genetic analysis of cellular adaptation to glucose starvation
Project/Area Number |
17K07394
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Cell biology
|
Research Institution | Kurume University |
Principal Investigator |
|
Project Period (FY) |
2017-04-01 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 栄養飢餓ストレス / グルコース / 細胞応答 / 解糖系 / TORキナーゼ / 栄養飢餓 / 細胞周期 / 細胞内シグナル伝達 / シグナル伝達 / 遺伝学 / 分子生物学 / ストレス応答 / 糖代謝 |
Outline of Final Research Achievements |
Eukaryotic cells can adapt to changes in nutrition in environment. To understand the mechanism underlying adaptation to glucose starvation stress, we performed genetic analyses of the glucose-sensing mechanism, and the mechanisms regulating the localization of glucose transporters on the cell surface. Here we show that the fission yeast cells monitor the intracellular glycolytic flux ( i.e. the rate of glucose metabolism), and the extracellular glucose level independently. Furthermore, we found that the intracellular localization of the hexose transporter is regulated by the TORC1 and TORC2 signaling pathways, and pathways regulating the endocytosis.
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Academic Significance and Societal Importance of the Research Achievements |
本研究の遂行により、グルコース輸送体の遺伝子発現コントロールの仕組みや、局在制御メカニズムの一端が明らかとなった。ヒトにおいては、グルコース輸送体GLUT4の機能異常が糖尿病発症原因となることが知られている。それゆえ本研究の成果は、糖尿病発症につながる遺伝子異常の解明に結び付くだろう。また、糖尿病治療の新薬開発にも役立つと期待できる。
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Report
(4 results)
Research Products
(11 results)