2015 Fiscal Year Final Research Report
A mechanism regulating the copper acquisition by intracellular proteins
| Project/Area Number |
25291028
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Functional biochemistry
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
NOMURA Takao 慶應義塾大学, 理工学部, 助教 (90597840)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 銅シャペロン / 神経変性疾患 / タンパク質フォールディング / SOD1 / タンパク質凝集 / 筋萎縮性側索硬化症 |
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| Outline of Final Research Achievements |
Copper ion is essential to various physiologies. Most of the copper ions in our bodies exist as the protein-bound form and function as active sites for enzymatic reactions. Also, the level of copper ions in our bodies is strictly controlled, and even slight deviation of the copper ions in physiological conditions will lead to pathological conditions and sometimes fatal diseases. Here, we investigated the mechanism regulating the acquisition of copper ions by intracellular proteins and also examined the molecular pathomechanism of the disease caused by the mis-regulation of copper metabolism in the cell. More precisely, we have noted the activation mechanism of Cu,Zn-superoxide dismutase (SOD1), which requires a copper ion for its enzymatic activity. Also, conformational changes of SOD1 upon dissociation of metal ions have been examined and discussed in relation to the pathogenesis of amyotrophic lateral sclerosis.
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| Free Research Field |
生物無機化学
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