Unraveling the mechanism by which G0S2 regulates mitochondrial ATP production under ischemia
| Project/Area Number |
15K19378
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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 |
Cardiovascular medicine
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| Research Institution | Osaka University |
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Principal Investigator |
Kato Hisakazu 大阪大学, 医学系研究科, 助教 (30589312)
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ミトコンドリア / 虚血 / ATP合成酵素 / タンパク質分解 / 分子心臓学 / 循環器・高血圧 / エネルギー代謝 / ユビキチン |
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| Outline of Final Research Achievements |
Heart tissue consumes more energy than other organs to maintain cardiac pump function. However, the mechanism by which mitochondrial ATP production is regulated under hypoxia is not fully understood. In this study, we revealed how G0S2 regulates mitochondrial ATP production via ATP synthase, mainly from the following experiments. (1) G0S2 is degraded by ubiquitin-proteasome system. (2) One amino acid within hydrophobic region of G0S2 is strongly involved in its protein degradation. (3) In cardiomyocytes, G0S2 mutants that have longer half-life improved the decreases in mitochondrial ATP concentration under hypoxic condition compared to wild-type. These results suggest that the enhancement of mitochondrial ATP production by inhibition of G0S2 protein degradation can lead to novel therapeutic target to ischemic heart diseases.
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Report
(3 results)
Research Products
(7 results)
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[Journal Article] Mutation in VPS33A affects metabolism of glycosaminoglycans: a new type of mucopolysaccharidosis with severe systemic symptoms2017
Author(s)
Kondo H, Maksimova N, Otomo T*,Kato H, Imai A, Asano Y, Kobayashi K, Nojima S, Nakaya A, Hamada Y, Irahara K, Gurinova E, Sukhomyasova A, Nogovicina A, Savvina M, Yoshimori T, Ozono K Sakai N*
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Journal Title
Human Molecular Genetics
Volume: 26
Pages: 173-183
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Btg2 is a Negative Regulator of Cardiomyocyte Hypertrophy through a Decrease in Cytosolic RNA.2016
Author(s)
Masumura Y, Higo S, Asano Y, Kato H, Yan Y, Ishino S, Tsukamoto O, Kioka H, Hayashi T, Shintani Y, Yamazaki S, Minamino T, Kitakaze M, Komuro I, Takashima S, Sakata Y.
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Journal Title
Sci Rep.
Volume: 6
Issue: 1
Pages: 28592-28592
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] A Development of Nucleic Chromatin Measurements as a New Prognostic Marker for Severe Chronic Heart Failure.2016
Author(s)
Kanzaki M, Asano Y, Ishibashi-Ueda H, Oiki E, Nishida T, Asanuma H, Kato H, Oka T, Ohtani T, Tsukamoto O, Higo S, Kioka H, Matsuoka K, Sawa Y, Komuro I, Kitakaze M, Takashima S, Sakata Y.
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Journal Title
PLoS One.
Volume: 11
Issue: 2
Pages: e0148209-e0148209
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] An interaction between GLP-1 and adenosine contributes to cardioprotection of a dipeptidyl peptidase 4 inhibitor from myocardial ischemia/reperfusion injury.2015
Author(s)
Ihara M, Asanuma H, Yamazaki S, Kato H, Asano Y, Shinozaki Y, Mori H, Minamino T, Asakura M, Sugimachi M, Mochizuki N, Kitakaze M.
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Journal Title
Am J Physiol Heart Circ Physiol.
Volume: in press
Issue: 10
Pages: 1287-1297
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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