| Project/Area Number |
22590950
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | National Center of Neurology and Psychiatry |
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Principal Investigator |
NAGATA Tetsuya 独立行政法人国立精神・神経医療研究センター, 神経研究所遺伝子疾患治療研究部, 室長 (50362976)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEDA Shin'ichi 独)国立精神・神経医療研究センター・神経研究所, 遺伝子疾患治療研究部, 部長 (90171644)
IWATA Yuko 独立行政法人国立循環器病研究センター, 分子生理部, 室長 (80171908)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 神経分子病態学 / SAC / TRPfamily / TRPV2 / DMD |
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| Research Abstract |
A number of studies have reported the elevation of the cytosolic Ca2+ concentration in skeletal and cardiac muscles of muscular dystrophy. Chronic elevation of the cytosolic Ca2+ concentration could activate Ca2+-dependent cell signaling cascade and induce cell necrosis. The cellular mechanism for controlling Ca2+ influx in muscular dystrophy, however, is still unknown. The TRP channels form a large family of cation channels that likely function as tetramers in various processes, such as sensory signaling, most of which are permeable for Ca2+, and some also for Mg2+. To determine the relationship between TRP family and muscle degeneration, we analyzed the expression of TRP channel in skeletal and cardiac muscle of Canine models of Duchenne muscular dystrophy.
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