Search results for "Protein Precursor"

showing 10 items of 169 documents

Propeptide glycosylation and galectin‐3 binding decrease proteolytic activation of human proMMP‐9/progelatinase B

2019

Matrix metalloproteinases (MMPs) are secreted as proenzymes, containing propeptides that interact with the catalytic zinc, thereby controlling MMP activation. The MMP‐9 propeptide is unique in the MMP family because of its post‐translational modification with an N‐linked oligosaccharide. ProMMP‐9 activation by MMP‐3 occurs stepwise by cleavage of the propeptide in an aminoterminal (pro‐AT) and carboxyterminal (pro‐CT) peptide. We chemically synthesized aglycosyl pro‐AT and pro‐CT and purified recombinant glycosylated pro‐ATS f−9. First, we report new cleavage sites in the MMP‐9 propeptide by MMP‐3 and neutrophil elastase. Additionally, we demonstrated with the use of western blot analysis a…

0301 basic medicinePNGase FN-linked glycosylationGlycosylationGlycosylationmatrix metalloproteinase‐9Galectin 3GalectinsProteolysisgalectin‐3Biochemistry03 medical and health scienceschemistry.chemical_compoundCongenital Disorders of Glycosylation0302 clinical medicineN-linked glycosylationmatrix metalloproteinase-9galectin-3medicineHumansZymographyAmino Acid SequenceProtein precursorMolecular BiologyN‐linked glycosylationEnzyme Precursorspropeptidemedicine.diagnostic_testbiologyBlood ProteinsOriginal ArticlesCell BiologyTrypsinEnzyme Activation030104 developmental biologyMatrix Metalloproteinase 9chemistryBiochemistryGelatinasesCase-Control Studiesproteolytic activation030220 oncology & carcinogenesisNeutrophil elastaseProteolysisbiology.proteinMatrix Metalloproteinase 3Original ArticleLeukocyte Elastasemedicine.drug
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Regulatory effects of simvastatin and apoJ on APP processing and amyloid-beta clearance in blood-brain barrier endothelial cells

2017

Amyloid-β peptides (Aβ) accumulate in cerebral capillaries indicating a central role of the blood-brain barrier (BBB) in the pathogenesis of Alzheimer’s disease (AD). Although a relationship between apolipoprotein-, cholesterol- and Aβ metabolism is evident, the interconnecting mechanisms operating in brain capillary endothelial cells (BCEC) are poorly understood. ApoJ (clusterin) is present in HDL that regulates cholesterol metabolism which is disturbed in AD. ApoJ levels are increased in AD brains and in plasma of cerebral amyloid angiopathy (CAA) patients. ApoJ may bind, prevent fibrillization, and enhance clearance of Aβ. We here define a connection of apoJ and cellular cholesterol home…

0301 basic medicineSimvastatinmedicine.medical_specialtyAmyloidSwineMice TransgenicBiologyBlood–brain barrierAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineInternal medicinemedicineAmyloid precursor proteinAnimalsMolecular BiologyCells CulturedAmyloid beta-PeptidesClusterinEndothelial CellsCell Biologymedicine.diseaseLRP1Peptide FragmentsMice Inbred C57BLClusterin030104 developmental biologyEndocrinologymedicine.anatomical_structureBlood-Brain Barrierbiology.proteinFemaleCerebral amyloid angiopathyblood-brain barrier ; amyloid-β ; cholesterol ; simvastatin ; clusterin/apoJ ; LRP1Protein Processing Post-Translational030217 neurology & neurosurgeryIntracellularLipoprotein
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Rescue of Hypovitaminosis A Induces Non-Amyloidogenic Amyloid Precursor Protein (APP) Processing.

