| Project/Area Number |
20590870
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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 |
Circulatory organs internal medicine
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
MIURA Tetsuji Sapporo Medical University, 医学部, 教授 (90199951)
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| Co-Investigator(Kenkyū-buntansha) |
MIKI Takayuki 札幌医科大学, 医学部, 講師 (00336405)
TANNO Masaya 札幌医科大学, 医学部, 講師 (00398322)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | コネキシン / 細胞シグナル / 心筋細胞 / 細胞死 / connexin-43 / signal transduction / G protein coupled receptor / β-subunit / mitochondria / 細胞内情報電達 / 細胞内情報伝達 |
|---|
| Research Abstract |
This study aimed to clarify role of connexin-43 (Cx43) in a major cytoprotective signaling, PI3K-Akt-GSK-3β signaling in cardiomyocytes. We found that Cx43 in the sarcolemma contributes to activation of class I_B P13K as a co-factor of β subunit of G proteins. This role of Cx43 is specific to regulation of class I_B P13K and is not required for activation of class I_A PI3K. Cx43 in mitochondria, being necessary for redox signaling by activated mitochondrial ATP-sensitive K^+ channel, was found to be dispensable in PI3K-Akt-GSK-3β signaling by G-protein coupled receptors.
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