Evidence map›Paper›PMID 30745421›Full record

ArticleThe Journal of cell biology2019

Protein stability of p53 targets determines their temporal expression dynamics in response to p53 pulsing.

Ryan L Hanson, Joshua R Porter, Eric Batchelor

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 16% of its field
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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  6. Systems Biology of the Cancer Cell.Annual review of biomedical engineering · 2025
    Review
  7. Review
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  10. A molecular mechanism for the "digital" response of p53 to stress.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. 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 · 2023
    Review
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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

3 authors at 1 institution in 1 country.

Ryan L HansonLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Joshua R PorterLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Eric BatchelorLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD batchelore@mail.nih.gov.ORCID 0000-0003-3870-5615
National Institutes of Health · US

Funding

Systems-level analysis of the regulation and function of p53 dynamicsZIABC011382 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BATCHELOR, ERIC · 2011 to 2020
$5.8M
Intramural NIH HHS ZIA BC011382
6 · The paper itself

Abstract

In response to DNA damage, the transcription factor p53 accumulates in a series of pulses. While p53 dynamics play a critical role in regulating stress responses, how p53 pulsing affects target protein expression is not well understood. Recently, we showed that p53 pulses generate diversity in target mRNA expression dynamics; however, given that mRNA and protein expression are not necessarily well correlated, it remains to be determined how p53 pulses impact target protein expression. Using computational and experimental approaches, we show that target protein decay rates filter p53 pulses: Distinct target protein expression dynamics are generated depending on the relationship between p53 pulse frequency and target mRNA and protein stability. Furthermore, by mutating the targets MDM2 and PUMA to alter their stabilities, we show that downstream pathways are sensitive to target protein decay rates. This study delineates the mechanisms by which p53 dynamics play a crucial role in orchestrating the timing of events in the DNA damage response network.

Indexed as

DNA Breaks, Double-StrandedApoptosis Regulatory ProteinsBreast NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansKineticsMCF-7 CellsModels, BiologicalMutationProtein StabilityProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2RNA, MessengerRNA StabilitySignal TransductionApoptosis Regulatory ProteinsBBC3 protein, humanMDM2 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2RNA, MessengerTP53 protein, humanTumor Suppressor Protein p53Zinostatin

Identifiers

PMID30745421
PMCPMC6446860
OpenAlexW2911789995

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.