ArticleScience signaling2017
p53 dynamics in response to DNA damage vary across cell lines and are shaped by efficiency of DNA repair and activity of the kinase ATM.
Article in Science signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 112 citations in OpenAlex.
- Transient peak of p53 induction persists at low radiation doses in MCF-7 cells.Molecular biology reports · 2026Article
- A dual role for cGAS in shaping cellular and organismal responses to genomic instability.Genes & development · 2026Article
- Methodological Landscape of DNA Damage Response Detection: From Conventional Assays to Future Innovations.Current issues in molecular biology · 2026Review
- Genetic resonance in the p53 signaling network.Cell systems · 2026Article
- DNA-damaging chemotherapy reshapes cardiac-resident macrophage composition and function.Science immunology · 2026Article
- Decoding the Central Dogma: Quantitative Insights into Transcription and Translation Dynamics in the p53-Mediated DNA Damage Response.Journal of molecular biology · 2026Review
- Harnessing Natural Extracellular Vesicles to Combat Age-Related Diseases: From Aging Drivers to Therapeutic Opportunities.International journal of nanomedicine · 2026Review
- p53 Regulates Nuclear Architecture to Reduce Carcinogen Sensitivity and Mutagenic Potential.bioRxiv : the preprint server for biology · 2025Article
- Cell confluency affects p53 dynamics in response to DNA damage.Molecular biology of the cell · 2025Article
- Deciphering UBE4B phosphorylation dynamics: a key mechanism in p53 accumulation and cancer cell response to DNA damage.Cell death discovery · 2025Article
- Cell Type Specific Suppression of Hyper-Recombination by Human RAD18 Is Linked to Proliferating Cell Nuclear Antigen K164 Ubiquitination.Biomolecules · 2025Article
- Linking signaling dynamics and cell fate decisions through single-cell imaging: evidence and challenges.Frontiers in cell and developmental biology · 2025Review
- Complex p53 dynamics regulated by miR-125b in cellular responses to reactive oxidative stress and DNA damage.Briefings in bioinformatics · 2024Article
- Temporal regulation of gene expression through integration of p53 dynamics and modifications.Science advances · 2024Article
- Entrainment and multi-stability of the p53 oscillator in human cells.Cell systems · 2024Article
- Low-frequency ERK and Akt activity dynamics are predictive of stochastic cell division events.NPJ systems biology and applications · 2024Article
- Increased cancer risk in HIV-infected individuals occupationally exposed to chemicals: Depression of p53 as the key driver.PLOS global public health · 2024Article
- Emerging role and therapeutic implications of p53 in intervertebral disc degeneration.Cell death discovery · 2023Review
- 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
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cellular systems show a wide range of signaling dynamics. Many of these dynamics are highly stereotyped, such as oscillations at a fixed frequency. However, most studies looking at the role of signaling dynamics focus on one or a few cell lines, leaving the diversity of dynamics across tissues or cell lines a largely unexplored question. We focused on the dynamics of the tumor suppressor protein p53, which regulates cell cycle arrest and apoptosis in response to DNA damage. We established live-cell reporters for 12 cancer cell lines expressing wild-type p53 and quantified p53 dynamics in response to double-strand break-inducing DNA damage. In many of the tested cell lines, we found that p53 abundance oscillated in response to ionizing radiation or the DNA-damaging chemotherapeutic neocarzinostatin and that the periodicity of the oscillations was fixed. In other cell lines, p53 abundance dynamically changed in different ways, such as a single broad pulse or a continuous induction. By combining single-cell assays of p53 signaling dynamics, small-molecule screening in live cells, and mathematical modeling, we identified molecules that perturbed p53 dynamics and determined that cell-specific variation in the efficiency of DNA repair and the activity of the kinase ATM (ataxia-telangiectasia mutated) controlled the signaling landscape of p53 dynamics. Because the dynamics of wild-type p53 varied substantially between cell lines, our study highlights the limitation of using one line as a model system and emphasizes the importance of studying the dynamics of other signaling pathways across different cell lines and genetic backgrounds.
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