Evidence map›Paper›PMID 14755247›Full record

ArticleOncogene2004

Attenuation of the p53 response to DNA damage by high cell density.

Jair Bar, Efrat Cohen-Noyman, Benjamin Geiger, Moshe Oren

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Live-cell imaging and mathematical analysis of the "community effect" in apoptosis.Apoptosis : an international journal on programmed cell death · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Hippo signaling: to die or not to die.Cell death and differentiation · 2013
    Article
  14. Article
  15. Ninjurin1, a target of p53, regulates p53 expression and p53-dependent cell survival, senescence, and radiation-induced mortality.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Jair BarDepartment of Molecular Cell Biology, Weizmann Institute of Science, POB26, Rehovot 76100, Israel.
Efrat Cohen-Noyman
Benjamin Geiger
Moshe Oren
Weizmann 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 CA 40099
6 · The paper itself

Abstract

The p53 tumor suppressor is critical for preventing cancer progression. Numerous observations suggest that p53 function can be modulated by the cells' microenvironment. We addressed specifically the impact of cell crowding on the induction of p53 by DNA damage. We report that cell crowding attenuates markedly p53 upregulation, transcriptional activation and subsequent p53-dependent apoptosis following exposure to genotoxic stress. The p53 protein remains short-lived in confluent cultures regardless of the extent of DNA damage, even though it undergoes efficient phosphorylation on the mouse equivalent of human p53 serine 15. This inhibitory effect of cell crowding is not a secondary consequence of density-dependent cell cycle arrest (contact inhibition). Microscopic examination indicates that dense cultures display prominent cadherin-mediated cell-cell junctions, and only poor cell-matrix focal adhesions, whereas sparse cells possess conspicuous matrix adhesions and essentially no cell-cell contacts. High-density cell culture might recapitulate the microenvironment of cells in a living organism, where the response of p53 to DNA damage is reported to be low in some organs and ages. The impact of cell density on p53 activation may have important bearings on the involvement of p53 in tumor suppression and the cellular response to anticancer therapy.

Indexed as

DNA DamageAnimalsCadherinsCell CountCell LineCisplatinCytoskeletal ProteinsFibroblastsMicePaxillinPhosphoproteinsRetroviridaeTranscriptional ActivationTumor Suppressor Protein p53Up-RegulationCadherinsCisplatinCytoskeletal ProteinsPaxillinPhosphoproteinsPxn protein, mouseTumor Suppressor Protein p53

Identifiers

PMID14755247
OpenAlexW1972842856

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.