TTC7 and Hyccin Regulate Neuronal A beta(42) Accumulation and its Associated Neural Deficits in A beta(42)-Expressing Drosophila
文献类型：期刊论文
| 作者 | Sun, Minghao1; Zhao, Yinghui1,2; Han, Men3; Zhang, Baozhu1; Zhang, Xiao1; Zhang, Qichao1,5; Lim, Nastasia K-H1,6; Wang, Wen-An4; Huang, Fu-De1,5 |
| 刊名 | JOURNAL OF ALZHEIMERS DISEASE
 |
| 出版日期 | 2018 |
| 卷号 | 65期号:3页码:1001-1010 |
| 关键词 | Alzheimer's disease amyloid-beta Drosophila Hyccin PI4KIII alpha TTC7 |
| ISSN号 | 1387-2877 |
| DOI | 10.3233/JAD-170907 |
| 文献子类 | Article |
| 英文摘要 | Neuronal amyloid-beta (A beta) accumulation plays an important role in the pathogenesis of Alzheimer's disease (AD). The conformation and toxicity of A beta are regulated by lipids on the plasma membrane. Previously, we found downregulation of Rolling Blackout (RBO) or phosphatidylinositol-4-kinase type III alpha (PI4KIII1 alpha) reduces neuronal A beta accumulation and associated neural deficits in a Drosophila model expressing A beta(42) . In mammals, the homologs of RBO and PI4KIII alpha were reported to form a plasma membrane-localized complex with a scaffold protein TTC7 and cytosolic protein Hyccin/FAM126A to tightly control the plasmalemmal level of phosphatidylinositol-4-phosphate. Here, we show genetic downregulation of Drosophila TTC7 and Hyccin also reduces neuronal A beta accumulation and associated synaptic and motor defects as well as premature death in A beta(42) -expressing flies, while overexpression of TTC7 and Hyccin produced the opposite effect. These results, together with our previous study, demonstrate that RBO/TTC7/PI4KIII alpha/Hyccin regulate neuronal A beta accumulation and associated neural deficits in the Drosophila model, further supporting the RBO/Efr3-PI4KIII alpha complex as a potential therapeutic target for AD. |
| WOS关键词 | BETA-AMYLOID PEPTIDES ; ALZHEIMERS-DISEASE ; PLASMA-MEMBRANE ; INTRANEURONAL ACCUMULATION ; RECEPTOR ; PROTEIN ; TRANSMISSION ; CONTRIBUTES ; MECHANISMS ; HYPOTHESIS |
| 资助项目 | National Natural Science Foundation of China[81571101] ; National Natural Science Foundation of China[81771416] ; National Natural Science Foundation of China[81650110527] |
| WOS研究方向 | Neurosciences & Neurology |
| 语种 | 英语 |
| WOS记录号 | WOS:000444339800023 |
| 出版者 | IOS PRESS |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/272297]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Huang, Fu-De |
| 作者单位 | 1.Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Adv Res Inst, Shanghai 201210, Peoples R China; 2.Shanghai Univ, Sch Life Sci, Lab Mol Neurobiol, Shanghai, Peoples R China; 3.Qingdao Univ, Sch Med, Qingdao Municipal Hosp, Dept Neurol, Qingdao, Peoples R China; 4.Shanghai Jiao Tong Univ, Sch Med, Chongming Branch, Xinhua Hosp,Dept Neurol, Shanghai, Peoples R China; 5.Univ Chinese Acad Sci, Chinese Acad Sci, Sinodanish Coll, Beijing, Peoples R China; 6.Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Materia Med, Shanghai, Peoples R China |
| 推荐引用方式 GB/T 7714 | Sun, Minghao,Zhao, Yinghui,Han, Men,et al. TTC7 and Hyccin Regulate Neuronal A beta(42) Accumulation and its Associated Neural Deficits in A beta(42)-Expressing Drosophila[J]. JOURNAL OF ALZHEIMERS DISEASE,2018,65(3):1001-1010. |
| APA | Sun, Minghao.,Zhao, Yinghui.,Han, Men.,Zhang, Baozhu.,Zhang, Xiao.,...&Huang, Fu-De.(2018).TTC7 and Hyccin Regulate Neuronal A beta(42) Accumulation and its Associated Neural Deficits in A beta(42)-Expressing Drosophila.JOURNAL OF ALZHEIMERS DISEASE,65(3),1001-1010. |
| MLA | Sun, Minghao,et al."TTC7 and Hyccin Regulate Neuronal A beta(42) Accumulation and its Associated Neural Deficits in A beta(42)-Expressing Drosophila".JOURNAL OF ALZHEIMERS DISEASE 65.3(2018):1001-1010. |
入库方式： OAI收割
来源：上海药物研究所
浏览0
下载0
收藏0
其他版本
除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。