Search results for "amyloid beta"

showing 10 items of 191 documents

The unsolved relationship of brain aging and late-onset Alzheimer disease.

2009

Late-onset Alzheimer disease is the most common form of dementia and is strongly associated with age. Today, around 24 million people suffer from dementia and with aging of industrial populations this number will significantly increase throughout the next decades. An effective therapy that successfully decelerates or prevents the progressive neurodegeneration does not exist. Histopathologically Alzheimer disease is characterized by extensive extracellular amyloid beta (Abeta) plaques, intracellular neurofibrillary tangles (NFTs), synaptic loss and neuronal cell death in distinct brain regions. The molecular correlation of Abeta or NFTs and development of late-onset Alzheimer disease needs f…

Programmed cell deathAgingAmyloid βFree RadicalsBiophysicsmedicine.disease_causeBiochemistryModels BiologicalAtrophyAlzheimer DiseasemedicineExtracellularDementiaAnimalsHumansMolecular BiologyAmyloid beta-Peptidesbusiness.industryBrainNeurodegenerative Diseasesmedicine.diseaseDementiaAlzheimer's diseasebusinessNeuroscienceOxidative stressIntracellularBiochimica et biophysica acta
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Diverse cell surface protein ectodomains are shed by a system sensitive to metalloprotease inhibitors.

1996

The extracellular domains of a diverse group of membrane proteins are shed in response to protein kinase C activators such as phorbol 12-myristate 13-acetate (PMA). The lack of sequence similarity in the cleavage sites suggests the involvement of many proteases of diverse specificity in this process. However, a mutant Chinese hamster ovary cell line recently isolated for being defective in PMA-activated shedding of the membrane-anchored growth factor transforming growth factor alpha precursor (proTGF-alpha) is concomitantly defective in the shedding of many other unrelated membrane proteins. Here we show that independent mutagenesis and selection experiments yield shedding mutants having th…

ProteasesCellCHO CellsBiologyHydroxamic AcidsTransfectionBiochemistryAmyloid beta-Protein PrecursorAntigens CDCricetinaemedicineAnimalsProtease InhibitorsL-SelectinProtein PrecursorsCell adhesionMolecular BiologyProtein kinase CMetalloproteinaseChinese hamster ovary cellCell MembraneGenetic Complementation TestMembrane ProteinsMetalloendopeptidasesCell BiologyReceptors InterleukinTransforming Growth Factor alphaReceptors Interleukin-6Cell biologyKineticsmedicine.anatomical_structurePhenotypeEctodomainMembrane proteinMutagenesisTetradecanoylphorbol AcetatePhenanthrolinesThe Journal of biological chemistry
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Metalloprotease meprin β is activated by transmembrane serine protease matriptase-2 at the cell surface thereby enhancing APP shedding.

2014

Increased expression of metalloprotease meprin β is associated with fibrotic syndromes and Alzheimer's disease (AD). Hence, regulation of meprin activity might be a suitable strategy for the treatment of these conditions. Meprin β is a type 1 transmembrane protein, but can be released from the cell surface by ectodomain shedding. The protease is expressed as an inactive zymogen and requires proteolytic maturation by tryptic serine proteases. In the present study, we demonstrate, for the first time, the differences in the activation of soluble and membrane bound meprin β and suggest transmembrane serine protease 6 [TMPRSS6 or matriptase-2 (MT2)] as a new potent activator, cleaving off the pr…

ProteasesTMPRSS6Swinemedicine.medical_treatmentMolecular Sequence DataBiologyBiochemistryProtein Structure SecondaryAmyloid beta-Protein PrecursorChlorocebus aethiopsmedicineAnimalsHumansAmino Acid SequenceMolecular BiologySerine proteaseProteaseCell MembraneSerine EndopeptidasesMetalloendopeptidasesCell BiologySheddaseTrypsinTransmembrane proteinHEK293 CellsBiochemistryEctodomainCOS Cellsbiology.proteinmedicine.drugThe Biochemical journal
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The Cleavage Product of Amyloid-β Protein Precursor sAβPPα Modulates BAG3-Dependent Aggresome Formation and Enhances Cellular Proteasomal Activity

