Identification and functional analysis of brain catechin-binding proteins using aliphatic catechin derivatives
| Project/Area Number |
15K14971
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Natural medicines
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| Research Institution | Nagasaki University |
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Principal Investigator |
IWATA Nobuhisa 長崎大学, 医歯薬学総合研究科(薬学系), 教授 (70246213)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | アルツハイマー病 / アミロイドβペプチド / ネプリライシン / αセクレターゼ / βセクレターゼ / カテキン / 結合タンパク質 / カテキン結合タンパク質 / カテキン受容体 |
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| Outline of Final Research Achievements |
I previously found that aliphatic catechin derivatives introduced an alkyl group not only upregulated major Aβ-degrading enzyme neprilysin and α-secretase that cleaves amyloid precursor protein not to generate Aβ, but also downregulated β-secretase via gene expression. In this study, to understand catechin-mediated regulatory mechanism of these gene expressions, I screened catechin-binding proteins for membrane or cytosolic proteins derived from neuronal cells or mouse brains using catechin-coupled magnetic beads and LC/MSMS method, and identified two candidate proteins; one is a secretory vesicle-related protein, and the other is gene expression-related protein. When the neuronal cells overexpressing the candidate protein A or B were treated with aliphatic catechin derivatives, neprilysin activity was more strongly increased than that in mock cells treated with aliphatic catechins, as well β-secrease activity was more prominently suppressed in cells overexpressing the protein A.
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Report
(3 results)
Research Products
(17 results)
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[Presentation] Disease-modifying therapy through enhancement of neuronal Aβ-degrading enzyme neprilysin activity for Alzheimer's disease.2016
Author(s)
Iwata N, Hori Y, Watanabe K, Kinoshita M, Kawano Y, Hatta D, Honda M, Asai M, Shirotani K, Ohyama K, Kuroda N, and Tanaka T.
Organizer
The 30th International College of Neuropsychopharmacology World Congress
Place of Presentation
ソウル（韓国)
Year and Date
2016-07-03
Related Report
Int'l Joint Research
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