Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1 - sprookjes - yvandenbroek - TriplyDB

Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1

Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1

http://www.wikidata.org/entity/Q24302464

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Mitochondria, calcium and cell death: a deadly triad in neurodegeneration Conditional forebrain inactivation of nicastrin causes progressive memory impairment and age-related neurodegeneration Role of ROS and RNS Sources in Physiological and Pathological Conditions The synaptic maintenance problem: membrane recycling, Ca2+ homeostasis and late onset degeneration Early etiology of Alzheimer's disease: tipping the balance toward autophagy or endosomal dysfunction?Protein transamidation by transglutaminase 2 in cells: a disputed Ca2+-dependent action of a multifunctional protein Deranged calcium signaling and neurodegeneration in spinocerebellar ataxia type 3 Alzheimer's disease-linked mutations in presenilin-1 result in a drastic loss of activity in purified γ-secretase complexes.A novel function for the presenilin family member spe-4: inhibition of spermatid activation in Caenorhabditis elegans Mitochondrial Ca2+ overload underlies Abeta oligomers neurotoxicity providing an unexpected mechanism of neuroprotection by NSAIDs Cardiomyocyte contractile dysfunction in the APPswe/PS1dE9 mouse model of Alzheimer's disease Reduced synaptic STIM2 expression and impaired store-operated calcium entry cause destabilization of mature spines in mutant presenilin mice.FAD mutations in amyloid precursor protein do not directly perturb intracellular calcium homeostasis.Alzheimer's disease and neuronal network activity Mutagenesis mapping of the presenilin 1 calcium leak conductance pore.Quantitative proteomic analysis of mitochondria in aging PS-1 transgenic mice.An overview of APP processing enzymes and products.Progressive age-related impairment of the late long-term potentiation in Alzheimer's disease presenilin-1 mutant knock-in mice Inositol trisphosphate receptor Ca2+ release channels in neurological diseases.Gain-of-function enhancement of IP3 receptor modal gating by familial Alzheimer's disease-linked presenilin mutants in human cells and mouse neurons.Role of presenilins in neuronal calcium homeostasis Proteases and proteolysis in Alzheimer disease: a multifactorial view on the disease process.NMDA-mediated Ca(2+) influx drives aberrant ryanodine receptor activation in dendrites of young Alzheimer's disease mice.Regulation of Ca2+ signaling with particular focus on mast cells.Early calcium dysregulation in Alzheimer's disease: setting the stage for synaptic dysfunction.Modulation of γ-secretase activity by multiple enzyme-substrate interactions: implications in pathogenesis of Alzheimer's disease Excitability and synaptic alterations in the cerebellum of APP/PS1 mice The C terminus of Bax inhibitor-1 forms a Ca2+-permeable channel pore.A platelet protein biochip rapidly detects an Alzheimer's disease-specific phenotype Presenilin 2 modulates endoplasmic reticulum (ER)-mitochondria interactions and Ca2+ cross-talk.Bilayer measurement of endoplasmic reticulum Ca2+ channels.Endoplasmic reticulum Ca(2+) handling in excitable cells in health and disease Constitutive cAMP response element binding protein (CREB) activation by Alzheimer's disease presenilin-driven inositol trisphosphate receptor (InsP3R) Ca2+ signaling.Presenilin-like GxGD membrane proteases have dual roles as proteolytic enzymes and ion channels.Presenilins and γ-secretase: structure, function, and role in Alzheimer Disease.Lack of evidence for presenilins as endoplasmic reticulum Ca2+ leak channels Physiology and pathology of calcium signaling in the brain.Presenilins: a novel link between intracellular calcium signaling and lysosomal function?Mitochondrial Ca(2+) and neurodegeneration Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease

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P2860

Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1

http://www.wikidata.org/entity/Q24302464

description

2007 nî lūn-bûn

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2007 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2007 թվականի մայիսին հրատարակված գիտական հոդված

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2007年の論文

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2007年学术文章

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2007年學術文章

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Familial Alzheimer disease-lin ...... leak function of presenilin 1

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Familial Alzheimer disease-lin ...... leak function of presenilin 1

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Journal of Clinical Investigation

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Familial Alzheimer disease-lin ...... leak function of presenilin 1

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Bart de Strooper

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Huiping Tu

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Ilya Bezprozvanny

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Mostafa Bentahir

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Omar Nelson

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Tianhua Lei

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P2860

Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations

Loss-of-function presenilin mutations in Alzheimer disease. Talking Point on the role of presenilin mutations in Alzheimer disease

The presenilins

A new generation of Ca2+ indicators with greatly improved fluorescence properties

Presenilin-1 maintains a nine-transmembrane topology throughout the secretory pathway

Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein

A nine-transmembrane domain topology for presenilin 1

Clinical phenotypic heterogeneity of Alzheimer's disease associated with mutations of the presenilin-1 gene

Presenilin clinical mutations can affect gamma-secretase activity by different mechanisms

Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration

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10.1172/JCI30447

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Alzheimer's disease

endoplasmic reticulum calcium ion homeostasis

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1847535

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