Revealing the molecular mechanism of regulating SOD1 proteostasis by zinc-related genes for understanding ALS pathogenesis
| Project/Area Number |
16K18513
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional biochemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Homma Kengo 東京大学, 大学院薬学系研究科(薬学部), 特任研究員 (60708171)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 亜鉛 / SOD1 / ALS / 亜鉛トランスポーター / 構造変化 |
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| Outline of Final Research Achievements |
ALS is a devastating neurodegenerative disease characterized by the selective motoneuron death. We have previously reported that SOD1 mutants interact with Derlin-1, leading to the motoneuron death. In addition, we have found that the zinc depletion induced the conformational change of wild-type SOD1 (SOD1WT) and the interaction between SOD1WT and Derlin-1. To evaluate the possibility that the conformationally-disordered SOD1WT could be involved in the pathogenesis of SOD1 mutation-negative ALS, we investigated the molecular mechanism of SOD1WT conformational change.
The analysis of ZIP13, a zinc transporter, that was identified as a mediator of zinc depletion-induced SOD1WT conformational change revealed the essential role of the Golgi apparatus in zinc depletion-induced SOD1WT conformational change.
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Report
(3 results)
Research Products
(1 results)
