| Project/Area Number |
13470009
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Nagoya University |
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Principal Investigator |
NARUSE Keiji Nagoya University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (40252233)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥9,500,000 (Direct Cost: ¥9,500,000)
Fiscal Year 2002: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥6,000,000 (Direct Cost: ¥6,000,000)
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| Keywords | SA channel / Ca-activated K chanel / SAKCA / structure-function relationship / Stretch-activated channel / 心筋 / 伸展刺激 / パッチクランプ法 |
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| Research Abstract |
Stretch-sensing mechanisms of stretch-activated (SA) channels have been extensively studied and many molecular models have been presented. Here we cloned a stretch-activated, large-conductance (BK) channel from cultured chick embryonic heart and found out that the channel contains "STREX" sequence, originally reported to be a target sequence of PKA and whose expression is regulated by stress hormones, and that it turned out to contain a mechano-sensive domain of the channel. Deletion of STREX or substitution of Ala^<674> to Thr^<674> diminished stretch-sensitivity of the channel. When compared the chick STREX with mouse, rabbit STREX, which did not have any stretch-sensitivity in CHO cells, it turned out that the sequence ERA is most likely to be important. When chick STREX-EGFP was co-expressed with SAKCA in CHO cells, a strong signal was detected at cell membrane and stretch-sensitivity of the channel was significantly inhibited.
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