ArticleInternational journal of molecular sciences2020
Dynamic Behavior of p53 Driven by Delay and a Microrna-34a-Mediated Feedback Loop.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Importance of ultradian oscillations in neurogenesis during development and its implications for spinal cord regeneration.Frontiers in cell and developmental biology · 2025Review
- Towards verifiable cancer digital twins: tissue level modeling protocol for precision medicine.Frontiers in physiology · 2024Review
- MicroRNAs in doxorubicin-induced cardiotoxicity: The DNA damage response.Frontiers in pharmacology · 2022Review
- Dual roles of SIRT1 in the BAX switch through the P53 module: A mathematical modeling study.Computational and structural biotechnology journal · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The tumor suppressor protein p53 is a critical hub in the comprehensive transcriptional network that inhibits the growth of cells after acute stress stimulation. In this paper, an integrated model of the p53 signaling pathway in response to DNA damage is proposed and the p53 stability and oscillatory dynamics are analyzed. Through theoretical analysis and numerical simulation, we find that the delay as a bifurcation parameter can drive the p53-Mdm2 module to undergo a supercritical Hopf bifurcation, thereby producing oscillation behavior. Moreover, we demonstrate how the positive feedback loop formed by p53* and microRNA-34a (miR-34a) with the feature of double-negative regulation produces limit-cycle oscillations. Further, we find that miR-34a can affect the critical value of Hopf bifurcation in delay-induced p53 networks. In addition, we show that ATM, once activated by DNA damage, makes p53* undergo two Hopf bifurcations. These results revealed that both time delay and miR-34a can have tumor suppressing roles by promoting p53 oscillation or high level expression, which will provide a perspective for promoting the development of anti-cancer drugs by targeting miR-34a and time delay.
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Registered trials
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