Evidence map›Paper›PMID 25704813›Full record

ArticleCell reports2015

Analysis of p53 transactivation domain mutants reveals Acad11 as a metabolic target important for p53 pro-survival function.

Dadi Jiang, Edward L LaGory, Daniela Kenzelmann Brož, Kathryn T Bieging, Colleen A Brady, Nichole Link, John M Abrams, Amato J Giaccia, Laura D Attardi

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Lipids as Regulators of Cellular Senescence.Frontiers in physiology · 2022
    Review
  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

9 authors at 2 institutions in 1 country.

Dadi JiangDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Edward L LaGoryDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Daniela Kenzelmann BrožDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Kathryn T BiegingDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Colleen A BradyDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Nichole LinkDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
John M AbramsDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Amato J GiacciaDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Laura D AttardiDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: attardi@stanford.edu.
Stanford University · USThe University of Texas Southwestern Medical Center · US

Funding

Molecular and Genetic Control of Programmed Cell DeathR01GM072124 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI ABRAMS, JOHN M · 2004 to 2016
$4.4M
Postdoctoral Training in the Radiation ScincesT32CA121940 · NCI · STANFORD UNIVERSITY · PI GRAVES, EDWARD E. · 2007 to 2018
$2.1M
Mouse Models to Dissect p53 Tumor Suppressor FunctionR01CA140875 · NCI · STANFORD UNIVERSITY · PI ATTARDI, LAURA D · 2011 to 2015
$1.7M
NCI NIH HHS CA140875NCI NIH HHS R01 CA140875NCI NIH HHS T32 CA121940NIGMS NIH HHS R01 GM072124
6 · The paper itself

Abstract

The p53 tumor suppressor plays a key role in maintaining cellular integrity. In response to diverse stress signals, p53 can trigger apoptosis to eliminate damaged cells or cell-cycle arrest to enable cells to cope with stress and survive. However, the transcriptional networks underlying p53 pro-survival function are incompletely understood. Here, we show that in oncogenic-Ras-expressing cells, p53 promotes oxidative phosphorylation (OXPHOS) and cell survival upon glucose starvation. Analysis of p53 transcriptional activation domain mutants reveals that these responses depend on p53 transactivation function. Using gene expression profiling and ChIP-seq analysis, we identify several p53-inducible fatty acid metabolism-related genes. One such gene, Acad11, encoding a protein involved in fatty acid oxidation, is required for efficient OXPHOS and cell survival upon glucose starvation. This study provides new mechanistic insight into the pro-survival function of p53 and suggests that targeting this pathway may provide a strategy for therapeutic intervention based on metabolic perturbation.

Indexed as

Acyl-CoA DehydrogenaseAmino Acid SequenceAmino Acid SubstitutionAnimalsCell Line, TumorCell SurvivalGene Regulatory NetworksGlucoseHumansMiceMice, NudeMolecular Sequence DataNeoplasmsOxidative PhosphorylationProtein Structure, TertiaryRNA InterferenceACAD11 protein, humanAcyl-CoA DehydrogenaseGlucoseTumor Suppressor Protein p53

Identifiers

PMID25704813
PMCPMC4365998
OpenAlexW1969265009

What OpenQuestion holds

Textmetadata
LicenceTDM
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.