Analysis of molecular mechanism of sensing endoplasmic reticulum stress and effect of failing in the endoplasmic reticulum stress response
| Project/Area Number |
20247026
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | Kyoto University |
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Principal Investigator |
MORI Kazutoshi Kyoto University, 大学院・理学研究科, 教授 (70182194)
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| Co-Investigator(Kenkyū-buntansha) |
OYADOMARI Seiichi 徳島大学, 疾患ゲノム研究センター, 教授 (90502534)
HARADA Akihiro 群馬大学, 生体調節研究所, 教授 (40251441)
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| Co-Investigator(Renkei-kenkyūsha) |
MINAMINO Tetsuo 大阪大学, 大学院・医学研究科, 助教 (30379234)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥43,290,000 (Direct Cost: ¥33,300,000、Indirect Cost: ¥9,990,000)
Fiscal Year 2010: ¥13,780,000 (Direct Cost: ¥10,600,000、Indirect Cost: ¥3,180,000)
Fiscal Year 2009: ¥13,780,000 (Direct Cost: ¥10,600,000、Indirect Cost: ¥3,180,000)
Fiscal Year 2008: ¥15,730,000 (Direct Cost: ¥12,100,000、Indirect Cost: ¥3,630,000)
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| Keywords | 小胞体 / 分子シャペロン / 転写誘導 / 膜結合性転写因子 / ノックアウトマウス / 選別輸送 / 還元 / 脂肪滴 / アポリポプロテイン / 心不全 |
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| Research Abstract |
The endoplasmic reticulum (ER) membrane-bound transcription factor ATF6 translocates to the Golgi apparatus upon ER stress to be activated by proteolysis. We demonstrate that the luminal domain of ATF6 alone is sufficient for sensing ER stress. ATF6α knockout mice develop normally, however, ATF6α knockout mice exhibit liver dysfunction and steatosis upon intraperitoneal injection of the ER stress-inducing reagent tunicamycin. We point out suppression of very-low-density lipoprotein formation, which is responsible for release of neutral lipids from liver, due to the destabilized apolipoprotein B-100 as a cause of liver steatosis.
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Report
(4 results)
Research Products
(15 results)
