| Project/Area Number |
24657141
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Cell biology
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
TAGAYA MITSUO 東京薬科大学, 生命科学部, 教授 (30179569)
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| Co-Investigator(Kenkyū-buntansha) |
谷 佳津子 東京薬科大学, 生命科学部, 教授 (40266896)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 小胞体 / ミトコンドリア / ペルオキシソーム / 脂肪滴 / Syntaxin 17 / Sec16B / サブコンパートメント / Sec16b / syntaxin17 / syntaxin 17 |
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| Research Abstract |
We examined whether the MAM (mitochondria-associated membrane), a subdomain of the endoplasmic reticulum, participates in lipid droplet formation and peroxisome biogenesis. Lipid droplet formation was suppressed by knockdown of MAM-organizing proteins, such as syntaxin17. Rab32 may also contribute to lipid droplet formation. Depletion of Sec16B caused lipid droplet formation and elongation of peroxisomes in a certain cell type, but suppressed lipid droplet formation and shortened peroxisomes in another type of cells. The data suggest that the MAM has an important role in lipid droplet formation, and that there is an intimate relation between lipid droplet formation and peroxisome biogenesis.
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