2014 Fiscal Year Final Research Report
Resolving the function of the ENH1-PKC/PKD-Calcium Channel function in the cardiac hypertrophy
Project/Area Number |
24570150
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Functional biochemistry
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Research Institution | Nagoya University |
Principal Investigator |
MATURANA ANDRES 名古屋大学, 生命農学研究科, 准教授 (10452004)
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Co-Investigator(Renkei-kenkyūsha) |
KURODA Shunichi 名古屋大学, 大学院生命農学研究科, 教授 (60263406)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | シグナル伝達 / 心臓肥大 |
Outline of Final Research Achievements |
Scaffolding proteins are essential for the transmission of intracellular signaling. Scaffolding proteins gather signaling proteins and their targets at precise subcellular locations to maximize the efficiency of the signal transduction. We are studying a scaffolding protein called ENH that is essential for the cardiac and skeletal muscle development. We have previously shown that ENH is essential for the development of cardiac hypertrophy but some ENH splice variants can on the contrary prevent cardiac hypertrophy. In the present study, we studied the splicing mechanisms of ENH. We generate a splice variant ENH trangenic mice to study in-vivo its ability to prevent cardiac hypertrophy. Finally, we analyzed the downstream signaling events downstream to the complex signaling composed by ENH1, the protein kinase D and the L-type calcium channels. Our work sustain the idea that ENH is a key player in the cardiac remodeling leading to heart hypertrophy.
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Free Research Field |
細胞情報伝達機構
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