Evidence map›Paper›PMID 31885199›Full record

ArticleMolecular systems biology2019

Stochastic transcription in the p53-mediated response to DNA damage is modulated by burst frequency.

Dhana Friedrich, Laura Friedel, Ana Finzel, Andreas Herrmann, Stephan Preibisch, Alexander Loewer

Abstract read
In one paragraph

Article in Molecular systems biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Systems Biology of the Cancer Cell.Annual review of biomedical engineering · 2025
    Review
  4. Article
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  6. Article
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  8. Article
  9. Analysis of developmental gene expression using smFISH andbioRxiv : the preprint server for biology · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Dhana FriedrichDepartment for Biology, Technische Universität Darmstadt, Darmstadt, Germany.ORCID 0000-0003-2144-9280
Laura FriedelDepartment for Biology, Technische Universität Darmstadt, Darmstadt, Germany.
Ana FinzelBerlin Institute for Medical Systems Biology, Max Delbrück Center in the Helmholtz Association, Berlin, Germany.
Andreas HerrmannDepartment for Biology, Humboldt Universität zu Berlin, Berlin, Germany.
Stephan PreibischBerlin Institute for Medical Systems Biology, Max Delbrück Center in the Helmholtz Association, Berlin, Germany.
Alexander LoewerDepartment for Biology, Technische Universität Darmstadt, Darmstadt, Germany.ORCID 0000-0002-8819-3040

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Discontinuous transcription has been described for different mammalian cell lines and numerous promoters. However, our knowledge of how the activity of individual promoters is adjusted by dynamic signaling inputs from transcription factors is limited. To address this question, we characterized the activity of selected target genes that are regulated by pulsatile accumulation of the tumor suppressor p53 in response to ionizing radiation. We performed time-resolved measurements of gene expression at the single-cell level by smFISH and used the resulting data to inform a mathematical model of promoter activity. We found that p53 target promoters are regulated by frequency modulation of stochastic bursting and can be grouped along three archetypes of gene expression. The occurrence of these archetypes cannot solely be explained by nuclear p53 abundance or promoter binding of total p53. Instead, we provide evidence that the time-varying acetylation state of p53's C-terminal lysine residues is critical for gene-specific regulation of stochastic bursting.

Indexed as

DNA DamageA549 CellsAcetylationCell NucleusGene Expression RegulationGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansIn Situ Hybridization, FluorescenceLysineModels, GeneticPromoter Regions, GeneticRadiation, IonizingSingle-Cell AnalysisSingle Molecule ImagingStochastic ProcessesLysineTP53 protein, humanTumor Suppressor Protein p53cellular heterogeneityDNA damagep53 signalingsingle-cell analysisstochastic transcription

Identifiers

PMID31885199
PMCPMC6886302

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Registered trials

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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.