Evidence map›Paper›PMID 10359590›Full record

ArticleMolecular biology of the cell1999

Transformation by v-Src: Ras-MAPK and PI3K-mTOR mediate parallel pathways.

E Penuel, G S Martin

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 130 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Review
  5. Article
  6. Article
  7. Functional selection in SH3-mediated activation of the PI3 kinase.bioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Article
  10. Isothiocyanate FromFrontiers in cell and developmental biology · 2021
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Mimicking transient activation of protein kinases in living cells.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  17. Article
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

E PenuelDepartment of Molecular and Cell Biology, University of California-Berkeley, Berkeley, California 94720-3204, USA.
G S Martin
University of California, Berkeley · US

Funding

THE MOLECULAR BASIS OF CELL FUNCTIONT32GM007232 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI BILDER, DAVID, UNAL, ELCIN · 1985 to 2022
$36.4M
GENETICS OF RNA TUMOR VIRUSESR37CA017542 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI MARTIN, G STEVEN · 1990 to 2010
$4.0M
GENETICS OF RNA TUMOR VIRUSESR01CA017542 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI MARTIN, G STEVEN · 1985 to 2002
$1.1M
NCI NIH HHS CA-17542NCI NIH HHS R01 CA017542NCI NIH HHS R37 CA017542NIGMS NIH HHS GM-07232NIGMS NIH HHS T32 GM007232
6 · The paper itself

Abstract

An increase in the level of active, GTP-bound Ras is not necessary for transformation of chicken embryo fibroblasts (CEF) by v-Src. This suggests that other Ras-independent pathways contribute to transformation by v-Src. To address the possibility that activation of phosphatidylinositol-3-kinase (PI3K) and the mammalian target of rapamycin (mTOR/FRAP), represents one of these pathways, we have examined the effect of simultaneous inhibition of the Ras-MAPK and PI3K-mTOR pathways on transformation of CEF by v-Src. Transformation was assessed by the standard parameters of morphological alteration, increased hexose uptake, loss of density inhibition, and anchorage-independent growth. Inhibition of the Ras-MAPK pathway by expression of the dominant-negative Ras mutant HRasN17 or by addition of the MAPK kinase (MEK) inhibitor PD98059 reduced several of these parameters but failed to block transformation. Similarly, inhibition of the PI3K-mTOR pathway by addition of the PI3K inhibitor 2-[4-morpholinyl]-8-phenyl-4H-1-benzopyran-4-one (LY294002) or the mTOR inhibitor rapamycin, although reducing several parameters of transformation, also failed to block transformation. However, simultaneous inhibition of signaling by the Ras-MAPK pathway and the PI3K-mTOR pathway essentially blocked transformation. These data indicate that transformation of CEF by v-Src is mediated by two parallel pathways, the Ras-MAPK pathway and the PI-3K-mTOR pathway, which both contribute to transformation. The possibility that simultaneous activation of other pathways is also required is not excluded.

Indexed as

Genes, rasGenes, srcMitogen-Activated Protein Kinase KinasesProtein KinasesAnimalsCalcium-Calmodulin-Dependent Protein KinasesChick EmbryoChromonesColony-Forming Units AssayEnzyme ActivationEnzyme InhibitorsFibroblastsFlavonoidsGene Expression RegulationHexosesMAP Kinase Kinase 12-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneCalcium-Calmodulin-Dependent Protein KinasesChromonesEnzyme InhibitorsFlavonoidsHexosesMAP Kinase Kinase 1Mitogen-Activated Protein Kinase KinasesMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphotransferases (Alcohol Group Acceptor)Protein KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID10359590
PMCPMC25360
OpenAlexW2115291382

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.