| Project/Area Number |
09044283
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Field |
Biophysics
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| Research Institution | NAGOYA UNIVERSITY |
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Principal Investigator |
SOKABE Masahiro SCH MED,NAGOYA UNIVERSITY,PROFESSOR, 医学部, 教授 (10093428)
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| Co-Investigator(Kenkyū-buntansha) |
SACHS Frederick SUNY/BUFFALO,BIOPHYS,PROFESSOR, 医学部, 教授
FREDERICK Sa ニューヨーク州立大学, 医学部, 教授
成瀬 恵治 名古屋大学, 医学部, 講師 (40252233)
SOCHS Freder ニューヨーク州立大学, 医学部, 教授
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | SA channel / cell volume regulation / endothelial cells / stretch stimulation / AFM / mec / mid-1 / リモデリング / 遺伝子クローニング / ブロッカー / チャネル遺伝子 / 伸展刺激装置 / チャネル解析法 / 原子間力顕微鏡 |
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| Research Abstract |
Stretch activated (SA) channels are expressed in a variety of cells and, thought to have important roles in fundamental cell functions. However their physiological functions are not yet known and their molecular entity has not yet be identified except for that in e. coli. To resolve these problems is the most important issue on the SA channel. The aim of this research project is to find out a clue to this goal through a collaboration between Japan and the U.S.As for the first problem, a cation selective SA channel has been found to have an important role in the regulatory volume decrease in A6 cells throuigh the estimation of whole cell activity of the SA channel by measuring intracellular Ca2+ incresae. Moreover the role of a cation selective SA channel has been clarified in stretch -induced cell remodeling in endothelial cells (Japan side). On the other hand ; the US researchers has developed a method to apply quantitative mechanical stimuli to cultured cells using canti-lever of AFM (atomic force microscope). They successfully explained the stretch induced-activity of heart cells by this method combined with sinultaneous whole cell recordings of SA channel currents.
The second problem has been a tough one. We tried to clone a Drosophila gene homologous to mec gene from c.elegance, a putative SA channel gene, but failed. The US side tried to purify a SA channel-specific blocker from spider venoms, but yet to be done. However, at the last moment, we (Japan side) could identify a gene (mid-1) encoding cation selective SA channel from yeast. This is the first identified gene for the cation selective SA channel. By this finding we can evisage a variety of intriguing research projects including structure-function study. Based on this result, we will pursue further collaboration between Japan and the US.
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