| Project/Area Number |
15K18373
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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 | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | オリゴデンドロサイト / Olig2 / 転写因子 / p53 / 神経幹細胞 / ノックアウトマウス / DNA損傷 / 細胞増殖 / 細胞死 / ミエリン / 分化促進 / 脱髄疾患 |
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| Outline of Final Research Achievements |
We identified a novel Olig2 binding factor, Obp2 and analyzed central nervous system-specific Obp2 mutant mice. These mice exhibited severe loss of oligodendrocyte differentiation without motor neuron defects.We further found that Obp2 contributed to the maintenance of Olig2-positive neural precursor cells and oligodendrocyte progenitor cells through the regulation of DNA damage-p53 axis in central nervous system.
We also demonstrated that OIF, which is a truncated form of Obp2 strongly induced the transcriptional activity of oligodendrocyte related genes such as PLP and MBP, and promoted oligodendrocyte differentiation in dysmyelinating mice.
In conclusion, we suggest that Obp2 is indispensable for oligodendrocyte development and OIF could be useful for the therapy of demyelinating diseases.
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