2015

Alzheimer's disease (AD) is the major age-associated form of dementia characterized by gradual cognitive decline. Aberrant cleavage of the amyloid-β protein precursor (AβPP) is thought to play an important role in the pathology of this disease. Two principal AβPP processing pathways exist: amyloidogenic cleavage of AβPP resulting in production of the soluble N-terminal fragment sAβPPβ, amyloid-β (Aβ), which accumulates in AD brain, and the AβPP intracellular domain (AICD) sAβPPα, p3 and AICD are generated in the non-amyloidogenic pathway. Prevalence of amyloidogenic versus non-amyloidogenic processing leads to depletion of sAβPPα and an increase in Aβ. Although sAβPPα is a well-accepted neu…

Proteasome Endopeptidase ComplexTime FactorsCell SurvivalLeupeptinsGreen Fluorescent ProteinsCysteine Proteinase InhibitorsProtein degradationProtein aggregationBiologyTransfectionBAG3Rats Sprague-DawleyAmyloid beta-Protein PrecursorAnimalsHumansRNA MessengerRNA Small InterferingProtein precursorCells CulturedAdaptor Proteins Signal TransducingNeuronsAmyloid beta-PeptidesDose-Response Relationship DrugGeneral NeuroscienceHEK 293 cellsBrainGeneral MedicineFibroblastsEmbryo MammalianRatsCell biologyPsychiatry and Mental healthClinical PsychologyHEK293 CellsProteostasisAggresomeGene Expression RegulationBiochemistryProteasomeProteolysisAmyloid Precursor Protein SecretasesGeriatrics and GerontologyApoptosis Regulatory ProteinsJournal of Alzheimer's Disease
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Calcium negatively regulates meprin β activity and attenuates substrate cleavage

2015

The meprin β metalloproteinase is an important enzyme in extracellular matrix turnover, inflammation, and neurodegeneration in humans and mice. Previous studies showed a diminished cleavage of certain meprin β substrates in the presence of calcium, although the mechanism was not clear. With the help of a specific fluorogenic peptide assay and the human amyloid precursor protein as substrate, we demonstrated that the influence of calcium is most likely a direct effect on human meprin β itself. Analyzing the crystal structures of pro- and mature meprin β helped to identify a cluster of negatively charged amino acids forming a potential calcium binding site. Mutation of 2 of these residues (D2…

Protein Foldingchemistry.chemical_elementCalciumEndoplasmic ReticulumBiochemistryCell LineSubstrate SpecificityAmyloid beta-Protein PrecursorChlorocebus aethiopsGeneticsAmyloid precursor proteinAnimalsHumansAmino Acid SequenceBinding siteProtein precursorMolecular BiologyCellular localizationSecretory pathwayMetalloproteinaseAmyloid beta-PeptidesBinding SitesbiologyEndoplasmic reticulumMetalloendopeptidasesCell biologyHEK293 CellschemistryCOS CellsMutationMetalloproteasesbiology.proteinCalciumAmyloid Precursor Protein SecretasesSequence AlignmentBiotechnologyThe FASEB Journal
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Thioflavin T templates amyloid β(1–40) conformation and aggregation pathway

2015

Aβ(1-40) peptide supramolecular assembly and fibril formation processes are widely recognized to have direct implications in the progression of Alzheimer's disease. The molecular basis of this biological process is still unknown and there is a strong need of developing effective strategies to control the occurring events. To this purpose the exploitation of small molecules interacting with Aβ aggregation represents one of the possible routes. Moreover, the use specific labeling has represented so far one of the most common and effective methods to investigate such a process. This possibility in turn rests on the reliability of the probe/labels involved. Here we present evidences of the effe…

