| Project/Area Number |
23650183
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Osaka University |
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Principal Investigator |
MORI Yasutake 大阪大学, 医学系研究科, 准教授 (00343252)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | タンパク質メチル化 / PRMT / 翻訳制御 / 翻訳後修飾 / ミクログリア細胞 / 翻訳因子 |
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| Research Abstract |
Protein arginine N-methyltransferase 8 (PRMT8) was originally reported as a neuron-specific type II PRMT with dominantly nuclear distribution. However, when we examined changes in PRMT8 expression level in the spinal cords injured by hemisection, unambiguous signals were observed in the cytoplasm of round-shaped cells that were densely packed around the lesion site. This group of cells were well-overlapped with CD11b-positive cells, not with neurons, demonstrating that PRMT8 is expressed in the activated microglia/macrophage cells. By Western blot analysis, PRMT8 from the injured spinal cord showed a slower mobility shift band with Mw of 60-62kDa than that from brain lysate with Mw of 42kDa. We demonstrated that the high molecular weight (HMW) PRMT8is due to phosphorylation and the myristoylation might be caused by an additional N-terminal stretch harboring consensus myristoylation site that would stem from usage of another in-frame translation initiation site. These data raise the possibility that membranebound type of PRMT8 can be a novel marker for activated microglia.
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