PS1 activates PI3K thus inhibiting GSK-3 activity and tau overphosphorylation: effects of FAD mutations
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Current Insights into Molecular Mechanisms of Alzheimer Disease and Their Implications for Therapeutic ApproachesTmem100, an ALK1 receptor signaling-dependent gene essential for arterial endothelium differentiation and vascular morphogenesisPresenilin-1 regulates the expression of p62 to govern p62-dependent tau degradationMetalloproteinase/Presenilin1 processing of ephrinB regulates EphB-induced Src phosphorylation and signalingA protease-independent function for SPPL3 in NFAT activationGAB2 alleles modify Alzheimer's risk in APOE epsilon4 carriersWhen loss is gain: reduced presenilin proteolytic function leads to increased Abeta42/Abeta40. Talking Point on the role of presenilin mutations in Alzheimer diseaseCellular Notch responsiveness is defined by phosphoinositide 3-kinase-dependent signalsInflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's DiseaseThe dynamic role of beta-catenin in synaptic plasticityEarly etiology of Alzheimer's disease: tipping the balance toward autophagy or endosomal dysfunction?mTOR/p70S6k signalling alteration by Abeta exposure as well as in APP-PS1 transgenic models and in patients with Alzheimer's diseaseEthyl Pyruvate Combats Human Leukemia Cells but Spares Normal Blood CellsSirt1 promotes axonogenesis by deacetylation of Akt and inactivation of GSK3Human neural stem cells alleviate Alzheimer-like pathology in a mouse model.Gamma-secretase-dependent and -independent effects of presenilin1 on beta-catenin.Tcf-4 transcriptional activityImpairments in fast axonal transport and motor neuron deficits in transgenic mice expressing familial Alzheimer's disease-linked mutant presenilin 1Transgenic Drosophila models of Alzheimer's disease and tauopathiesNeuropathological role of PI3K/Akt/mTOR axis in Down syndrome brain.Inhibition of glycogen synthase kinase-3β by Angelica sinensis extract decreases β-amyloid-induced neurotoxicity and tau phosphorylation in cultured cortical neurons.Mechanisms of tau-induced neurodegeneration.Genetics and biology of Alzheimer's disease and frontotemporal lobar degenerationPharmacological and genetic reversal of age-dependent cognitive deficits attributable to decreased presenilin functionModeling presenilin-dependent familial Alzheimer's disease: emphasis on presenilin substrate-mediated signaling and synaptic function.Presenilin-1 regulates induction of hypoxia inducible factor-1α: altered activation by a mutation associated with familial Alzheimer's diseasePresenilin-1 regulates the constitutive turnover of the fibronectin matrix in endothelial cellsN-cadherin regulates p38 MAPK signaling via association with JNK-associated leucine zipper protein: implications for neurodegeneration in Alzheimer diseaseAn Alzheimer's disease-relevant presenilin-1 mutation augments amyloid-beta-induced oligodendrocyte dysfunctionTelencephalin protects PAJU cells from amyloid beta protein-induced apoptosis by activating the ezrin/radixin/moesin protein family/phosphatidylinositol-3-kinase/protein kinase B pathway.Linking protective GAB2 variants, increased cortical GAB2 expression and decreased Alzheimer's disease pathologyPathological and physiological functions of presenilins.Amyloid-β as a modulator of synaptic plasticityDysregulation of protein phosphorylation/dephosphorylation in Alzheimer's disease: a therapeutic targetDeregulation of the phosphatidylinositol-3 kinase signaling cascade is associated with neurodegeneration in Npc1-/- mouse brain.Immunotherapy targeting pathological tau prevents cognitive decline in a new tangle mouse modelAlzheimer neurofibrillary degeneration: significance, etiopathogenesis, therapeutics and prevention.Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.Presenilin 1 regulates homeostatic synaptic scaling through Akt signaling.Presenilins regulate the cellular level of the tumor suppressor PTEN.Presenilin mutations linked to familial Alzheimer's disease cause an imbalance in phosphatidylinositol 4,5-bisphosphate metabolism.
P2860
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P248
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P2860
PS1 activates PI3K thus inhibiting GSK-3 activity and tau overphosphorylation: effects of FAD mutations
description
2004 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2004 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2004
@ast
im Juli 2004 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2004/07/07)
@sk
vědecký článek publikovaný v roce 2004
@cs
wetenschappelijk artikel (gepubliceerd op 2004/07/07)
@nl
наукова стаття, опублікована в липні 2004
@uk
مقالة علمية (نشرت في 7-7-2004)
@ar
name
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@ast
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@en
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@nl
type
label
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@ast
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@en
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@nl
prefLabel
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@ast
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@en
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@nl
P2093
P2860
P921
P3181
P356
P1433
P1476
PS1 activates PI3K thus inhibi ...... tion: effects of FAD mutations
@en
P2093
Alexander Schwarzman
Junichi Shioi
Miguel Gama-Sosa
Nikolaos K. Robakis
Rachael Neve
Zhiping Shao
P2860
P304
P3181
P356
10.1038/SJ.EMBOJ.7600251
P407
P577
2004-07-07T00:00:00Z