• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

基于简化二维弛豫振荡器模型揭示γ射线辐照下P53网络两相动力学的决定因素。

Revealing determinants of two-phase dynamics of P53 network under gamma irradiation based on a reduced 2D relaxation oscillator model.

作者信息

Demirkıran Gökhan, Kalaycı Demir Güleser, Güzeliş Cüneyt

机构信息

The Graduate School of Natural and Applied Sciences, Dokuz Eylül University, Buca, İzmir 35160, Turkey.

Department of Electrical and Electronics Engineering, Dokuz Eylül University, Buca, İzmir 35160, Turkey.

出版信息

IET Syst Biol. 2018 Feb;12(1):26-38. doi: 10.1049/iet-syb.2017.0041.

DOI:10.1049/iet-syb.2017.0041
PMID:29337287
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8687238/
Abstract

This study proposes a two-dimensional (2D) oscillator model of p53 network, which is derived via reducing the multidimensional two-phase dynamics model into a model of ataxia telangiectasia mutated (ATM) and Wip1 variables, and studies the impact of p53-regulators on cell fate decision. First, the authors identify a 6D core oscillator module, then reduce this module into a 2D oscillator model while preserving the qualitative behaviours. The introduced 2D model is shown to be an excitable relaxation oscillator. This oscillator provides a mechanism that leads diverse modes underpinning cell fate, each corresponding to a cell state. To investigate the effects of p53 inhibitors and the intrinsic time delay of Wip1 on the characteristics of oscillations, they introduce also a delay differential equation version of the 2D oscillator. They observe that the suppression of p53 inhibitors decreases the amplitudes of p53 oscillation, though the suppression increases the sustained level of p53. They identify Wip1 and P53DINP1 as possible targets for cancer therapies considering their impact on the oscillator, supported by biological findings. They model some mutations as critical changes of the phase space characteristics. Possible cancer therapeutic strategies are then proposed for preventing these mutations' effects using the phase space approach.

摘要

本研究提出了一种p53网络的二维(2D)振荡器模型,该模型是通过将多维两相动力学模型简化为共济失调毛细血管扩张突变(ATM)和Wip1变量的模型而推导出来的,并研究了p53调节因子对细胞命运决定的影响。首先,作者确定了一个6D核心振荡器模块,然后在保留定性行为的同时将该模块简化为一个2D振荡器模型。所引入的2D模型被证明是一个可激发的弛豫振荡器。这个振荡器提供了一种机制,导致支持细胞命运的多种模式,每种模式对应一种细胞状态。为了研究p53抑制剂和Wip1的固有时间延迟对振荡特性的影响,他们还引入了2D振荡器的延迟微分方程版本。他们观察到,抑制p53抑制剂会降低p53振荡的幅度,尽管这种抑制会提高p53的持续水平。考虑到Wip1和P53DINP1对振荡器的影响,他们将其确定为癌症治疗的可能靶点,生物学研究结果也支持这一点。他们将一些突变建模为相空间特征的关键变化。然后提出了可能的癌症治疗策略,以使用相空间方法预防这些突变的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/f1b26eafbe78/SYB2-12-26-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/265c02c6d0be/SYB2-12-26-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/0c891d38a450/SYB2-12-26-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/a275a84b459e/SYB2-12-26-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/e41c1dd3abd0/SYB2-12-26-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/db60c9f24fb4/SYB2-12-26-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/bfb37c811bb3/SYB2-12-26-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/d02035ff24a8/SYB2-12-26-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/f1b26eafbe78/SYB2-12-26-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/265c02c6d0be/SYB2-12-26-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/0c891d38a450/SYB2-12-26-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/a275a84b459e/SYB2-12-26-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/e41c1dd3abd0/SYB2-12-26-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/db60c9f24fb4/SYB2-12-26-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/bfb37c811bb3/SYB2-12-26-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/d02035ff24a8/SYB2-12-26-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bcf/8687238/f1b26eafbe78/SYB2-12-26-g002.jpg

