Evidence map›Paper›PMID 12776195›Full record

ArticleOncogene2003

Hypoxia attenuates the p53 response to cellular damage.

Marcus Achison, Ted R Hupp

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. HIF-transcribed p53 chaperones HIF-1α.Nucleic acids research · 2019
    Article
  7. Article
  8. Review
  9. Induction of dormancy in hypoxic human papillomavirus-positive cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  10. Article
  11. Article
  12. Tumor suppressor p53 stole the AKT in hypoxia.The Journal of clinical investigation · 2015
    Article
  13. Article
  14. Article
  15. Toxicogenomic effect of nickel and beyond.Archives of toxicology · 2014
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Passage-dependent cancerous transformation of human mesenchymal stem cells under carcinogenic hypoxia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    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

2 authors at 1 institution in 1 country.

Marcus AchisonThe Cancer Research UK Laboratories, Department of Molecular and Cellular Pathology, The University of Dundee, Dundee, DD1 9SY, UK.
Ted R Hupp
Cancer Research UK · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumour suppressor activity of p53 in vivo can be subject to pressure from the physiological stress of hypoxia and we report on the development of a cell system to define the p53-dependent stages in the adaptation of cells to hypoxia. p53(+/+) cells exposed to hypoxia exhibited a transient arrest in G2/M, but escaped from this checkpoint and entered a long-term G(0)/G(1) arrest. By contrast, isogenic p53-null cells exposed to hypoxic conditions exhibited a 6-10-fold higher level of apoptosis, suggesting that p53 acts as a survival factor under limiting oxygen concentrations. Surprisingly, hypoxia-dependent growth arrest in p53(+/+) cells did not result in either p21(WAF1) or HIF-1 protein stabilization, but rather promoted a significant decrease in Ser(392)-site phosphorylation at the CK2/FACT site. However, chemically induced anoxia induced Ser(392)-site phosphorylation as well as stabilization of both p53 and HIF-1 proteins. In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels. Hypoxia inhibited 5-FU-induced p53-dependent cell death and attenuated p53 phosphorylation at the ATM and CK2/FACT phosphorylation sites. Although anoxia activates the p53 response, hypoxia silences the p53 transactivation pathway and identifies a physiological signalling model to study mechanisms of p53 inactivation under hypoxic conditions.

Indexed as

ApoptosisCell SurvivalDown-RegulationFluorouracilHumansHypoxiaPhosphorylationTumor Cells, CulturedTumor Suppressor Protein p53FluorouracilTumor Suppressor Protein p53

Identifiers

PMID12776195
OpenAlexW2023553772

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.