2014 Fiscal Year Annual Research Report
心肥大状態を誘導するＥＮＨ１－ＰＫＣ／ＰＫＤ－Ｃａチャネル複合体の調節機構の解析
| Project/Area Number |
24570150
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
MATURANA ANDRES 名古屋大学, 生命農学研究科, 准教授 (10452004)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Keywords | intracellular signaling / scaffolding protein / cardiac hypetrophy / PDZ LIM protin |
|---|
| Outline of Annual Research Achievements |
Our aim was to study the function and expression mechanisms of the scaffolding protein ENH1 (PDLIM5) in the heart and in the development of cardiac hypertrophy.
We have studied the expression of ENH1 and its alternative splicing homologue ENH2 and ENH3 in the cardiac and skeletal muscle development.
We identified the target of the ENH1-PKC-PKD1 signaling complex. And we tested the inhibitory property of the ENH3 splice variants on the ENH1 dependent signaling pathway. We found out that ENH3 expression prevents the activation of the ENH-PKC-PKD1 signaling pathway thus resolving the mechanism that was still elusive when this project started. Finally, we generated a transgenic mice to test in-vivo the cardiac hypertrophy preventive action of ENH3.
In addition, we identified an ENH1 interacting protein and uncovered that this protein has a high cardioprotective capacity. To study in-vivo the function of this identified protein, we generated a transgenic mice.
Finally, we study the splicing mechanism of the enh gene to understand how the various ENH isoforms are expressed in the heart.
|
