Evidence map›Paper›PMID 11016968›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Generation of oscillations by the p53-Mdm2 feedback loop: a theoretical and experimental study.

R Lev Bar-Or, R Maya, L A Segel, U Alon, A J Levine, M Oren

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 222 papers.

0numbers the graph read from it
0cells of the map it votes in
222citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

222 citing papers in PubMed, 593 citations in OpenAlex.

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  5. Negative feedback and oscillations in a model for mRNA translation.Journal of the Royal Society, Interface · 2025
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  17. 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
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162 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 2 countries.

R Lev Bar-OrDepartments of Molecular Cell Biology and Applied Mathematics and Computer Science, The Weizmann Institute of Science, P. O. Box 26, 76100 Rehovot, Israel.
R Maya
L A Segel
U Alon
A J Levine
M Oren
Rockefeller University · USWeizmann Institute of Science · IL

Funding

FUNCTIONAL ANALYSIS OF THE P53 CELLULAR TUMOR ANTIGENR01CA040099 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI OREN, MOSHE · 1985 to 2002
$546k
NCI NIH HHS R01 CA040099NCI NIH HHS R01 CA-40099
6 · The paper itself

Abstract

The intracellular activity of the p53 tumor suppressor protein is regulated through a feedback loop involving its transcriptional target, mdm2. We present a simple mathematical model suggesting that, under certain circumstances, oscillations in p53 and Mdm2 protein levels can emerge in response to a stress signal. A delay in p53-dependent induction of Mdm2 is predicted to be required, albeit not sufficient, for this oscillatory behavior. In line with the predictions of the model, oscillations of both p53 and Mdm2 indeed occur on exposure of various cell types to ionizing radiation. Such oscillations may allow cells to repair their DNA without risking the irreversible consequences of continuous excessive p53 activation.

Indexed as

FeedbackNuclear Proteins3T3 CellsAnimalsHumansMiceProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Tumor Cells, CulturedMDM2 protein, humanMdm2 protein, mouseNuclear ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2

Identifiers

PMID11016968
PMCPMC17186
OpenAlexW2152750766

What OpenQuestion holds

Textmetadata
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.