ADAM10 missense mutations potentiate β-amyloid accumulation by impairing prodomain chaperone function - Wikidata - awgldk - TriplyDB

ADAM10 missense mutations potentiate β-amyloid accumulation by impairing prodomain chaperone function

ADAM10 missense mutations potentiate β-amyloid accumulation by impairing prodomain chaperone function

http://www.wikidata.org/entity/Q33926960

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Genes associated with Alzheimer's disease: an overview and current status Misframed ubiquitin and impaired protein quality control: an early event in Alzheimer's disease Deletion of aquaporin-4 in APP/PS1 mice exacerbates brain Aβ accumulation and memory deficits Alzheimer Disease: Crosstalk between the Canonical Wnt/Beta-Catenin Pathway and PPARs Alpha and Gamma Current and future implications of basic and translational research on amyloid-β peptide production and removal pathways Genetic diagnosis and prognosis of Alzheimer's disease: challenges and opportunities Cerebrospinal fluid biomarkers of neurovascular dysfunction in mild dementia and Alzheimer's disease Function, therapeutic potential and cell biology of BACE proteases: current status and future prospects.Opposing effects of membrane-anchored CX3CL1 on amyloid and tau pathologies via the p38 MAPK pathway Targeting the β secretase BACE1 for Alzheimer's disease therapy.Alzheimer's disease risk genes and mechanisms of disease pathogenesis Inhibition of ADAM10 promotes the clearance of Aβ across the BBB by reducing LRP1 ectodomain shedding.SAP97-mediated ADAM10 trafficking from Golgi outposts depends on PKC phosphorylation.Dietary (-)-epicatechin as a potent inhibitor of βγ-secretase amyloid precursor protein processing.Low-variance RNAs identify Parkinson's disease molecular signature in blood Activation of peroxisome proliferator-activated receptor α stimulates ADAM10-mediated proteolysis of APP Mapping Breakpoints of Complex Chromosome Rearrangements Involving a Partial Trisomy 15q23.1-q26.2 Revealed by Next Generation Sequencing and Conventional Techniques.Massachusetts Alzheimer's Disease Research Center: progress and challenges.Non-alcoholic fatty liver disease induces signs of Alzheimer's disease (AD) in wild-type mice and accelerates pathological signs of AD in an AD model The IgLON Family Member Negr1 Promotes Neuronal Arborization Acting as Soluble Factor via FGFR2.Fluorescent Analogue of Batimastat Enables Imaging of α-Secretase in Living Cells The Alzheimer's disease peptide β-amyloid promotes thrombin generation through activation of coagulation factor XII.Redundant Gs-coupled serotonin receptors regulate amyloid-β metabolism in vivo.An activated form of ADAM10 is tumor selective and regulates cancer stem-like cells and tumor growth.Consumption of pomegranates improves synaptic function in a transgenic mice model of Alzheimer's disease.Alzheimer's disease genetics: from the bench to the clinic.Common and Rare Genetic Variants Associated With Alzheimer's Disease.Modulation of Neuroinflammation in the Central Nervous System: Role of Chemokines and Sphingolipids.Monoaminergic neuropathology in Alzheimer's disease.Hypoxia/ischemia activate processing of Amyloid Precursor Protein: impact of vascular dysfunction in the pathogenesis of Alzheimer's disease.Clearance of cerebral Aβ in Alzheimer's disease: reassessing the role of microglia and monocytes.Therapeutic Potential of Secreted Amyloid Precursor Protein APPsα.The Role of ADAM10 in Alzheimer's Disease.Increase of α-Secretase ADAM10 in Platelets Along Cognitively Healthy Aging.State of Play in Alzheimer's Disease Genetics.Untangling Genetic Risk for Alzheimer's Disease.Viral gene transfer of APPsα rescues synaptic failure in an Alzheimer's disease mouse model.Molecular systems evaluation of oligomerogenic APP(E693Q) and fibrillogenic APP(KM670/671NL)/PSEN1(Δexon9) mouse models identifies shared features with human Alzheimer's brain molecular pathology.Shedding the epilepsy comorbidity in Alzheimer's disease.Targeting amyloid precursor protein shuttling and processing - long before amyloid beta formation.

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P2860

ADAM10 missense mutations potentiate β-amyloid accumulation by impairing prodomain chaperone function

http://www.wikidata.org/entity/Q33926960

description

2013 nî lūn-bûn

@nan

2013 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2013年の論文

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年學術文章

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name

ADAM10 missense mutations pote ...... g prodomain chaperone function

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ADAM10 missense mutations pote ...... g prodomain chaperone function

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type

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ADAM10 missense mutations pote ...... g prodomain chaperone function

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ADAM10 missense mutations pote ...... g prodomain chaperone function

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ADAM10 missense mutations pote ...... g prodomain chaperone function

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ADAM10 missense mutations pote ...... g prodomain chaperone function

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ADAM10 missense mutations pote ...... g prodomain chaperone function

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Andrea N Lesinski

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Donna M Romano

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Doo Yeon Kim

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Jaehong Suh

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Moira A Gannon

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Se Hoon Choi

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P2860

APP binds DR6 to trigger axon pruning and neuron death via distinct caspases

Role of Genes and Environments for Explaining Alzheimer Disease

The disintegrin/metalloprotease ADAM 10 is essential for Notch signalling but not for alpha-secretase activity in fibroblasts

SIRT1 suppresses beta-amyloid production by activating the alpha-secretase gene ADAM10.

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

The PSIPRED protein structure prediction server

Alzheimer's disease: genes, proteins, and therapy

Constitutive and regulated alpha-secretase cleavage of Alzheimer's amyloid precursor protein by a disintegrin metalloprotease

Autolytic processing at Glu586-Ser587 within the cysteine-rich domain of human adamalysin 19/disintegrin-metalloproteinase 19 is necessary for its proteolytic activity

ADAM-10 over-expression increases cortical synaptogenesis

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Rudolph E. Tanzi

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256928740

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24055016

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molecular chaperones

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4105199

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