Evidence map›Paper›PMID 15342912›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Proteasomal degradation of the FoxO1 transcriptional regulator in cells transformed by the P3k and Akt oncoproteins.

Masahiro Aoki, Hao Jiang, Peter K Vogt

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing 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

117 citing papers in PubMed, 254 citations in OpenAlex.

  1. A renaissance in targeting the PI3K/AKT/mTOR pathway.Nature reviews. Drug discovery · 2026
    Review
  2. Article
  3. A Protective Role of Canonical Wnt/Mediators of inflammation · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Assessing the Activity of Transcription Factor FoxO1.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  9. Article
  10. Article
  11. Angiotensin II Inhibits Insulin Receptor Signaling in Adipose Cells.International journal of molecular sciences · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. PI3K in T Cell Adhesion and Trafficking.Frontiers in immunology · 2021
    Review
  19. Article
  20. Review

57 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.

Masahiro AokiDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. maoki@mfour.med.kyoto-u.ac.jp
Hao Jiang
Peter K Vogt
Kyoto University · JPScripps Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The P3k oncoprotein [homolog of the catalytic subunit p110alpha of class 1A phosphoinositide 3-kinase (PI3K)] and its downstream effector Akt induce oncogenic transformation in cultures of chicken embryo fibroblasts (CEF). The winged helix transcription factor FoxO1 is a growth-attenuating and proapoptotic protein and serves as a substrate of Akt. Here we show that FoxO1 expression is constitutively suppressed in CEF transformed by P3k or Akt. The FoxO1 protein level is high in serum-starved normal CEF, but platelet-derived growth factor treatment induces rapid phosphorylation and disappearance of FoxO1. PI3K inhibitors or the proteasome inhibitor lactacystin interfere with this process. These data suggest that phosphorylation-dependent degradation of FoxO1 by means of proteasomes plays a role in oncogenic transformation by P3k and Akt. A dominant negative mutant of FoxO1 containing the repressor domain of the Drosophila Engrailed protein induces partial oncogenic transformation of CEF and interferes with FoxO1-dependent transcriptional activation. The FoxG1 oncoprotein also inhibits transcriptional activation by FoxO1. Inhibition of FoxO1, albeit by different mechanisms, appears to be a common denominator of the PI3K and FoxG1 oncogenic pathways.

Indexed as

Cell Transformation, NeoplasticAnimalsCell DivisionCell Line, TransformedChickensCysteine EndopeptidasesDNA-Binding ProteinsDown-RegulationForkhead Box Protein O1Forkhead Transcription FactorsGene ExpressionHumansMultienzyme ComplexesOncogene ProteinsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsAKT1 protein, humanCysteine EndopeptidasesDNA-Binding ProteinsForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanMultienzyme ComplexesOncogene ProteinsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProteasome Endopeptidase ComplexProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTranscription Factors

Identifiers

PMID15342912
PMCPMC518802
OpenAlexW1974178287

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.