Evidence map›Paper›PMID 8393576›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1993

A mutant alpha subunit of G12 potentiates the eicosanoid pathway and is highly oncogenic in NIH 3T3 cells.

N Xu, L Bradley, I Ambdukar, J S Gutkind

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

71 citing papers in PubMed, 174 citations in OpenAlex.

  1. Review
  2. Review
  3. GRespiratory research · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. GαFrontiers in cell and developmental biology · 2022
    Review
  9. Article
  10. Review
  11. Naturally occurring hotspot cancer mutations in GαThe Journal of biological chemistry · 2020
    Article
  12. Review
  13. Article
  14. Review
  15. Signaling mechanisms and physiological functions of G-protein GαProtein science : a publication of the Protein Society · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Gα12 regulates osteoclastogenesis by modulating NFATc1 expression.Journal of cellular and molecular medicine · 2018
    Article
  20. Article

11 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 1 country.

N XuLaboratory of Cellular Development and Oncology, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892.
L Bradley
I Ambdukar
J S Gutkind
National Institutes of Health · USNational Institute of Dental and Craniofacial Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery of GTPase-inhibiting mutations in genes for alpha subunits of Gs or G(i2) in certain human endocrine tumors has raised the possibility that heterotrimeric guanine nucleotide-binding regulatory proteins (G proteins) might contribute to neoplastic disease. Expression of GTPase-deficient alpha s or alpha i2 polypeptides in rodent fibroblasts increases or decreases cAMP, respectively, and induces certain alterations in cell growth but only a few of the phenotypic changes associated with cellular transformation. In contrast, an analogous mutation in the alpha subunit of Gq, which activates phosphatidylinositol (PI)-specific phospholipase C, is fully oncogenic. However, activated alpha q is cytotoxic and several orders of magnitude less potent as an oncogene than certain G protein-coupled receptors. Thus, G proteins other than those inducing PI hydrolysis might possess high transforming efficiency. In the present study, we explored the G12 family of G proteins for their oncogenic potential. Our results show that whereas overexpression of wild-type alpha 12 in NIH 3T3 cells is itself weakly transforming, an activated alpha 12 behaves as a remarkably potent oncogene. Transformation by alpha 12 correlates with alterations in the eicosanoid pathway but not with PI-specific phospholipase C or other G protein-linked second messengers.

Indexed as

3T3 CellsAmino Acid SequenceAnimalsBase SequenceCell DivisionCell Transformation, NeoplasticCyclic AMPEicosanoidsEnzyme ActivationGTP-Binding ProteinsInositol PhosphatesMiceMice, NudeMolecular Sequence DataMultigene FamilyMutationCyclic AMPEicosanoidsGTP-Binding ProteinsInositol Phosphates

Identifiers

PMID8393576
PMCPMC47008
OpenAlexW2047454594

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.