| Project/Area Number |
23790342
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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 |
General medical chemistry
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| Research Institution | Yokohama City University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 神経幹細胞 / 発生・分化 / 細胞極性 / PAR3 / 大脳形成 |
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| Research Abstract |
During mammalian cerebral development, neural precursor cells (NPCs) first expand their population and next generate neurons. However, the molecular mechanisms regulating this transition of NPC division modes have not been clarified yet. To elucidate the molecular mechanisms regulating this transition, I analyzed the roles of PAR3, the evolutionarily conserved polarity protein, in mouse NPCs at E10.5. I found that PAR3-deficient NPCs were significantly biased to self-renewal divisions and altered expression of several transcription factors. These observations suggest that PAR3 is involved in the regulation of the transition of NPC division modes in mice.
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