2016 Fiscal Year Final Research Report
Regulation of asymmetric cell division by the machinery maintaining genome stability
| Project/Area Number |
15K14376
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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 |
Tumor biology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MIYAGAWA KIYOSHI 東京大学, 大学院医学系研究科(医学部), 教授 (40200133)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Keywords | 細胞周期 / 不均等細胞分裂 |
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| Outline of Final Research Achievements |
To clarify the molecular mechanism underlying the nature of cancer stem cells characterized by tolerance to cancer treatment, we tried to identify the machinery regulating both the DNA double-strand break response and asymmetric cell division. We found that Rad54B, which repairs double-strand breaks by homologous recombination and regulates cell-cycle checkpoint by degrading p53, promotes asymmetric cell division in the neuroblastoma-derived cell line. Furthermore, we found that Rad54B activates the Notch-signaling pathway by inhibiting Numb, which may be involved in asymmetric cell division.
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| Free Research Field |
医学
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