2015

Retinoic acid, the bioactive metabolite of beta-carotene or vitamin A, plays a pleiotropic, multifunctional role in vertebrate development. Studies in rodents revealed that a diet deficient in vitamin A results in a complex neonatal syndrome (the VAD syndrome), manifested in many organs. In humans, the function of retinoic acid (RA) extends into adulthood, where it has important roles in fertility, vision, and suppression of neoplastic growth. In recent years, it has also been suggested that retinoic acid might potentially act as a therapeutically relevant drug in attenuating or even preventing neurodegenerative diseases such as Alzheimer's disease (AD). Here, we report that VAD leads to an…

0301 basic medicineVitaminmedicine.medical_specialtyADAM10Retinoic acidTretinoin03 medical and health scienceschemistry.chemical_compoundADAM10 ProteinAmyloid beta-Protein PrecursorMiceNeuroblastoma0302 clinical medicineKeratolytic AgentsTretinoinInternal medicineNeuroblastomaGene expressionPresenilin-2medicineAmyloid precursor proteinAnimalsHumansGene Regulatory NetworksRats WistarCells CulturedCerebral CortexNeuronsAmyloid beta-PeptidesbiologyVitamin A Deficiencymedicine.diseaseAcitretinPeptide FragmentsVitamin A deficiencyDisease Models Animal030104 developmental biologyEndocrinologyNeurologychemistryAnimals Newbornbiology.proteinFemaleNeurology (clinical)030217 neurology & neurosurgerymedicine.drugCurrent Alzheimer research
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Statins and the squalene synthase inhibitor zaragozic acid stimulate the non-amyloidogenic pathway of amyloid-beta protein precursor processing by su…

2010

Cholesterol-lowering drugs such as statins influence the proteolytic processing of the amyloid-beta protein precursor (AbetaPP) and are reported to stimulate the activity of alpha-secretase, the major preventive secretase of Alzheimer's disease. Statins can increase the alpha-secretase activity by their cholesterol-lowering properties as well as by impairment of isoprenoids synthesis. In the present study, we elucidate the contribution of these pathways in alpha-secretase activation. We demonstrate that zaragozic acid, a potent inhibitor of squalene synthase which blocks cholesterol synthesis but allows synthesis of isoprenoids, also stimulates alpha-secretase activity. Treatment of human n…

ADAM10Blotting Westernchemistry.chemical_compoundSqualeneADAM10 ProteinAmyloid beta-Protein PrecursorCell Line TumormedicineHumansLovastatinRNA Small InterferingProtein precursorLuciferasesLipid raftNeuronsbiologyATP synthaseChemistryReverse Transcriptase Polymerase Chain ReactionTerpenesGeneral NeuroscienceAnticholesteremic AgentsCell MembraneMembrane ProteinsTricarboxylic AcidsZaragozic acidGeneral MedicineBridged Bicyclo Compounds HeterocyclicEnzyme ActivationPsychiatry and Mental healthClinical PsychologyADAM ProteinsCholesterolFarnesyl-Diphosphate FarnesyltransferaseBiochemistrybiology.proteinlipids (amino acids peptides and proteins)LovastatinGeriatrics and GerontologyAmyloid Precursor Protein SecretasesHydroxymethylglutaryl-CoA Reductase InhibitorsAmyloid precursor protein secretasemedicine.drugJournal of Alzheimer's disease : JAD
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Brothers in arms: proBDNF/BDNF and sAPPα/Aβ-signaling and their common interplay with ADAM10, TrkB, p75NTR, sortilin, and sorLA in the progression of…

2021

Abstract Brain-derived neurotrophic factor (BDNF) is an important modulator for a variety of functions in the central nervous system (CNS). A wealth of evidence, such as reduced mRNA and protein level in the brain, cerebrospinal fluid (CSF), and blood samples of Alzheimer’s disease (AD) patients implicates a crucial role of BDNF in the progression of this disease. Especially, processing and subcellular localization of BDNF and its receptors TrkB and p75 are critical determinants for survival and death in neuronal cells. Similarly, the amyloid precursor protein (APP), a key player in Alzheimer’s disease, and its cleavage fragments sAPPα and Aβ are known for their respective roles in neuropro…

