| Project/Area Number |
25293080
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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 |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
OYADOMARI Seiichi 徳島大学, 先端酵素学研究所(プロテオ), 教授 (90502534)
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| Co-Investigator(Kenkyū-buntansha) |
親泊 美帆 徳島大学, 疾患プロテオゲノム研究センター, 特任助教 (00596158)
三宅 雅人 徳島大学, 疾患プロテオゲノム研究センター, 助教 (30588976)
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| Co-Investigator(Renkei-kenkyūsha) |
MORI Kazutoshi 京都大学, 理学系研究科, 教授 (70182194)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥17,160,000 (Direct Cost: ¥13,200,000、Indirect Cost: ¥3,960,000)
Fiscal Year 2015: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2014: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
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| Keywords | 分子病態学 / 小胞体ストレス / ATF6 |
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| Outline of Final Research Achievements |
The living organisms have a response against unfolded proteins in the endoplasmic reticulum (ER), the so-called UPR. ATF6 is a main regulator of the UPR. Mammalian cells have two genes that encode ATF6 (ATF6α and ATF6β) at different loci on the chromosome, and it has been reported that ATF6α, not ATF6β, is important for protein folding. In this study, we found that ATF6β is important for cartilage differentiation and colitis development from analysis using ATF6β knockout mouse. Thus, the UPR signaling pathway can control biological functions such as metabolism and immunity beside maintaining ER protein homeostasis.
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