| Project/Area Number |
21790236
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
General pharmacology
|
|---|
| Research Institution | Hokkaido University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | エンドセリン受容体 / TRPCチャネル / 受容体作動性Ca^<2+>流入 / ストア作動性Ca^<2+>流入 / カルモジュリン / プロテインキナーゼA / リン酸化 / エンドセリンA型受容体 / 抑制性制御機構 / Phos-tag / in vitro kinase assay / カルシウムイオン / HEK293細胞 / エンドセリン受容体結合蛋白質 / STIM1 / ORAI1 / 蛋白-蛋白相互作用 |
|---|
| Research Abstract |
The purpose of this study is to elucidate transient receptor potential canonical(TRPC) channels functioning as endothelin type A receptor(ET_AR)-operated Ca^<2+> channel and its regulatory mechanism. The results obtained from molecular pharmacological studies indicate that(1) both TRPC3 and TRPC6 contribute to ET_AR-operated Ca^<2+> entry,(2) G_<q/11> protein, phospholipase C, Src, phosphoinositide 3-kinase, calmodulin(CaM), and CaM/IP_3 receptor binding domain at the C terminus of TRPC3 and TRPC6 are involved in ET_AR-mediated Ca^<2+> entry via TRPC3 and TRPC6, and(3) TRPC6 is negatively regulated by protein kinase A-mediated phosphorylation of Ser^<28>
|