相似文献

1
Revealing determinants of two-phase dynamics of P53 network under gamma irradiation based on a reduced 2D relaxation oscillator model.基于简化二维弛豫振荡器模型揭示γ射线辐照下P53网络两相动力学的决定因素。
IET Syst Biol. 2018 Feb;12(1):26-38. doi: 10.1049/iet-syb.2017.0041.
2
Two-dimensional polynomial type canonical relaxation oscillator model for p53 dynamics.用于p53动力学的二维多项式型规范弛豫振荡器模型。
IET Syst Biol. 2018 Aug;12(4):138-147. doi: 10.1049/iet-syb.2017.0077.
3
Oscillatory Dynamics of p53 Genetic Network Induced by Feedback Loops and Time Delays.由反馈环和时滞引起的 p53 基因网络的振荡动力学。
IEEE Trans Nanobioscience. 2019 Oct;18(4):611-621. doi: 10.1109/TNB.2019.2924079. Epub 2019 Jun 20.
4
P65-mediated miR-590 inhibition modulates the chemoresistance of osteosarcoma to doxorubicin through targeting wild-type p53-induced phosphatase 1.P65 介导的 miR-590 抑制通过靶向野生型 p53 诱导的磷酸酶 1 调节骨肉瘤对阿霉素的化疗耐药性。
J Cell Biochem. 2019 Apr;120(4):5652-5665. doi: 10.1002/jcb.27849. Epub 2018 Nov 1.
5
Wild-type p53-induced phosphatase 1 dephosphorylates histone variant gamma-H2AX and suppresses DNA double strand break repair.野生型 p53 诱导的磷酸酶 1 去磷酸化组蛋白变体 γ-H2AX 并抑制 DNA 双链断裂修复。
J Biol Chem. 2010 Apr 23;285(17):12935-47. doi: 10.1074/jbc.M109.071696. Epub 2010 Jan 29.
6
Abrogation of Wip1 expression by RITA-activated p53 potentiates apoptosis induction via activation of ATM and inhibition of HdmX.通过 RITA 激活的 p53 消除 Wip1 的表达,通过激活 ATM 和抑制 HdmX 增强细胞凋亡诱导。
Cell Death Differ. 2011 Nov;18(11):1736-45. doi: 10.1038/cdd.2011.45. Epub 2011 May 6.
7
Regulation of ATM/p53-dependent suppression of myc-induced lymphomas by Wip1 phosphatase.Wip1磷酸酶对ATM/p53依赖的myc诱导淋巴瘤抑制作用的调控。
J Exp Med. 2006 Dec 25;203(13):2793-9. doi: 10.1084/jem.20061563. Epub 2006 Dec 11.
8
DNA damage-induced regulatory interplay between DAXX, p53, ATM kinase and Wip1 phosphatase.DNA损伤诱导的DAXX、p53、ATM激酶和Wip1磷酸酶之间的调控相互作用。
Cell Cycle. 2015;14(3):375-87. doi: 10.4161/15384101.2014.988019.
9
A novel mathematical model of ATM/p53/NF- κB pathways points to the importance of the DDR switch-off mechanisms.一种新型的ATM/p53/NF-κB信号通路数学模型揭示了DNA损伤应答关闭机制的重要性。
BMC Syst Biol. 2016 Aug 15;10(1):75. doi: 10.1186/s12918-016-0293-0.
10
Two-phase dynamics of p53 in the DNA damage response.p53 在 DNA 损伤反应中的两相动力学。
Proc Natl Acad Sci U S A. 2011 May 31;108(22):8990-5. doi: 10.1073/pnas.1100600108. Epub 2011 May 16.

引用本文的文献

1
Two-dimensional polynomial type canonical relaxation oscillator model for p53 dynamics.用于p53动力学的二维多项式型规范弛豫振荡器模型。
IET Syst Biol. 2018 Aug;12(4):138-147. doi: 10.1049/iet-syb.2017.0077.
2
Bifurcation analysis of bistable and oscillatory dynamics in biological networks using the root-locus method.使用根轨迹法对生物网络中的双稳态和振荡动力学进行分岔分析。
IET Syst Biol. 2019 Dec;13(6):333-345. doi: 10.1049/iet-syb.2019.0043.

本文引用的文献

1
Application of bifurcation theory and siRNA-based control signal to restore the proper response of cancer cells to DNA damage.应用分岔理论和基于小干扰RNA的控制信号来恢复癌细胞对DNA损伤的正常反应。
J Theor Biol. 2016 Nov 7;408:213-221. doi: 10.1016/j.jtbi.2016.08.017. Epub 2016 Aug 15.
2
A novel mathematical model of ATM/p53/NF- κB pathways points to the importance of the DDR switch-off mechanisms.一种新型的ATM/p53/NF-κB信号通路数学模型揭示了DNA损伤应答关闭机制的重要性。
BMC Syst Biol. 2016 Aug 15;10(1):75. doi: 10.1186/s12918-016-0293-0.
3
Feedbacks, Bifurcations, and Cell Fate Decision-Making in the p53 System.
p53系统中的反馈、分岔与细胞命运决定
PLoS Comput Biol. 2016 Feb 29;12(2):e1004787. doi: 10.1371/journal.pcbi.1004787. eCollection 2016 Feb.
4
Knockdown of Wip1 Enhances Sensitivity to Radiation in HeLa Cells Through Activation of p38 MAPK.敲低Wip1通过激活p38丝裂原活化蛋白激酶增强HeLa细胞对辐射的敏感性。
Oncol Res. 2014;22(4):225-233. doi: 10.3727/096504015X14386062091479.
5
Dynamics of P53 in response to DNA damage: Mathematical modeling and perspective.P53对DNA损伤反应的动力学:数学建模与展望
Prog Biophys Mol Biol. 2015 Nov;119(2):175-82. doi: 10.1016/j.pbiomolbio.2015.08.017. Epub 2015 Aug 13.
6
Phosphatase Wip1 controls antigen-independent B-cell development in a p53-dependent manner.磷酸酶Wip1以p53依赖的方式控制抗原非依赖性B细胞发育。
Blood. 2015 Jul 30;126(5):620-8. doi: 10.1182/blood-2015-02-624114. Epub 2015 May 26.
7
WIP1 phosphatase as a potential therapeutic target in neuroblastoma.WIP1磷酸酶作为神经母细胞瘤的潜在治疗靶点。
PLoS One. 2015 Feb 6;10(2):e0115635. doi: 10.1371/journal.pone.0115635. eCollection 2015.
8
Investigation of oscillation accumulation triggered genetic switch in gene regulatory networks.基因调控网络中振荡积累触发的遗传开关研究。
J Theor Biol. 2014 Jul 21;353:61-6. doi: 10.1016/j.jtbi.2014.03.017. Epub 2014 Mar 18.
9
Singular Hopf bifurcation in a differential equation with large state-dependent delay.具有大状态依赖时滞的微分方程中的奇异霍普夫分岔
Proc Math Phys Eng Sci. 2014 Feb 8;470(2162):20130596. doi: 10.1098/rspa.2013.0596.
10
Correlation between oncogenic mutations and parameter sensitivity of the apoptosis pathway model.致癌突变与细胞凋亡途径模型参数敏感性之间的相关性。
PLoS Comput Biol. 2014 Jan;10(1):e1003451. doi: 10.1371/journal.pcbi.1003451. Epub 2014 Jan 23.