Inhibition of intracellular transport involved in fluoride-induced hepatotoxicity.
| Project/Area Number |
24780297
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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 |
Applied veterinary science
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
NAKAGAWA HIROSHI 大阪府立大学, 生命環境科学研究科(系), 助教 (60336807)
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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 |
¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | トキシコロジー / 細胞シグナリング / 脂肪代謝 / 細胞内小胞輸送 / 小胞輸送 / 細胞内シグナリング / 細胞死 / アポトーシス / ERストレス / 肝毒性 |
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| Research Abstract |
Fluoride hepatotoxicity reveals lipid retention in hepatocyte. We assumed that a disruption of intra-cellular lipid vesicle transport retained the lipid in endoplasmic reticulum. We examined the role of lipid metabolism relating proteins CD36, ApoB, CIDE-B, Vamp-7, FABP-1 in intra-cellular vesicle traffic systems. CIDE-B was recruited from cytosol to endoplasmic reticulum membrane with the formation of protein transport vesicle. On the other hand, inhibition of protein transport vesicle formation blocked CIDE-B recruitment from cytosol to endoplasmic reticulum membrane. These results indicate lipid metabolism relating protein CIDE-B recruited from cytosol to endoplasmic reticulum membrane like a coat protein of protein transport vesicles.
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Report
(3 results)
Research Products
(27 results)
