Search results for "Erich"

showing 10 items of 805 documents

Fitness Trade-Offs Determine the Role of the Molecular Chaperonin GroEL in Buffering Mutations

2015

Molecular chaperones fold many proteins and their mutated versions in a cell and can sometimes buffer the phenotypic effect of mutations that affect protein folding. Unanswered questions about this buffering include the nature of its mechanism, its influence on the genetic variation of a population, the fitness trade-offs constraining this mechanism, and its role in expediting evolution. Answering these questions is fundamental to understand the contribution of buffering to increase genetic variation and ecological diversification. Here, we performed experimental evolution, genome resequencing, and computational analyses to determine the trade-offs and evolutionary trajectories of Escherich…

PopulationGenetic FitnessBiologyGroELCell LineChaperonin10127 Institute of Evolutionary Biology and Environmental StudiesGenetic drift1311 Geneticsmutational bufferingOperonGenetic variationGenetics1312 Molecular BiologyEscherichia coliexperimental evolutioneducationMolecular BiologyDiscoveriesEcology Evolution Behavior and Systematics2. Zero hungerGeneticseducation.field_of_studyExperimental evolutionGenetic DriftChaperonin 60Gene Expression Regulation BacterialGroEL1105 Ecology Evolution Behavior and SystematicsGenes BacterialMutation570 Life sciences; biology590 Animals (Zoology)bacteriaProtein foldingGenetic FitnessDirected Molecular EvolutionSubcellular Fractions
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The transcriptome of Spodoptera exigua larvae exposed to different types of microbes.

2012

We have obtained and characterized the transcriptome of Spodoptera exigua larvae with special emphasis on pathogen-induced genes. In order to obtain a highly representative transcriptome, we have pooled RNA from diverse insect colonies, conditions and tissues. Sequenced cDNA included samples from 3 geographically different colonies. Enrichment of RNA from pathogen-related genes was accomplished by exposing larvae to different pathogenic and non-pathogenic microbial agents such as the bacteria Bacillus thuringiensis, Micrococcus luteus, and Escherichia coli, the yeast Saccharomyces cerevisiae, and the S. exigua nucleopolyhedrovirus (SeMNPV). In addition, to avoid the loss of tissue-specific …

PopulationMolecular Sequence DataBacillus thuringiensisGenes InsectSaccharomyces cerevisiaeSpodopteraSpodopteraBiochemistryPolymorphism Single NucleotideTranscriptomeINDEL MutationExiguaEscherichia coliAnimalsRNA VirusesAmino Acid SequenceeducationMolecular BiologyGeneGeneticsExpressed Sequence TagsExpressed sequence tageducation.field_of_studybiologyfungiRNARNA virusbiology.organism_classificationMicrococcus luteusInsect ScienceLarvaInsect ProteinsTranscriptomeMicrosatellite RepeatsInsect biochemistry and molecular biology
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Pore-forming toxins activate MAPK p38 by causing loss of cellular potassium.

2009

Mitogen activated protein kinase (MAPK) p38 has emerged as a survival protein in cells that are attacked by bacterial toxins forming small membrane pores. Activation of p38 by pore forming toxins (PFT) has been attributed to osmotic stress, but here we show that loss of K+ is likely to be the critical parameter. Several lines of evidence support this conclusion: first, osmoprotection did not prevent p38-phosphorylation in alpha-toxin-loaded cells. Second, treatment of cells with a K+ ionophore, or simple incubation in K+-free medium sufficed to cause robust p38-phosphorylation. Third, media containing high [K+] prevented p38-activation by Staphylococcus aureus alpha-toxin, Vibrio cholerae c…

Pore Forming Cytotoxic ProteinsOsmotic shockp38 mitogen-activated protein kinasesBacterial ToxinsBiophysicsBiologyHemolysin ProteinsBiochemistryp38 Mitogen-Activated Protein KinasesCell LineCell membraneHemolysin ProteinsmedicineHumansPhosphorylationMolecular BiologyPore-forming toxinEscherichia coli ProteinsCell MembraneHemolysinEpithelial CellsCell BiologyCell biologyEnzyme Activationmedicine.anatomical_structureBiochemistryPotassiumStreptolysinCalciumCytolysinBiochemical and biophysical research communications
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Cytocidal effects of Escherichia coli hemolysin on human T lymphocytes.

