| Project/Area Number |
15K08183
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Kyoto Gakuen University |
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Principal Investigator |
Niisato Naomi 京都学園大学, 健康医療学部, 教授 (00237645)
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| Co-Investigator(Kenkyū-buntansha) |
丸中 良典 京都府立医科大学, 医学(系)研究科(研究院), 教授 (00127036)
宮崎 裕明 京都府立医科大学, 医学(系)研究科(研究院), 助教 (30360027)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | proteasome / ENaC / p97 / MG132 / Ubiquitin / プロテアソーム / p38 / ERAD |
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| Outline of Final Research Achievements |
In this study, we hypothesized that membrane proteins containing ENaC might be degraded in proteasome through a similar mechanism to “retrotranslocation” in ERAD (endoplasmic reticulum associated degradation. As results, we indicate that 1) a p97 (a AAA+ ATPase) inhibitor accumulated ENaC in the plasma membrane when ENaC degradation was induced by a p38 inhibitor, 2) p97 colocalized with ENaC by inducing ENaC degradation with a p38 inhibitor, 3) a composition of proteasome also colocalized with ENaC by a p38 inhibitor. Based on these results, ENaC might be degrated in proteasome through a p97-dependent mechanism.
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