Evidence map›Paper›PMID 15226433›Full record

ArticleMolecular and cellular biology2004

Distinct mechanisms determine the patterns of differential activation of H-Ras, N-Ras, K-Ras 4B, and M-Ras by receptors for growth factors or antigen.

Annette Ehrhardt, Muriel D David, Götz R A Ehrhardt, John W Schrader

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

38 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Active GTPase Pulldown Protocol.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  4. Article
  5. The Interdependent Activation of Son-of-Sevenless and Ras.Cold Spring Harbor perspectives in medicine · 2019
    Review
  6. The Many Faces of Rap1 GTPase.International journal of molecular sciences · 2018
    Review
  7. Article
  8. Article
  9. Article
  10. Kras Is Critical for B Cell Lymphopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Regulatory domain phosphorylation to distinguish the mechanistic basis underlying acute CFTR modulators.American journal of physiology. Lung cellular and molecular physiology · 2011
    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

4 authors at 2 institutions in 2 countries.

Annette EhrhardtThe Biomedical Research Centre, University of British Columbia, Vancouver, Canada.
Muriel D David
Götz R A Ehrhardt
John W Schrader
University of British Columbia · CAUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although GTPases of the Ras family have been implicated in many aspects of the regulation of cells, little is known about the roles of individual family members. Here, we analyzed the mechanisms of activation of H-Ras, N-Ras, K-Ras 4B, and M-Ras by two types of external stimuli, growth factors and ligation of the antigen receptors of B or T lymphocytes (BCRs and TCRs). The growth factors interleukin-3, colony-stimulating factor 1, and epidermal growth factor all preferentially activated M-Ras and K-Ras 4B over H-Ras or N-Ras. Preferential activation of M-Ras and K-Ras 4B depended on the presence of their polybasic carboxy termini, which directed them into high-buoyant-density membrane domains where the activated receptors, adapters, and mSos were also present. In contrast, ligation of the BCR or TCR resulted in activation of H-Ras, N-Ras, and K-Ras 4B, but not M-Ras. This pattern of activation was not influenced by localization of the Ras proteins to membrane domains. Activation of H-Ras, N-Ras, and K-Ras 4B instead depended on the presence of phospholipase C-gamma and RasGRP. Thus, the molecular mechanisms leading to activation of Ras proteins vary with the stimulus and can be influenced by either colocalization with activated receptors or differential sensitivity to the exchange factors activated by a stimulus.

Indexed as

Adaptor Proteins, Signal TransducingGenes, rasAdaptor Proteins, Vesicular TransportAnimalsCell LineEnzyme ActivationEpidermal Growth FactorGRB2 Adaptor ProteinGrowth SubstancesHumansInterleukin-3Macrophage Colony-Stimulating FactorMembrane MicrodomainsMiceMonomeric GTP-Binding ProteinsPhorbol EstersAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportEpidermal Growth FactorGRB2 Adaptor ProteinGRB2 protein, humanGrb2 protein, mouseGrowth SubstancesHRAS protein, humanInterleukin-3KRAS protein, humanMacrophage Colony-Stimulating FactorMonomeric GTP-Binding ProteinsMras protein, mousePhorbol EstersPhospholipase C gammaProteinsProto-Oncogene Proteins p21(ras)ras ProteinsReceptors, Antigen, T-CellSHC1 protein, humanShc1 protein, mouseShc Signaling Adaptor ProteinsSOS1 ProteinSrc Homology 2 Domain-Containing, Transforming Protein 1Type C Phospholipases

Identifiers

PMID15226433
PMCPMC434254
OpenAlexW2150273078

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.