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Differential regulation of BACE1 expression by oxidative and nitrosative signals

Author(s): Kwak Young-Don | Wang Ruishan | Li Jing | Zhang Yun-Wu | Xu Huaxi | Liao Francesca-Fang

Journal: Molecular Neurodegeneration
ISSN 1750-1326

Volume: 6;
Issue: 1;
Start page: 17;
Date: 2011;
Original page

Abstract Background It is well established that both cerebral hypoperfusion/stroke and type 2 diabetes are risk factors for Alzheimer's disease (AD). Recently, the molecular link between ischemia/hypoxia and amyloid precursor protein (APP) processing has begun to be established. However, the role of the key common denominator, namely nitric oxide (NO), in AD is largely unknown. In this study, we investigated redox regulation of BACE1, the rate-limiting enzyme responsible for the β-cleavage of APP to Aβ peptides. Results Herein, we studied events such as S-nitrosylation, a covalent modification of cysteine residues by NO, and H2O2-mediated oxidation. We found that NO and H2O2 differentially modulate BACE1 expression and enzymatic activity: NO at low concentrations (
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