Evidence map›Paper›PMID 1716764›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1991

Association of p21ras with phosphatidylinositol 3-kinase.

A Sjölander, K Yamamoto, B E Huber, E G Lapetina

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.5field-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

55 citing papers in PubMed, 185 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Structural insights into Ras regulation by SIN1.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. RAS pathway regulation in melanoma.Disease models & mechanisms · 2022
    Review
  12. Article
  13. Review
  14. TargetingFrontiers in oncology · 2022
    Review
  15. Review
  16. Article
  17. The Hallmarks of Flavonoids in Cancer.Molecules (Basel, Switzerland) · 2021
    Review
  18. Review
  19. Review
  20. Synthetic Lethal Vulnerabilities inCold Spring Harbor perspectives in medicine · 2018
    Review
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 1 institution in 1 country.

A SjölanderDivision of Cell Biology, Burroughs Wellcome Co., Research Triangle Park, NC 27709.
K Yamamoto
B E Huber
E G Lapetina
Burroughs Wellcome Fund · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In mammalian cells, ras genes code for 21-kDa GTP-binding proteins. Increased expression and mutations in specific amino acids have been closely linked to alterations of normal cell morphology, growth, and differentiation and, in particular, to neoplastic transformation. The signal transduction induced by these p21ras proteins is largely unknown; however, the signaling pathways of several growth factors have been reported to involve phosphatidylinositol (PtdIns) 3-kinase. In the present study of a Ha-ras-transformed epithelial cell line, we demonstrated increased PtdIns 3-kinase activity in anti-phosphotyrosine and anti-receptor (insulin and hybrid insulin-like growth factor I) immunoprecipitates of cells that had been stimulated with insulin or insulin-like growth factor I. The PtdIns 3-kinase activity was also immunoprecipitated in these experiments by the anti-Ras monoclonal antibody Y13-259. The specificity of this association with p21ras was ascertained by the neutralizing effect of the antigen peptide and the absence of PtdIns 3-kinase activity in Y13-259 immunoprecipitates from cells in which the ras gene was turned off. These data indicate that PtdIns 3-kinase activity is an important step in the cascade of reactions in p21ras signal transduction, suggesting that the alterations of the cytoskeleton and growth in ras-transformed cells could be mediated by PtdIns 3-kinase activity.

Indexed as

1-Phosphatidylinositol 4-KinaseAnimalsCells, CulturedInsulinInsulin-Like Growth Factor IIn Vitro TechniquesLiverPhosphatidylinositolsPhosphotransferasesPhosphotyrosineProto-Oncogene Proteins p21(ras)RatsSignal TransductionTyrosine1-Phosphatidylinositol 4-KinaseInsulinInsulin-Like Growth Factor IPhosphatidylinositolsPhosphotransferasesPhosphotyrosineProto-Oncogene Proteins p21(ras)Tyrosine

Identifiers

PMID1716764
PMCPMC52414
OpenAlexW2058078993

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.