Overexpression of Ubiquilin-1 Alleviates Alzheimer’s Disease-Caused Cognitive and Motor Deficits and Reduces Amyloid-β Accumulation in Mice
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Title
Overexpression of Ubiquilin-1 Alleviates Alzheimer’s Disease-Caused Cognitive and Motor Deficits and Reduces Amyloid-β Accumulation in Mice
Authors
Keywords
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Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 59, Issue 2, Pages 575-590
Publisher
IOS Press
Online
2017-06-09
DOI
10.3233/jad-170173
References
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Note: Only part of the references are listed.- Relationship between ubiquilin-1 and BACE1 in human Alzheimer's disease and APdE9 transgenic mouse brain and cell-based models
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- Ubiquilin-1 Is a Molecular Chaperone for the Amyloid Precursor Protein
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- Ubiquilin functions in autophagy and is degraded by chaperone-mediated autophagy
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- Alzheimer's Disease-Associated Ubiquilin-1 Regulates Presenilin-1 Accumulation and Aggresome Formation
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- PLIC proteins or ubiquilins regulate autophagy-dependent cell survival during nutrient starvation
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- Acute predator stress impairs the consolidation and retrieval of hippocampus-dependent memory in male and female rats
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- Mutant Presenilin 1 Increases the Levels of Alzheimer Amyloid β-Peptide Aβ42 in Late Compartments of the Constitutive Secretory Pathway
- (2003) Suzana S. Petanceska et al. JOURNAL OF NEUROCHEMISTRY
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