Cell Reports · 2015 · 55 citations · 32 references
Life SciencesBiochemistryNeuroscienceApoptosisMolecular NeurobiologyMolecular NeuroscienceMitochondrial DysfunctionMitochondrial Stress ResponsesMolecular Basis Of NeurodegenerationNeurodegenerative DiseasesNeurodegenerative DisordersProtein DegradationFrameshift MutationsNeuronal DysfunctionProteasome SystemUbiquitin BindingUbiquitin SystemUbiquitin-mediated DegradationUbiquitin-proteasome ProteolysisUbiquitin-proteasome System Dysfunction
-induced enhancement of the basic amino acids arginine, ornithine, and lysine at mitochondria as a decisive toxic event, which can be reversed by Cdc48/Vms1-mediated proteolysis. The fact that AD-induced cellular dysfunctions can be avoided by UPS activity at mitochondria has potentially far-reaching pathophysiological implications.
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