1993

Escherichia coli hemolysin is the prototype of a large family of pore-forming toxins produced by gram-negative organisms. Besides its known cytotoxic activities against granulocytes, monocytes, endothelial cells, and renal epithelial cells, we now demonstrate that the toxin potently kills human T lymphocytes. Evidence based on different and independent approaches indicates that lymphocidal activity is due to formation of transmembrane pores. Additionally, cells prestimulated with phytohemagglutinin respond to low doses of E. coli hemolysin with DNA fragmentation similar to that observed in cells undergoing programmed cell death. Kinetic considerations lead us to conclude that DNA degradatio…

Programmed cell deathCell Membrane PermeabilityTime FactorsDNA damageT-LymphocytesImmunologyBiologyIn Vitro Techniquesmedicine.disease_causeHemolysin ProteinsLymphocyte ActivationMicrobiologyMicrobiologyHemolysin ProteinsAdenosine TriphosphatemedicineEscherichia coliCytotoxic T cellHumansEscherichia coliCell DeathDose-Response Relationship DrugHemolysinT lymphocyteDNAInfectious DiseasesDNA fragmentationParasitologyResearch ArticleDNA Damage
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Evaluation of Changes in Gut Microbiota in Patients with Crohn’s Disease after Anti-Tnfα Treatment: Prospective Multicenter Observational Study

2020

Background: Crohn’s disease is believed to result from the interaction between genetic susceptibility, environmental factors and gut microbiota, leading to an aberrant immune response. The objectives of this study are to evaluate the qualitative and quantitative changes in the microbiota of patients with Crohn’s disease after six months of anti-tumor-necrosis factor (anti-TNFα) (infliximab or adalimumab) treatment and to determine whether these changes lead to the recovery of normal microbiota when compared to a control group of healthy subjects. In addition, we will evaluate the potential role of the Faecalibacterium prausnitzii/Escherichia coli and Faecalibacterium prausnitzii/Clostridium…

Project ReportCrohn’s diseasemedicine.medical_specialtyanti-TNFαHealth Toxicology and MutagenesisFaecalibacterium prausnitziilcsh:MedicineDiseaseGut flora03 medical and health sciences0302 clinical medicineCrohn DiseaseInternal medicinemedicineAdalimumabEscherichia coli and Clostridium coccoides groupHumansProspective Studies030304 developmental biology0303 health sciencesCrohn's diseasebiologygut microbiotabusiness.industryFaecalibacterium prausnitziiTumor Necrosis Factor-alphalcsh:RPublic Health Environmental and Occupational Healthmedicine.diseasebiology.organism_classificationInfliximabGastrointestinal MicrobiomeDysbiosis030211 gastroenterology & hepatologyCalprotectinbusinessDysbiosismedicine.drugInternational Journal of Environmental Research and Public Health
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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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Characterization of EprA, a major extracellular protein of Oenococcus oeni with protease activity

2008

International audience; Extracellular proteins from Oenococcus oeni. a wine-making bacterium, were isolated during growth on media differing by their nitrogen content. Analysis by two-dimensional electrophoresis revealed a low number of protein signals. Among the main spots, one signal corresponded to a single protein, which contained a lysine repeat domain characteristic of cell-wall hydrolases. We demonstrated that this major protein, named EprA, was able to hydrolyse several proteins. The heterologous production of this protein in Escherichia coli confirmed the protease activity of EprA. With a MW of 21.3 kDa and a pl of 5.3, EprA presents optimal activity at pH 7.0 and 45 degrees C. Thi…

ProteasesHydrolyzed proteinNitrogenmedicine.medical_treatmentWinemedicine.disease_causeMicrobiology[ CHIM ] Chemical SciencesMicrobiology03 medical and health sciencesBacterial Proteinsmedicine[CHIM]Chemical SciencesElectrophoresis Gel Two-DimensionalPolyacrylamide gel electrophoresisEscherichia coli030304 developmental biologyOenococcus oenichemistry.chemical_classification0303 health sciencesProteasebiology030306 microbiologyTemperatureGeneral MedicineHydrogen-Ion Concentrationbiology.organism_classificationCulture MediaMolecular WeightEnzymeBiochemistrychemistryFermentationFood MicrobiologyElectrophoresis Polyacrylamide GelOenococcusLeuconostocFood SciencePeptide Hydrolases
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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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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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