| Project/Area Number |
21659454
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Dental engineering/Regenerative dentistry
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
IKEDA Masaaki 東京医科歯科大学, 大学院・医歯学総合研究科, 准教授 (20193211)
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|---|
| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,430,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2009: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | 再生歯学 / iPS細胞 / 最終分化細胞 / エピジェネティック / 核マトリクス結合因子 / 核内高次構造 / 細胞増殖 / 前駆細胞 / クロマチン |
|---|
| Research Abstract |
The pathways regulated by p53 and RB tumor suppressors play important roles in differentiation and irreversible cell-cycle arrest in terminally differentiated cells. To induce dedifferentiation and proliferation of terminally differentiated cells, we investigated functional roles of DRIL1 and its closely related DRIL2, family members of ARID(AT-rich interaction domain) DNA-binding proteins, in these major tumor suppressor pathways. We found that DRIL1 cooperates with p53 to activate pro-arrest p21^WAF1 transcription, and that DRIL1 and DRIL2 play important roles in E2F-target gene expression and cell cycle progression, and that DRIL2 function is required for osteogenic differentiation. In addition, our results suggest that, in addition to DRIL1 or DRIL2 knockdown, inhibition of p53 and RB functions is required for inducing dedifferentiation and proliferation of terminally differentiated cells. These results provide important insights to the conversion of terminally differentiated cells into progenitor cells.
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