The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
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The Function of Autophagy in Neurodegenerative DiseasesPalmitate Increases β-site AβPP-Cleavage Enzyme 1 Activity and Amyloid-β Genesis by Evoking Endoplasmic Reticulum Stress and Subsequent C/EBP Homologous Protein Activation.Knock-in of human BACE1 cleaves murine APP and reiterates Alzheimer-like phenotypesL655,240, acting as a competitive BACE1 inhibitor, efficiently decreases β-amyloid peptide production in HEK293-APPswe cells.A peptide binding to the β-site of APP improves spatial memory and attenuates Aβ burden in Alzheimer's disease transgenic miceCancer and neurodegenerative disorders: pathogenic convergence through microRNA regulation.Unveiling a novel transient druggable pocket in BACE-1 through molecular simulations: Conformational analysis and binding mode of multisite inhibitors.Association of BACE1 Gene Polymorphism with Cerebellar Volume but Not Cognitive Function in Normal Individuals.Circulating miRNAs as biomarkers for neurodegenerative disorders.BACE1-Deficient Mice Exhibit Alterations in Immune System Pathways.Hypercholesterolemia induces short-term spatial memory impairments in mice: up-regulation of acetylcholinesterase activity as an early and causal event?PPARs in the central nervous system: roles in neurodegeneration and neuroinflammation.Multiple Mechanisms Linking Type 2 Diabetes and Alzheimer's Disease: Testosterone as a Modifier.The precision of axon targeting of mouse olfactory sensory neurons requires the BACE1 proteaseInvestigation of flap flexibility of β-secretase using molecular dynamic simulations.p75 neurotrophin receptor interacts with and promotes BACE1 localization in endosomes aggravating amyloidogenesis.Sildenafil Decreases BACE1 and Cathepsin B Levels and Reduces APP Amyloidogenic Processing in the SAMP8 Mouse.Systems Pharmacology Analysis of the Amyloid Cascade after β-Secretase Inhibition Enables the Identification of an Aβ42 Oligomer Pool.Increased BACE1-AS long noncoding RNA and β-amyloid levels in heart failure.β-Site APP-cleaving enzyme 1 (BACE1) cleaves cerebellar Na+ channel β4-subunit and promotes Purkinje cell firing by slowing the decay of resurgent Na+ current.
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The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on December 2007
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
@en
The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
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type
label
The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
@en
The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
@nl
prefLabel
The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
@en
The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
@nl
P2860
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P1476
The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimer's Disease.
@en
P2093
P2860
P304
P356
10.2174/138920207783769512
P577
2007-12-01T00:00:00Z