| Project/Area Number |
24700373
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 運動ニューロン / 神経発生 / アルツハイマー病 / 分子・細胞・神経生物学 |
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| Research Abstract |
We studied the physiological functions of CLAC-P/collagen XXV, a transmembrane-type collagen originally identified as a component of senile plaque amyloid of Alzheimer's disease brains, by means of generating CLAC-P knockout and conditional knockout mice. In CLAC-P KO mice, motor axons failed to elongate and branch within the muscle, followed by degeneration of axons. Failure of muscular innervation in KO mice led to excessive apoptosis during development, resulting in almost complete and exclusive loss of spinal motoneurons. Bax deletion in CLAC-P KO mice rescued motoneurons from apoptosis, although motor axons remained halted around the muscle entry site. These observations indicate that CLAC-P/collagen XXV is a novel essential factor that regulates the initial phase of intramuscular motor innervation, which is required for subsequent target-dependent motoneuron survival and NMJ formation during development.
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