemistryOligodeoxyribonucleotidesMutagenesisMutagenesis Site-DirectedThermodynamicsSpectrophotometry UltravioletIsoleucineCysteineResearch Article
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Mutilation of RNA phage Qβ virus-like particles: from icosahedrons to rods

2000

Icosahedral virus-like particles (VLPs) of RNA phage Qbeta are stabilized by four disulfide bonds of cysteine residues 74 and 80 within the loop between beta-strands F and G (FG loop) of the monomeric subunits, which determine the five-fold and quasi-six-fold symmetry contacts of the VLPs. In order to reduce the stability of Qbeta VLPs, we mutationally converted the amino acid stretch 76-ANGSCD-81 within the FG loop into the 76-VGGVEL-81 sequence. It led to production in Escherichia coli cells of aberrant rod-like Qbeta VLPs, along with normal icosahedral capsids. The length of the rod-like particles exceeded 4-30 times the diameter of icosahedral Qbeta VLPs.

Icosahedral symmetryvirusesGenetic VectorsMolecular Sequence DataBiophysicsBiologymedicine.disease_causecomplex mixturesBiochemistryVirus-like particleStructural BiologyGeneticsmedicineAmino Acid SequenceCysteineMolecular BiologyEscherichia coliPeptide sequenceIcosahedronAlloleviviruschemistry.chemical_classificationSequence Homology Amino AcidRod-like structureVirionvirus diseasesRNASelf-assemblyCell Biologybiochemical phenomena metabolism and nutritionAmino acidCrystallographyCapsidchemistryMutagenesis Site-DirectedRNA ViralRNA phage QβVirus-like particleCysteineFEBS Letters
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AML-associated Flt3 kinase domain mutations show signal transduction differences compared with Flt3 ITD mutations

2005

Activating mutations of Flt3 are found in approximately one third of patients with acute myeloid leukemia (AML) and are an attractive drug target. Two classes of Flt3 mutations occur: internal tandem duplications (ITDs) in the juxtamembrane and point mutations in the tyrosine kinase domain (TKD). We and others have shown that Flt3-ITD induced aberrant signaling including strong activation of signal transducer and activator of transcription 5 (STAT5) and repression of CCAAT/estradiol-binding protein α (c/EBPα) and Pu.1. Here, we compared the signaling properties of Flt3-ITD versus Flt3-TKD in myeloid progenitor cells. We demonstrate that Flt3-TKD mutations induced autonomous growth of 32D ce…

ImmunologyApoptosisBiologymedicine.disease_causeBiochemistryCell Linefluids and secretionsProto-Oncogene Proteinshemic and lymphatic diseasesSTAT5 Transcription FactormedicineAnimalsHumansPoint MutationMyeloid CellsPhosphorylationProtein kinase BProtein kinase CMutationPoint mutationAutophosphorylationIntracellular Signaling Peptides and ProteinsReceptor Protein-Tyrosine Kinaseshemic and immune systemsCell BiologyHematologyMilk ProteinsStaurosporineMolecular biologyProtein Structure TertiaryDNA-Binding ProteinsMuridaefms-Like Tyrosine Kinase 3Leukemia MyeloidTandem Repeat SequencesAcute Diseaseembryonic structuresFms-Like Tyrosine Kinase 3Mutagenesis Site-DirectedTrans-ActivatorsSignal transductionTyrosine kinaseSignal TransductionTranscription FactorsBlood
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Histidine residues near the N terminus of staphylococcal alpha-toxin as reporters of regions that are critical for oligomerization and pore formation.

1994

Chemical modification of histidine residues in staphylococcal alpha-toxin leads to loss of functional activity. Site-directed mutants of the toxin in which each of the four histidine residues was replaced by several amino acids were therefore produced. The mutant proteins were purified and characterized. Exchange of H-259 or H-144 was sometimes tolerated without reduction in hemolytic activity. These histidine residues are thus not essential for toxin function. Exchange of H-35 and H-48, however, had marked effects. H-35 mutant toxins bound with high affinity to rabbit erythrocytes but displayed faulty oligomerization and were unable to form pores. H-48 mutant toxins also had severely impai…

ImmunologyMutantBacterial ToxinsBiologyHemolysin Proteinsmedicine.disease_causeMicrobiologyHemolysisHemolysin ProteinsStructure-Activity RelationshipmedicineStructure–activity relationshipAnimalsHistidineHistidinechemistry.chemical_classificationToxinErythrocyte Membranebiology.organism_classificationAmino acidN-terminusInfectious DiseaseschemistryBiochemistryMutagenesis Site-DirectedParasitologyRabbitsBacteriaResearch Article
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The Fibril-associated Collagen IX Provides a Novel Mechanism for Cell Adhesion to Cartilaginous Matrix

2004

Collagen IX is the prototype fibril-associated collagen with interruptions in triple helix. In human cartilage it covers collagen fibrils, but its putative cellular receptors have been unknown. The reverse transcription-PCR analysis of human fetal tissues suggested that based on their distribution all four collagen receptor integrins, namely alpha1beta1, alpha2beta1, alpha10beta1, and alpha11beta1, are possible receptors for collagen IX. Furthermore primary chondrocytes and chondrosarcoma cells express the four integrins simultaneously. Chondrosarcoma cells, as well as Chinese hamster ovary cells transfected to express alpha1beta1, alpha2beta1, or alpha10beta1 integrin as their only collage…

Integrin alpha1Integrin alpha2LigandsPolymerase Chain ReactionBiochemistryCollagen receptorMiceCricetinaeReceptorbiologyReverse Transcriptase Polymerase Chain ReactionChemistryChinese hamster ovary cellRecombinant ProteinsCell biologyBiochemistryCollagenIntegrin alpha ChainsProtein BindingMolecular Sequence DataIntegrinChondrosarcomaCHO CellsFibrilCollagen Type IXCell LineChondrocytesMicroscopy Electron TransmissionCell Line TumorCell AdhesionEscherichia coliAnimalsHumansImmunoprecipitationAmino Acid SequenceRNA MessengerBinding siteCell adhesionMolecular BiologyBinding SitesSequence Homology Amino AcidCell BiologyProtein Structure TertiaryRatsMicroscopy ElectronCollagen type I alpha 1CartilageMutationMutagenesis Site-Directedbiology.proteinRNAPeptidesJournal of Biological Chemistry
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Integrin alpha(2)I domain recognizes type I and type IV collagens by different mechanisms.

2000

The collagens are recognized by the alphaI domains of the collagen receptor integrins. A common structural feature in the collagen-binding alphaI domains is the presence of an extra helix, named helix alphaC. However, its participation in collagen binding has not been shown. Here, we have deleted the helix alphaC in the alpha(2)I domain and tested the function of the resultant recombinant protein (DeltaalphaCalpha(2)I) by using a real-time biosensor. The DeltaalphaCalpha(2)I domain had reduced affinity for type I collagen (430 +/- 90 nM) when compared with wild-type alpha(2)I domain (90 +/- 30 nM), indicating both the importance of helix alphaC in type I collagen binding and that the collag…

IntegrinsIntegrinIntegrin alpha2CHO CellsBiochemistryCollagen receptorType IV collagenIntegrin alpha2Antigens CDCricetinaeAnimalsBinding siteMolecular BiologyBinding SitesbiologyChemistryChinese hamster ovary cellCell BiologyMolecular biologyRecombinant ProteinsCollagen type I alpha 1biology.proteinMutagenesis Site-DirectedCollagenType I collagenProtein BindingThe Journal of biological chemistry
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