Protein StructureSecondaryAβ(1–40) peptideAmyloidProtein ConformationMolecular Sequence DataBiophysicsSupramolecular chemistryMolecular Dynamics SimulationProtein aggregationProtein Aggregation PathologicalBiochemistryProtein Structure SecondarySupramolecular assemblyProtein Aggregateschemistry.chemical_compoundProtein structureAlzheimer DiseasePathologicalSecondary structureAβ(1-40) peptideHumansBenzothiazolesAmino Acid SequenceFluorescent DyesAmyloid beta-PeptidesProtein StabilityOrganic ChemistryAlzheimer's diseaseProtein AggregationSmall moleculePeptide FragmentsSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)Peptide ConformationAlzheimer's disease; Aβ(1–40) peptide; Protein aggregation; Protein conformation; Secondary structure; Thioflavin T; Alzheimer Disease; Amino Acid Sequence; Amyloid beta-Peptides; Fluorescence Recovery After Photobleaching; Fluorescent Dyes; Humans; Molecular Dynamics Simulation; Molecular Sequence Data; Peptide Fragments; Protein Aggregates; Protein Aggregation Pathological; Protein Conformation; Protein Multimerization; Protein Stability; Protein Structure Secondary; ThiazolesThiazolesBiophysicBiochemistrychemistryThioflavin TBiophysicsThioflavinProtein MultimerizationFluorescence Recovery After PhotobleachingBiophysical Chemistry
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Effects of sulindac sulfide on the membrane architecture and the activity of gamma-secretase.

2007

gamma-Secretase is a membrane-embedded multi-protein complex that catalyzes the final cut of the Alzheimer's disease-related amyloid precursor protein (APP) to amyloid-beta peptides of variable length (37-43 amino acids) via an unusual intramembrane cleavage. Recent findings propose that some commonly used non-steroidal anti-inflammatory drugs (NSAIDs) have the ability to modulate specifically gamma-secretase activity without inhibiting the enzyme as a whole. These drugs may shift the processing of APP from the longer amyloid-beta 42 peptide towards shorter, less fibrillogenic and less toxic amyloid-beta species. We hypothesize that gamma-secretase activity, as an enzyme that is strictly as…

Protein subunitBlotting WesternPeptideCHO CellsSarcoplasmic Reticulum Calcium-Transporting ATPasesCellular and Molecular NeuroscienceAmyloid beta-Protein PrecursorCricetulusMembrane MicrodomainsSulindacCricetinaemental disordersAmyloid precursor proteinPresenilin-1AnimalsHumansLipid raftCells CulturedPharmacologychemistry.chemical_classificationbiologyAnti-Inflammatory Agents Non-SteroidalCell MembraneP3 peptideAmino acidMembraneBiochemistrychemistrybiology.proteinBiophysicsAmyloid Precursor Protein SecretasesAmyloid precursor protein secretaseNeuropharmacology
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The Metalloprotease Meprin β Generates Amino Terminal-truncated Amyloid β Peptide Species

2012

The amyloid β (Aβ) peptide, which is abundantly found in the brains of patients suffering from Alzheimer disease, is central in the pathogenesis of this disease. Therefore, to understand the processing of the amyloid precursor protein (APP) is of critical importance. Recently, we demonstrated that the metalloprotease meprin β cleaves APP and liberates soluble N-terminal APP (N-APP) fragments. In this work, we present evidence that meprin β can also process APP in a manner reminiscent of β-secretase. We identified cleavage sites of meprin β in the amyloid β sequence of the wild type and Swedish mutant of APP at positions p1 and p2, thereby generating Aβ variants starting at the first or seco…

ProteomicsMolecular Sequence DataMutantPeptideBiologyHydroxamic AcidsCleavage (embryo)BiochemistryCatalysis03 medical and health sciences0302 clinical medicineAlzheimer Diseasemental disordersmedicineAmyloid precursor proteinHumansProtein IsoformsAmino Acid SequenceMolecular Biology030304 developmental biologychemistry.chemical_classification0303 health sciencesMetalloproteinaseAmyloid beta-PeptidesWild typeBrainMetalloendopeptidasesMolecular Bases of DiseaseCell Biologymedicine.diseaseMolecular biologyProtein Structure TertiaryKineticsHEK293 CellsEnzymechemistryBiochemistryMutationMetalloproteasesbiology.proteinAmyloid Precursor Protein SecretasesAlzheimer's diseasePeptides030217 neurology & neurosurgeryJournal of Biological Chemistry
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Discovery of γ-secretase modulators with a novel activity profile by text-based virtual screening.

