MECHANISM OF CELL CYCLE DISRUPTION BY MULTIPLE P53 PULSES
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- IWAMOTO KAZUNARI
- Laboratory for Bioinformatics, Graduate School of Systems Life Sciences, Kyushu University Japan Society for the Promotion of Science
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- HAMADA HIROYUKI
- Laboratory for Bioinformatics, Graduate School of Systems Life Sciences, Kyushu University
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- OKAMOTO MASAHIRO
- Laboratory for Bioinformatics, Graduate School of Systems Life Sciences, Kyushu University
説明
When the DNA damage is generated, the tumor suppressor gene p53 is activated and selects the cell fate such as the cell cycle arrest, the DNA repair and the induction of apoptosis. Recently, the p53 oscillation was observed in MCF7 cell line. However, the biological meaning of p53 oscillation was still unclear. Here, we constructed a novel mathematical model of cell cycle regulatory system with p53 signaling network to investigate the relationship between the p53 oscillation and the cell cycle progression. First, the simulated result without DNA damage agreed with the biological findings. Next, the simulations with DNA damage realized both the p53 oscillation and the cell cycle arrest, and indicated that the generation of multiple p53 pulses disrupted the cell cycle progression. Moreover, the simulated results showed that the cell cycle disruption was caused by the catastrophe of M phase in the cell cycle, which resulted from the decline in cyclin A/cyclin-dependent kinase 2. The results in this study suggested that the generation of multiple p53 pulses against DNA damage may be used as a marker of cell cycle disruption.
収録刊行物
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- Ｇｅｎｏｍｅ Ｉｎｆｏｒｍａｔｉｃｓ
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Ｇｅｎｏｍｅ Ｉｎｆｏｒｍａｔｉｃｓ 25 (1), 12-24, 2011
日本バイオインフォマティクス学会
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詳細情報 詳細情報について
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- CRID
- 1390282679465554176
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- NII論文ID
- 130004567840
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- ISSN
- 2185842X
- 09199454
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可