Evidence map›Paper›PMID 30287508›Full record

ReviewBiochemical Society transactions2018

RAS variant signalling.

Stephanie P Mo, Judy M Coulson, Ian A Prior

Open access · hybridAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

51 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Inhibition mechanism of MRTX1133 on KRASJournal of computer-aided molecular design · 2023
    Article
  15. Exploiting the intrinsic misfolding propensity of the KRAS oncoprotein.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Review
  17. Fluorescent Biosensor for Measuring Ras Activity in Living Cells.Journal of the American Chemical Society · 2022
    Article
  18. Review
  19. Review
  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

3 authors at 1 institution in 1 country.

Stephanie P MoDivision of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3BX, U.K.
Judy M CoulsonDivision of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3BX, U.K.
Ian A PriorDivision of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3BX, U.K. iprior@liv.ac.uk.ORCID 0000-0002-4055-5161
University of Liverpool · GB

Funding

Wellcome Trust WT109309
6 · The paper itself

Abstract

RAS proteins are small GTPases that regulate signalling networks that control cellular proliferation and survival. They are frequently mutated in cancer and a commonly occurring group of developmental disorders called RASopathies. We discuss recent findings describing how RAS isoforms and different activating mutations differentially contribute to normal and disease-associated biology and the mechanisms that have been proposed to underpin this.

Indexed as

Signal TransductionAnimalsCell MembraneCell ProliferationDevelopmental DisabilitiesHumansMutationNeoplasmsProtein IsoformsProtein Multimerizationras ProteinsProtein Isoformsras ProteinscancercodonisoformsmutationRASsignalling

Identifiers

PMID30287508
PMCPMC6195641
OpenAlexW2895665486

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.