Evidence map›Paper›PMID 16432180›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Oncogenic transformation induced by the p110beta, -gamma, and -delta isoforms of class I phosphoinositide 3-kinase.

Sohye Kang, Adam Denley, Bart Vanhaesebroeck, Peter K Vogt

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

141 citing papers in PubMed, 269 citations in OpenAlex.

  1. Review
  2. Review
  3. Molecular mechanisms of PI3K isoform dependence in embryonic growth.Journal of the Turkish German Gynecological Association · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. PI3K inhibitors are finally coming of age.Nature reviews. Drug discovery · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. SUMOylation modulates the stability and function of PI3K-p110β.Cellular and molecular life sciences : CMLS · 2021
    Article
  17. Article
  18. Review
  19. PI 3-kinase delta enhances axonal PIPEMBO molecular medicine · 2020
    Article
  20. Article

81 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

4 authors at 2 institutions in 2 countries.

Sohye KangDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, BCC 239, La Jolla, CA 92037, USA.
Adam Denley
Bart Vanhaesebroeck
Peter K Vogt
University College London · GBLudwig Cancer Research · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Class I phosphoinositide 3-kinase contains four isoforms of the catalytic subunit, p110alpha, -beta, -gamma, and -delta. At physiological levels of expression, the wild-type p110alpha isoform lacks oncogenic potential, but gain-of-function mutations and overexpression of p110alpha are correlated with oncogenicity. The p110beta, -gamma, and -delta isoforms induce transformation of cultured cells as wild-type proteins. This oncogenic potential requires kinase activity and can be suppressed by the target of rapamycin inhibitor rapamycin. The p110delta isoform constitutively activates the Akt signaling pathway; p110gamma activates Akt only in the presence of serum. The isoforms differ in their requirements for upstream signaling. The transforming activity of the p110gamma isoform depends on rat sarcoma viral oncogene homolog (Ras) binding; preliminary data suggest the same for p110beta and indicate Ras-independent oncogenic potential of p110delta. The surprising oncogenic potential of the wild-type non-alpha isoforms of class I phosphoinositide 3-kinase may explain the dearth of cancer-specific mutations in these proteins, because these non-alpha isoforms could contribute to the oncogenic phenotype of the cell by differential expression.

Indexed as

Cell Transformation, NeoplasticAnimalsAntibiotics, AntineoplasticBlotting, WesternCell DifferentiationCell Line, TumorCells, CulturedChick EmbryoClass I Phosphatidylinositol 3-KinasesCulture Media, Serum-FreeHumansMutagenesis, Site-DirectedMutationPhosphatidylinositol 3-KinasesPlasmidsPoint MutationAntibiotics, AntineoplasticClass I Phosphatidylinositol 3-KinasesCulture Media, Serum-FreeMTOR protein, humanmTOR protein, ratPhosphatidylinositol 3-KinasesPIK3CB protein, humanProtein IsoformsProtein Kinasesras ProteinsSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID16432180
PMCPMC1360601
OpenAlexW2024676945

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.