| Project/Area Number |
20790216
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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 | Fukuoka University |
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Principal Investigator |
KITA Satomi Fukuoka University, 医学部, 講師 (10461500)
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| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 脂質キナーゼ / 心肥大 / シグナル伝達 / 脂質代謝異常 / Na^+ / Ca^<2+>交換輸送体 / 薬理学 / PIP5Kα / 心肥大・心不全 / イノシトールリン脂質代謝 / 遺伝子改変マウス |
|---|
| Research Abstract |
Phosphatidylinositol 4-phosphate 5-kinase α, a major cardiac isoform, catalyzes the synthesis of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P_2), which is a critical cell signal transducer. Although phosphoinositide 3-kinase (PI3K) signaling to Akt is involved in physiological cardiac hypertrophy, whether PIP5Ka promotes cardiac hypertrophy and functions is largely unknown. To address this issue, we generated a model of cardiac-specific transgenic mice with wild-type (WT) or dominant negative (DN) of PIP5K α.
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