| Project/Area Number |
13670088
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Nagasaki University Graduate School of Biomedical Science |
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Principal Investigator |
KAIBARA Muneshige Nagasaki Univ. Grad. Sch. Biomed. Sci. Ass. Prof., 大学院・医歯薬学総合研究科, 助教授 (40274633)
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| Co-Investigator(Kenkyū-buntansha) |
TANIYAMA Kohtaro Nagasaki Univ. Grad. Sch. Biomed. Sci. Prof., 大学院・医歯薬学総合研究科, 教授 (70030898)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | L-type / calcium channel / CACNA1C / inactivation / phosphorylation / cAMP / protein kinase / patch clamp / Cavl2 / Cav1.2 |
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| Research Abstract |
Calcium channel currents activate with membrane depolarization and inactivate overtime. The inactivating property has an important role in regulating intracellular Ca2+ concentration. Inactivation of the currents is modulated by at least tree factors : 1)membrane potential, 2) Ca2+, and 3) phosphorylation.
In this study, we investigated molecular mechanisms of the inactivation process related to phosphorylation using expression system. We cloned CACNA1C from guinea pig heart. And we investigated the role of phosphorylation sites in CACNA1C with mutagenesis study using whole-cell patch clamp study.
Our data indicate that 1) multiple phosphorylation sites in CACNA1are involved in the regulation of the channel activity, 2)other subunit regulates roles of each phosphorylation site in CACNA1C.
We have cloned CACNA1C(AB092629) and KCNJ12 (AB074970).
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