Project/Area Number |
18K06201
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 44010:Cell biology-related
|
Research Institution | Hokkaido University |
Principal Investigator |
Kitamura Akira 北海道大学, 先端生命科学研究院, 講師 (10580152)
|
Project Period (FY) |
2018-04-01 – 2021-03-31
|
Project Status |
Completed (Fiscal Year 2020)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | タンパク質恒常性 / タンパク質凝集体 / 神経変性疾患 / 筋萎縮性側索硬化症 / RNA / 分子シャペロン / ALS / TDP-43 / 蛍光相関分光法 / 線虫 / CD / FRAP / FCCS / RNA-タンパク質相互作用 / リコンビナントタンパク質 / タンパク質凝集 / 蛍光測定 |
Outline of Final Research Achievements |
Protein aggregates are frequently observed in neurons from neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). In addition, various studies have suggested that protein aggregates may be responsible for neuronal cell death. In this study, we showed that an aggregate-prone protein, which is the cause of ALS, directly interacts with RNA using fluorescence cross-correlation spectroscopy (FCCS), an interaction analysis technique with single-molecule sensitivity. Furthermore, we demonstrated that the intracellular expression of the RNA prevents aggregate formation.
|
Academic Significance and Societal Importance of the Research Achievements |
これまでタンパク質の凝集形成を抑制する細胞内在性因子として,分子シャペロンが知られていた.分子シャペロンはタンパク質の一群である.本研究は,RNAがタンパク質凝集を直接抑制する効果を新規に実証したものである.また,このようなRNAは将来的にALSなどの治療医薬品として開発対象になりうる.本研究はその応用につながる道筋を拓いたものである.
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