| Budget Amount *help |
¥82,940,000 (Direct Cost: ¥63,800,000、Indirect Cost: ¥19,140,000)
Fiscal Year 2023: ¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2022: ¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2021: ¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2020: ¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2019: ¥19,500,000 (Direct Cost: ¥15,000,000、Indirect Cost: ¥4,500,000)
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| Outline of Final Research Achievements |
Copper is an essential trace metal for sustaining life, and its deficiency or excess can lead to disease. This study aimed to elucidate, at the molecular level, the mechanisms by which SOD1 and its copper chaperone CCS acquire copper ions, with a focus on metal-binding abnormalities and structural alterations of SOD1 implicated in neurodegenerative diseases. Through collaborations within the research area, we employed advanced techniques such as native mass spectrometry, cryo-electron microscopy, and synthetic monobody tools to uncover the mechanisms of SOD1 misfolding, disruption of metal selectivity, and dysregulation of intracellular metal networks. Furthermore, by analyzing metal binding and structural stability in bacterial SOD1-like proteins, we advanced our understanding of the copper acquisition process and folding mechanisms of human SOD1.
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