ArticleCell reports2020
A Switch in p53 Dynamics Marks Cells That Escape from DSB-Induced Cell Cycle Arrest.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 57 citations in OpenAlex.
- A dual role for cGAS in shaping cellular and organismal responses to genomic instability.Genes & development · 2026Article
- Decoding the Central Dogma: Quantitative Insights into Transcription and Translation Dynamics in the p53-Mediated DNA Damage Response.Journal of molecular biology · 2026Review
- Article
- DNA damage checkpoints balance a tradeoff between diploid- and polyploid-derived arrest failures.Cell reports · 2025Article
- The interplay between driver mutation and oxidative stress in colorectal cancer: from pathogenesis to therapeutics.Journal of translational medicine · 2025Review
- DNA damage checkpoints balance a tradeoff between diploid- and polyploid-derived arrest failures.bioRxiv : the preprint server for biology · 2025Article
- Complex p53 dynamics regulated by miR-125b in cellular responses to reactive oxidative stress and DNA damage.Briefings in bioinformatics · 2024Article
- Caspase-2 kills cells with extra centrosomes.Science advances · 2024Article
- TOPAS-Tissue: A Framework for the Simulation of the Biological Response to Ionizing Radiation at the Multi-Cellular Level.International journal of molecular sciences · 2024Article
- Identification of genes with oscillatory expression in glioblastoma: the paradigm of SOX2.Scientific reports · 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
- SCML2 contributes to tumor cell resistance to DNA damage through regulating p53 and CHK1 stability.Cell death and differentiation · 2023Article
- Long-term p21 and p53 dynamics regulate the frequency of mitosis events and cell cycle arrest following radiation damage.Cell death and differentiation · 2023Article
- When cell death goes wrong: inflammatory outcomes of failed apoptosis and mitotic cell death.Cell death and differentiation · 2023Review
- Therapeutic Potential of Nanomedicine in Management of Alzheimer's Disease and Glioma.International journal of nanomedicine · 2023Review
- Comparative analysis of chlorambucil-induced DNA lesion formation and repair in a spectrum of different human cell systems.Toxicology reports · 2023Article
- PIDD1 in cell cycle control, sterile inflammation and cell death.Biochemical Society transactions · 2022Review
- Moonlighting at the Poles: Non-Canonical Functions of Centrosomes.Frontiers in cell and developmental biology · 2022Review
- Progress and challenges in understanding the regulation and function of p53 dynamics.Biochemical Society transactions · 2021Review
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Cellular responses to stimuli can evolve over time, resulting in distinct early and late phases in response to a single signal. DNA damage induces a complex response that is largely orchestrated by the transcription factor p53, whose dynamics influence whether a damaged cell will arrest and repair the damage or will initiate cell death. How p53 responses and cellular outcomes evolve in the presence of continuous DNA damage remains unknown. Here, we have found that a subset of cells switches from oscillating to sustained p53 dynamics several days after undergoing damage. The switch results from cell cycle progression in the presence of damaged DNA, which activates the caspase-2-PIDDosome, a complex that stabilizes p53 by inactivating its negative regulator MDM2. This work defines a molecular pathway that is activated if the canonical checkpoints fail to halt mitosis in the presence of damaged DNA.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.