2013 Fiscal Year Research-status 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
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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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Keywords | 細胞内シグナル / Zでぃすく / 足場タンパク質 |
Research Abstract |
Our aim is to study the function of the PDZ-LIM protein ENH1 in the development of cardiac hypertrophy. ENH alternative splice variants have an opposite function than ENH1 in the heart. ENH splice variants prevent the cardiac hypertrophy while ENH1 promote cardiac hypertrophy. Therefore, we also aim at resolving the mechanisms of ENH1 expression and alternative splicing. In this fiscal year, we identify two splicing factors essential for the mechanisms of enh gene splicing. By altering their expression we could modify the expression of ENH splice variants. In addition we confirmed that ENH1 LIM regions interact with the transcription factor CREB and localized at specific nuclear regions. Our research led to the publication of one paper and several presentation in national and international meetings. And we are now preparing another publication to be submitted.
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Current Status of Research Progress |
Current Status of Research Progress
2: Research has progressed on the whole more than it was originally planned.
Reason
Our work lead to one publication last year and we are preparing another manuscript for submission.
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Strategy for Future Research Activity |
We proceed the research as planned.
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Expenditure Plans for the Next FY Research Funding |
We have planned to generate a transgenic mice but experimental problems have delayed our plan, we are planning to generate the transgenic mice in the next fiscal year. The amount incurred in the next fiscal year is planned to be used to generate a transgenic mice.
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[Journal Article] Structural basis for the counter-transport mechanism of a H+/Ca2+ exchanger.2014
Author(s)
Nishizawa T, Kita S, Maturana AD, Furuya N, Hirata K, Kasuya G, Ogasawara S, Dohmae N, Iwamoto T, Ishitani R, Nureki O.
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Journal Title
Science
Volume: 341
Pages: 168-172
DOI
Peer Reviewed
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