ADAM10Clinical BiochemistryNerve Tissue ProteinsTropomyosin receptor kinase BReceptors Nerve Growth FactorBiochemistryNeuroprotectionADAM10 ProteinAmyloid beta-Protein PrecursorNeurotrophic factorsAlzheimer DiseaseAmyloid precursor proteinHumansReceptor trkBMolecular BiologyLDL-Receptor Related ProteinsAmyloid beta-PeptidesMembrane GlycoproteinsbiologyBrain-Derived Neurotrophic FactorMembrane ProteinsMembrane Transport ProteinsAdaptor Proteins Vesicular Transportnervous systembiology.proteinSignal transductionAmyloid Precursor Protein SecretasesNeuroscienceAmyloid precursor protein secretaseNeurotrophinBiological chemistryReferences
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Constitutive and regulated α-secretase cleavage of Alzheimer’s amyloid precursor protein by a disintegrin metalloprotease

1999

Amyloid β peptide (Aβ), the principal proteinaceous component of amyloid plaques in brains of Alzheimer’s disease patients, is derived by proteolytic cleavage of the amyloid precursor protein (APP). Proteolytic cleavage of APP by a putative α-secretase within the Aβ sequence precludes the formation of the amyloidogenic peptides and leads to the release of soluble APPsα into the medium. By overexpression ofa disintegrinandmetalloprotease (ADAM), classified as ADAM 10, in HEK 293 cells, basal and protein kinase C-stimulated α-secretase activity was increased severalfold. The proteolytically activated form of ADAM 10 was localized by cell surface biotinylation in the plasma membrane, but the m…

ADAM10Molecular Sequence DataBiologyKidneyTransfectionCell LineSubstrate SpecificityADAM10 ProteinAmyloid beta-Protein PrecursorEndopeptidasesAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesHumansPoint MutationADAM17 ProteinAmino Acid SequenceCloning MolecularProtein kinase AProtein Kinase CSecretory pathwayBinding SitesMultidisciplinaryHEK 293 cellsP3 peptideMembrane ProteinsMetalloendopeptidasesBiological SciencesPeptide FragmentsRecombinant Proteinscarbohydrates (lipids)ADAM ProteinsKineticsZincAlpha secretaseBiochemistryMutagenesis Site-Directedbiology.proteinCattleAmyloid Precursor Protein SecretasesProceedings of the National Academy of Sciences
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Effect of a dominant-negative form of ADAM10 in a mouse model of Alzheimer's disease.

2009

The alpha-secretase cleaves in the non-amyloidogenic pathway the amyloid-beta protein precursor (AbetaPP) within the region of the amyloid-beta peptides to prevent their formation and aggregation in the brain. Members of the ADAM family (a disintegrin and metalloprotease) are the main candidates for physiologically relevant alpha-secretases. We recently demonstrated that overexpression of ADAM10 in mice transgenic for human AbetaPP (ADAM10 x APP[V717I]) alleviated functional deficits related to Alzheimer's disease. To further demonstrate that this is due to the specific activity of alpha-secretase, we characterized mice overexpressing an inactive form of ADAM10 (ADAM10[E384A]; ADAM10-dn). T…

ADAM10Morris water navigation taskGlutamic AcidStimulationMice TransgenicADAM10 ProteinAmyloid beta-Protein PrecursorMiceIn vivoAlzheimer DiseaseDisintegrinReaction TimeAnimalsHumansIsoleucineProtein precursorMaze LearningSwimmingMetalloproteinaseAlaninebiologyBehavior AnimalChemistryGeneral NeuroscienceAge FactorsMembrane ProteinsValineGeneral MedicineCell biologyMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyADAM ProteinsDisease Models Animalbiology.proteinSpecific activityGeriatrics and GerontologyAmyloid Precursor Protein SecretasesJournal of Alzheimer's disease : JAD
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Down-regulation of Endogenous Amyloid Precursor Protein Processing due to Cellular Aging

