期刊
NEUROBIOLOGY OF AGING
卷 27, 期 9, 页码 1239-1249出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2005.07.001
关键词
Alzheimer's disease; amyloid beta-peptide; protein oxidation; proteomics; C. elegans
资金
- NIA NIH HHS [AG12423, AG-05119, AG-10836, AG21037] Funding Source: Medline
Protein oxidation has been shown to lead to loss of protein function, increased protein aggregation, decreased protein turnover, decreased membrane fluidity, altered cellular redox poteintial, loss of Ca2+ homeostaisis, and cell death. There is increasing evidence that protein oxidation is involved in the pathogenesis of Alzheimer's disease and amyloid beta-peptide (1-42) has been implicated as a mediator of oxidative stress in AD. However, the specific implications of the oxidation induced by A beta(1-42) on the neurodegeneration evident in AD are unknown. In this study, we used proteomic techniques to identify specific targets of oxidation in transgenic Caenorhabditis elegans (C. elegans) expressing human A beta(1-42). We identified 16 oxidized proteins involved in energy metabolism, proteasome function, and scavenging of oxidants that are more oxidized compared to control lines. These results are discussed with reference to Alzheimer's disease. (c) 2005 Elsevier Inc. All rights reserved.
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