Role of Gene33/RALT in oxidative stress-induced signal transduction in cardiac cells.
| Project/Area Number |
20790557
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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 |
Circulatory organs internal medicine
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
TAKEDA Kenji Kanazawa Medical University, 医学部, 助教 (90340009)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 分子心臓病態学 / 蛋白質間相互作用 / 心筋細胞 / Mig-6 / Ralt / 2014 / 03 / 酸化ストレス / 負の制御因子 / 心肥大 / HB-EGF / RALT |
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| Research Abstract |
We found that rat embryonic heart-derived H9c2 cells treated with oxidative stress exhibited a significant induction in Ralt mRNA and protein. Stable overexpression of Ralt in H9c2 cells prevented HB-EGF-induced signal transduction. To identify endogenous proteins that bind to Ralt in cardiac cells, we carried out a proteomic analysis and found that Ralt specifically bound to several different isoforms of 14-3-3 proteins independently of its phosphorylation status.
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Report
(3 results)
Research Products
(6 results)
