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Frequency switching between oscillatory homeostats and the regulation of p53.
https://doi.org/10.24517/00058255
https://doi.org/10.24517/00058255653fa98a-ae62-4ecf-a531-ea3a1e5cc315
| 名前 / ファイル | ライセンス | アクション |
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GS-PR-NOSHIYAMA-N-0227786.pdf (6.3 MB)
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| アイテムタイプ | 学術雑誌論文 / Journal Article(1) | |||||||
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| 公開日 | 2020-05-25 | |||||||
| タイトル | ||||||||
| タイトル | Frequency switching between oscillatory homeostats and the regulation of p53. | |||||||
| 言語 | en | |||||||
| 言語 | ||||||||
| 言語 | eng | |||||||
| 資源タイプ | ||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||
| 資源タイプ | journal article | |||||||
| ID登録 | ||||||||
| ID登録 | 10.24517/00058255 | |||||||
| ID登録タイプ | JaLC | |||||||
| 著者 |
Ruoff, Peter
× Ruoff, Peter× Nishiyama, Nobuaki |
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| 著者別表示 |
西山, 宣昭
× 西山, 宣昭
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| 提供者所属 | ||||||||
| 内容記述タイプ | Other | |||||||
| 内容記述 | 金沢大学国際基幹教育院 | |||||||
| 書誌情報 |
PLOS ONE 巻 15, 号 5, p. e0227786-26p., 発行日 2020-05-20 |
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| ISSN | ||||||||
| 収録物識別子タイプ | ISSN | |||||||
| 収録物識別子 | 1932-6203 | |||||||
| DOI | ||||||||
| 関連タイプ | isIdenticalTo | |||||||
| 識別子タイプ | DOI | |||||||
| 関連識別子 | 10.1371/journal.pone.0227786 | |||||||
| 出版者 | ||||||||
| 出版者 | Public Library of Science | |||||||
| 抄録 | ||||||||
| 内容記述タイプ | Abstract | |||||||
| 内容記述 | Homeostasis is an essential concept to understand the stability of organisms and their adaptive behaviors when coping with external and internal assaults. Many hormones that take part in homeostatic control come in antagonistic pairs, such as glucagon and insulin reflecting the inflow and outflow compensatory mechanisms to control a certain internal variable, such as blood sugar levels. By including negative feedback loops homeostatic controllers can exhibit oscillations with characteristic frequencies. In this paper we demonstrate the associated frequency changes in homeostatic systems when individual controllers -in a set of interlocked feedback loops- gain control in response to environmental changes. Taking p53 as an example, we show how Per2, ATM and Mdm2 feedback loops -interlocked with p53- gain individual control in dependence to the level of DNA damage, and how each of these controllers provide certain functionalities in their regulation of p53. In unstressed cells, the circadian regulator Per2 ensures a basic p53 level to allow its rapid up-regulation in case of DNA damage. When DNA damage occurs the ATM controller increases the level of p53 and defends it towards uncontrolled degradation, which despite DNA damage, would drive p53 to lower values and p53 dysfunction. Mdm2 on its side keeps p53 at a high but sub-apoptotic level to avoid premature apoptosis. However, with on-going DNA damage the Mdm2 set-point is increased by HSP90 and other p53 stabilizers leading finally to apoptosis. An emergent aspect of p53 upregulation during cell stress is the coordinated inhibition of ubiquitin-independent and ubiquitin-dependent degradation reactions. Whether oscillations serve a function or are merely a by-product of the controllers are discussed in view of the finding that homeostatic control of p53, as indicated above, does in principle not require oscillatory homeostats. | |||||||
| 内容記述 | ||||||||
| 内容記述タイプ | Other | |||||||
| 内容記述 | Creative Commons Attribution License 4.0 | |||||||
| 権利 | ||||||||
| 権利情報 | Copyright: © 2020 Ruoff, Nishiyama. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, andreproduction in any medium, provided the original author and source are credited. | |||||||
| 著者版フラグ | ||||||||
| 出版タイプ | VoR | |||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||
| 関連URI | ||||||||
| 関連タイプ | isIdenticalTo | |||||||
| 識別子タイプ | URI | |||||||
| 関連識別子 | https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0227786 | |||||||
| 関連名称 | https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0227786 | |||||||
