| Project/Area Number |
15K18680
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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 biochemistry
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MAKI Masatoshi 名古屋大学, 大学院生命農学研究科・応用分子生命科学専攻, 教授 (40183610)
SHIBATA Hideki 名古屋大学, 大学院生命農学研究科・応用分子生命科学専攻, 准教授 (30314470)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | mTOR / アミノ酸 / カルシウム / mTORC1 / 細胞内情報伝達 |
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| Outline of Final Research Achievements |
In this study, we sought to clarify the role of Ca2+ in the cellular mechanism of amino acids sensing and the cellular response. Addition of amino acids to the amino acid-starved cell induces the Ca2+ entry from extracellular space, leading to the increase of intracellular Ca2+ concentration. By using the several inhibitors that target particular Ca2+ channels, we identified that Amiloride-sensitive Ca2+ channel appears to responsible for the Ca2+ entry. In addition, we also investigated how increased Ca2+ levels affect the mTORC1, which is a central regulator of amino acid sensing pathway. It is known that amino acids activate mTORC1 via two distinct small GTPases, called Rag GTPases and Rheb GTPase. We found that the action of Rheb GTPase but not Rag was affected by Ca2+. These results suggest a novel regulatory mechanism of mTORC1 through the change of intracellular Ca2+ concentration in response to amino acids.
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