Evidence map›Paper›PMID 10930452›Full record

ArticleMolecular biology of the cell2000

The tumor suppressor p53 can both stimulate and inhibit ultraviolet light-induced apoptosis.

B C McKay, F Chen, C R Perumalswami, F Zhang, M Ljungman

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Autophagy in UV Damage Response.Photochemistry and photobiology · 2017
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Involvement of stromal p53 in tumor-stroma interactions.Seminars in cell & developmental biology · 2010
    Review
  10. Cells from long-lived mutant mice exhibit enhanced repair of ultraviolet lesions.The journals of gerontology. Series A, Biological sciences and medical sciences · 2008
    Article
  11. Article
  12. Article
  13. Regulation of ultraviolet light-induced gene expression by gene size.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

5 authors at 1 institution in 1 country.

B C McKayDepartment of Radiation Oncology, Division of Cancer Biology, University of Michigan Comprehensive Cancer Center, Ann Arbor 48109-0936, USA.
F Chen
C R Perumalswami
F Zhang
M Ljungman
University of Michigan · US

Funding

REGULATION OF P53 STABILITY BY SER315 PHOSPHORYLATIONR01CA082376 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LJUNGMAN, MATS · 1999 to 2002
$627k
NCI NIH HHS CA82376-01
6 · The paper itself

Abstract

We have previously shown that the tumor suppressor p53 can play a protective role against UV-induced apoptosis in human fibroblasts. In the present study, we investigated whether the protective function of p53 expression is established before or after UV irradiation. Using a stable human cell line expressing a murine temperature-sensitive p53 in which p53 function could be tightly and reversibly regulated, we found that functional p53 stimulated the induction of apoptosis when expressed for as little as 4-12 h after UV irradiation and that this induction was not dependent on de novo protein synthesis. In contrast, expression of p53 for 12 h or more before UV irradiation reduced the extent of apoptosis even when functional p53 expression was maintained after irradiation. The protection conferred by p53 required ongoing protein synthesis and correlated with enhanced recovery of mRNA synthesis. Together, these results suggest that p53 induces distinct proapoptotic and antiapoptotic signals and that these opposing activities can be separated both temporally and by their requirement for de novo protein synthesis. These findings may have important implications for the refinement of gene therapy approaches combining p53 with pharmacological agents that target transcription or translation.

Indexed as

ApoptosisCell CycleCycloheximideFlow CytometryHT29 CellsHumansModels, BiologicalProtein BiosynthesisProtein Synthesis InhibitorsTemperatureTime FactorsTranscription, GeneticTumor Suppressor Protein p53Ultraviolet RaysCycloheximideProtein Synthesis InhibitorsTumor Suppressor Protein p53

Identifiers

PMID10930452
PMCPMC14938
OpenAlexW2148394866

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.