2012

We present an integrated approach to identify and optimize a novel class of γ-secretase modulators (GSMs) with a unique pharmacological profile. Our strategy included (i) virtual screening through application of a recently developed protocol (PhAST), (ii) synthetic chemistry to discover structure–activity relationships, and (iii) detailed in vitro pharmacological characterization. GSMs are promising agents for treatment or prevention of Alzheimer’s disease. They modulate the γ-secretase product spectrum (i.e., amyloid-β (Aβ) peptides of different length) and induce a shift from toxic Aβ42 to shorter Aβ species such as Aβ38 with no or minimal effect on the overall rate of γ-secretase cleavag…

PyridinesPyridonesMolecular Sequence DataPeptideComputational biologyCHO CellsBiochemistryStructure-Activity RelationshipAlzheimer DiseaseCricetinaeAnimalsHumansγ secretaseAmino Acid Sequencechemistry.chemical_classificationVirtual screeningActivity profileAmyloid beta-PeptidesChemistryGeneral MedicineIntegrated approachIn vitroMinimal effectDrug DesignMolecular MedicineAmyloid Precursor Protein SecretasesACS chemical biology
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Amyloid-Beta Induces Different Expression Pattern of Tissue Transglutaminase and Its Isoforms on Olfactory Ensheathing Cells: Modulatory Effect of In…

2021

Abstract Alzhèimer Disease (AD) is characterized by protein aggregates in the brain, including amyloid-beta (Aβ), a substrate for tissue transglutaminase (TG2). We assessed the effect of full native peptide of Aβ (1–42), the fragments (25–35 and 35–25) on TG2 expression and its isoforms (Long and Short) on mouse Olfactory Ensheathing Cells (OECs). The levels of cytoskeletal proteins, Vimentin and Glial Fibrillary Acid Protein, were also studied. The effect of the pre-treatment with Indicaxanthin on cell viability, total Reactive Oxygen Species, superoxide anion and apoptotic pathway activation was assessed. Since Nestin is co-expressed in pluripotent stem cells with cyclin D1, their levels …

Pyridinestissue transglutaminase; olfactory ensheathing cells; amyloid-beta; oxidative stress; Indicaxanthin; self-renewalApoptosisAmyloid‐betaIndicaxanthinVimentinself-renewallcsh:ChemistryNestinMicechemistry.chemical_compoundProtein IsoformsCyclin D1lcsh:QH301-705.5SpectroscopybiologySuperoxideOpuntiaCell DifferentiationGeneral MedicineOlfactory Bulbamyloid-betaBetaxanthinsComputer Science ApplicationsCell biologyIndicaxanthinAmyloid betaTissue transglutaminase; Olfactory Ensheathing Cells; Amyloid-Beta; oxidative stress; In-dicaxanthin; self-renewalArticleGene Expression Regulation EnzymologicCatalysisInorganic ChemistryCyclin D1Alzheimer DiseaseGTP-Binding ProteinsGlial Fibrillary Acidic ProteinAnimalsHumansVimentinProtein Glutamine gamma Glutamyltransferase 2Viability assayPhysical and Theoretical ChemistryMolecular BiologyAmyloid beta-PeptidesTransglutaminasesOrganic ChemistryTissue transglutaminaseNestinSelf‐renewalNerve Regenerationlcsh:Biology (General)lcsh:QD1-999chemistryOxidative stressOlfactory ensheathing cellsbiology.proteinOlfactory ensheathing gliaReactive Oxygen SpeciesInternational Journal of Molecular Sciences
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