GULP1/CED-6 ameliorates amyloid-β toxicity in a Drosophila model of Alzheimer’s disease
Publication in refereed journal

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其它資訊
摘要Amyloidogenic processing of APP by β- and γ-secretases leads to the generation of amyloid-β peptide (Aβ), and the accumulation of Aβ in senile plaques is a hallmark of Alzheimer’s disease (AD). Understanding the mechanisms of APP processing is therefore paramount. Increasing evidence suggests that APP intracellular domain (AICD) interacting proteins influence APP processing. In this study, we characterized the overexpression of AICD interactor GULP1 in a Drosophila AD model expressing human BACE and APP695. Transgenic GULP1 significantly lowered the levels of both Aβ1-40 and Aβ1-42 without decreasing the BACE and APP695 levels. Overexpression of GULP1 also reduced
APP/BACE-mediated retinal degeneration, rescued motor dysfunction and extended longevity of the flies. Our results indicate that GULP1 regulate APP processing and reduce neurotoxicity in a Drosophila AD model.
出版社接受日期30.07.2017
著者Wai Yin Vivien Chiu, Alex Chun Koon, Jacky Chi Ki Ngo, Ho Yin Edwin Chan, Kwok-Fai Lau
期刊名稱Oncotarget
出版年份2017
月份11
日期21
卷號8
期次59
出版社Impact Journals
出版地USA
頁次99274 - 99283
國際標準期刊號1949-2553
語言美式英語
關鍵詞CED-6, APP, Aβ, neurodegeneration, neurotoxicity

上次更新時間 2020-23-11 於 01:38