2005

Processing of amyloid precursor protein (APP) is a well acknowledged central pathogenic mechanism in Alzheimer disease. However, influences of age-associated cellular alterations on the biochemistry of APP processing have not been studied in molecular detail so far. Here, we report that processing of endogenous APP is down-regulated during the aging of normal human fibroblasts (IMR-90). The generation of intracellular APP cleavage products C99, C83, and AICD gradually declines with increasing life span and is accompanied by a reduced secretion of soluble APP (sAPP) and sAPPalpha. Further, the maturation of APP was reduced in senescent cells, which has been shown to be directly mediated by a…

ADAM10NicastrinEndogenyBiochemistryCell LineAmyloid beta-Protein PrecursorMembrane MicrodomainsDownregulation and upregulationEndopeptidasesmental disordersPresenilin-1Amyloid precursor proteinAspartic Acid EndopeptidasesHumansSecretionMolecular BiologyCellular SenescenceMembrane GlycoproteinsbiologyChemistryMembrane ProteinsCell BiologyFibroblastsCholesterolBiochemistrybiology.proteinAmyloid Precursor Protein SecretasesProtein Processing Post-TranslationalAmyloid precursor protein secretaseIntracellularJournal of Biological Chemistry
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Influence of training and a maximal exercise test in analytical variability of muscular, hepatic, and cardiovascular biochemical variables.

2014

Short, middle, and long-term exercise, as well as the relative intensity of the physical effort, may influence a broad array of laboratory results, and it is thereby of pivotal importance to appropriately differentiate the 'physiologic' from the 'pathological' effects of exercise. Therefore, the values of some biomarkers in physically active subjects may be cautiously interpreted since the results may fall outside the conventional reference ranges. It has been demonstrated that middle and long-term endurance and/or strenuous exercise triggers transient elevations of muscular and cardiac biomarkers. However, no data have been published about the effect of short-term maximal exercise test on …

AdultCalcitoninMalemedicine.medical_specialtyCardiac biomarkersCardiovascular biomarkersCalcitonin Gene-Related PeptideClinical BiochemistryPhysical ExertionPhysical medicine and rehabilitationReference ValuesInternal medicineNatriuretic Peptide BrainmedicineCreatine Kinase MB FormHumansAspartate AminotransferasesProtein PrecursorsMuscle SkeletalPathologicalExerciseRelative intensitybiologyL-Lactate Dehydrogenasebusiness.industryC-reactive proteinSkeletal muscleHeartGeneral Medicinegamma-GlutamyltransferaseLaboratory resultsPeptide FragmentsTroponinmedicine.anatomical_structureexercise; laboratory; biomarkersC-Reactive ProteinLiverCardiologybiology.proteinExercise TestPhysical EnduranceMaximal exerciseSedentary BehaviorbusinesslaboratoryBiomarkersScandinavian journal of clinical and laboratory investigation
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Erythrocyte Membrane Phosphatidylserine Exposure in Obesity

2008

It has been suggested that increased erythrocyte membrane phosphatidylserine (PS) exposure could contribute to hypercoagulability and hemorheological disturbances in obesity. The aim of our study was to evaluate PS exposure in obese patients and in a control group and to correlate this with hemorheological properties, i.e., erythrocyte aggregability (EA) and deformability, and to evaluate the effect of weight loss on these parameters. An anthropometric and analytical evaluation was performed at baseline and after 3 months on a diet (very low-calorie diet for 4 weeks and low-calorie diet for 2 months) on 49 severe or morbid obese patients (37 women, 12 men) and 55 healthy volunteers (39 wome…

AdultErythrocyte AggregationMalemedicine.medical_specialtyAdolescentEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Phosphatidylserinesmedicine.disease_causeErythrocyte aggregationFlow cytometrychemistry.chemical_compoundYoung AdultEndocrinologyWeight lossInternal medicineErythrocyte DeformabilityMalondialdehydeWeight LossMedicineErythrocyte deformabilityHumansObesityProtein PrecursorsNutrition and Dieteticsmedicine.diagnostic_testbusiness.industryErythrocyte MembranePhosphatidylserineMiddle AgedMalondialdehydePathophysiologyPeptide FragmentsOxidative StressEndocrinologychemistryCase-Control StudiesImmunologyFemaleProthrombinmedicine.symptombusinessOxidative stress
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