ArticleScientific reports2017
Excitability in the p53 network mediates robust signaling with tunable activation thresholds in single cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Time after time - circadian clocks through the lens of oscillator theory.FEBS letters · 2026Review
- LncTRDMT1-5 promotes chromosomal instability through MSRB3-mediated cell cycle and DNA damage in breast cancer.Frontiers in oncology · 2026Article
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- Amplitude and frequency encoding result in qualitatively distinct informational landscapes in cell signaling.Scientific reports · 2025Article
- Decoding stimulus-specific regulation of promoter activity of p53 target genes.Frontiers in cell and developmental biology · 2025Article
- p53 and p21 dynamics encode single-cell DNA damage levels, fine-tuning proliferation and shaping population heterogeneity.Communications biology · 2023Article
- Permission to pass: on the role of p53 as a gatekeeper for aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- Review
- A nested bistable module within a negative feedback loop ensures different types of oscillations in signaling systems.Scientific reports · 2023Article
- Combined multiple transcriptional repression mechanisms generate ultrasensitivity and oscillations.Interface focus · 2022Article
- Nonmodular oscillator and switch based on RNA decay drive regeneration of multimodal gene expression.Nucleic acids research · 2022Article
- Intermittent ERK oscillations downstream of FGF in mouse embryonic stem cells.Development (Cambridge, England) · 2022Article
- Identification, visualization, statistical analysis and mathematical modeling of high-feedback loops in gene regulatory networks.BMC bioinformatics · 2021Article
- Mathematical Modelling of p53 Signalling during DNA Damage Response: A Survey.International journal of molecular sciences · 2021Review
- Dual roles of SIRT1 in the BAX switch through the P53 module: A mathematical modeling study.Computational and structural biotechnology journal · 2021Article
- Theoretical study of the impact of adaptation on cell-fate heterogeneity and fractional killing.Scientific reports · 2020Article
- Article
- Developmental function and state transitions of a gene expression oscillator in Caenorhabditis elegans.Molecular systems biology · 2020Article
- p53 dynamics in single cells are temperature-sensitive.Scientific reports · 2020Article
- Inferring Leading Interactions in the p53/Mdm2/Mdmx Circuit through Live-Cell Imaging and Modeling.Cell systems · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular signaling systems precisely transmit information in the presence of molecular noise while retaining flexibility to accommodate the needs of individual cells. To understand design principles underlying such versatile signaling, we analyzed the response of the tumor suppressor p53 to varying levels of DNA damage in hundreds of individual cells and observed a switch between distinct signaling modes characterized by isolated pulses and sustained oscillations of p53 accumulation. Guided by dynamic systems theory we show that this requires an excitable network structure comprising positive feedback and provide experimental evidence for its molecular identity. The resulting data-driven model reproduced all features of measured signaling responses and is sufficient to explain their heterogeneity in individual cells. We present evidence that heterogeneity in the levels of the feedback regulator Wip1 sets cell-specific thresholds for p53 activation, providing means to modulate its response through interacting signaling pathways. Our results demonstrate how excitable signaling networks can provide high specificity, sensitivity and robustness while retaining unique possibilities to adjust their function to the physiology of individual cells.
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