| Project/Area Number |
26870067
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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 |
Pathological medical chemistry
Cell biology
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Research Collaborator |
OTSUKA Rina
INOUE Hiroaki
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ミトコンドリア / 鉄代謝 / 小胞 / 神経変性疾患 / オートファジー / 品質管理 / 鉄動態 / 膜ダイナミクス |
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| Outline of Final Research Achievements |
Mitochondria produce cellular energy in response to cellular demands. Accumulation of dysfunctional mitochondria due to impaired quality control system, links to multiple human disorders. Recent studies revealed that elimination of damaged mitochondria through the autophagy is important for the quality and quantity control of them.
We have revealed that autophagy-deficient mice develop multiple liver tumors with accumulation of cellular stress and damaged mitochondria. During mitochondrial collapse in autophagy deficit tissues, we observed that liver mitochondria in autophagy-deficient mice show decreased iron content, however total iron contents in a cell is normal. These results suggested that insufficiently amounts of iron cause deformation of oxidative phosphorylation complex in a mitochondrion, then mitochondrion turn to be inactive. Alos abnormal iron distribution in a cell might cause an aggravating factor for the cellular environment, such as a trigger for fenton reaction.
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