Elucidation for pathophysiological significance of Jab1 as an inducer of endothelin type A receptor degradation in cardiovascular diseases
| Project/Area Number |
21790237
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General pharmacology
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| Research Institution | Hokkaido University |
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Principal Investigator |
NISHIMOTO Arata Hokkaido University, 大学院・医学研究科, 助教 (90396325)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 酵母ツーハイブリッド法 / エンドセリン受容体 / Jab1 / 蛋白質分解 / ユビキチン化 / エンドサイトーシス |
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| Research Abstract |
I identified Jun activation domain-binding protein 1 (Jab1) as an endothelin type A receptor (ET_AR)-interacting protein. Jab1 overexpression accelerated ubiquitination and degradation of ET_AR. Long-term ET-1 stimulation markedly accelerated the rate of ET_AR degradation and increased the amount of Jab1 bound to ET_AR. The degradation rate of ET_BR was markedly faster than that of ET_AR. Notably, the amount of Jab1 bound to ET_BR and ubiquitination level of ET_BR were markedly higher than those for ET_AR (Nishimoto A. et al., Biochem Biophys Res Commun., 391, p1616-22, 2010).
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Report
(3 results)
Research Products
(11 results)
