Evidence map›Paper›PMID 19101635›Full record

ReviewSeminars in cancer biology2009

Homeostatic functions of the p53 tumor suppressor: regulation of energy metabolism and antioxidant defense.

Ivan A Olovnikov, Julia E Kravchenko, Peter M Chumakov

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

83 citing papers in PubMed, 153 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Cells · 2024
    Review
  6. Review
  7. Review
  8. Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024
    Review
  9. Article
  10. Article
  11. Role of p53 in Regulating Radiation Responses.Life (Basel, Switzerland) · 2022
    Review
  12. Article
  13. Article
  14. Reviewing physical exercise in non-obese diabetic Goto-Kakizaki rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022
    Review
  15. Oxidative stress in melanogenesis and melanoma development.Contemporary oncology (Poznan, Poland) · 2022
    Review
  16. Mitochondrial CaCells · 2021
    Review
  17. Article
  18. Review
  19. Article
  20. Article

23 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

3 authors at 2 institutions in 2 countries.

Ivan A OlovnikovEngelhardt Institute of Molecular Biology, Moscow, Russia.
Julia E Kravchenko
Peter M Chumakov
Cleveland Clinic · USEngelhardt Institute of Molecular Biology · RU

Funding

Potentials of reactivated mutant p53R01CA104903 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI CHUMAKOV, PETER M · 2004 to 2008
$1.5M
Role of sestrin family genes in antioxidant defenseR01AG025278 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI CHUMAKOV, PETER M · 2005 to 2009
$1.5M
Howard Hughes Medical InstituteNCI NIH HHS R01CA10490NCI NIH HHS R01 CA104903NIA NIH HHS R01 AG025278NIA NIH HHS R01AG025278
6 · The paper itself

Abstract

The p53 tumor suppressor plays pivotal role in the organism by supervising strict compliance of individual cells to needs of the whole organisms. It has been widely accepted that p53 acts in response to stresses and abnormalities in cell physiology by mobilizing the repair processes or by removing the diseased cells through initiating the cell death programs. Recent studies, however, indicate that even under normal physiological conditions certain activities of p53 participate in homeostatic regulation of metabolic processes and that these activities are important for prevention of cancer. These novel functions of p53 help to align metabolic processes with the proliferation and energy status, to maintain optimal mode of glucose metabolism and to boost the energy efficient mitochondrial respiration in response to ATP deficiency. Additional activities of p53 in non-stressed cells tune up the antioxidant defense mechanisms reducing the probability of mutations caused by DNA oxidation under conditions of daily stresses. The deficiency in the p53-mediated regulation of glycolysis and mitochondrial respiration greatly accounts for the deficient respiration of the predominance of aerobic glycolysis in cancer cells (the Warburg effect), while the deficiency in the p53-modulated antioxidant defense mechanisms contributes to mutagenesis and additionally boosts the carcinogenesis process.

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsAntioxidantsAutophagyEnergy MetabolismGlycolysisHomeostasisHumansInsulin-Like Growth Factor IMitochondriaNeoplasmsPhosphorylationProtein KinasesSignal TransductionTOR Serine-Threonine KinasesTumor Suppressor Protein p53AMP-Activated Protein Kinase KinasesAntioxidantsInsulin-Like Growth Factor IMTOR protein, humanProtein KinasesTOR Serine-Threonine KinasesTumor Suppressor Protein p53

Identifiers

PMID19101635
PMCPMC2646792
OpenAlexW2068549818

What OpenQuestion holds

Textmetadata
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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.