Evidence map›Paper›PMID 20173116›Full record

ArticleBlood2010

Alternative modes of GM-CSF receptor activation revealed using activated mutants of the common beta-subunit.

Michelle Perugini, Anna L Brown, Diana G Salerno, Grant W Booker, Cvetan Stojkoski, Timothy R Hercus, Angel F Lopez, Margaret L Hibbs, Thomas J Gonda, Richard J D'Andrea

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. GM-CSF in inflammation.The Journal of experimental medicine · 2020
    Review
  7. Review
  8. Review
  9. Review
  10. GM-CSF-Dependent Inflammatory Pathways.Frontiers in immunology · 2019
    Review
  11. Role of the β Common (βc) Family of Cytokines in Health and Disease.Cold Spring Harbor perspectives in biology · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. G-CSF and GM-CSF in Neutropenia.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Review
  17. Dual Role of GM-CSF as a Pro-Inflammatory and a Regulatory Cytokine: Implications for Immune Therapy.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015
    Review
  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

10 authors at 5 institutions in 2 countries.

Michelle PeruginiDivision of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia.
Anna L Brown
Diana G Salerno
Grant W Booker
Cvetan Stojkoski
Timothy R Hercus
Angel F Lopez
Margaret L Hibbs
Thomas J Gonda
Richard J D'Andrea
South Australia Pathology · AUCentre for Cancer Biology · AUUniversity of Adelaide · AULudwig Cancer Research · BEUniversity of Queensland · AU

Funding

ACTIVATED MUTANTS AS PROBES OF GM/CSF RECEPTOR FUNCTIONR01HL060657 · NHLBI · WOMEN'S &CHILDREN'S HEALTH RES/INST · PI D'ANDREA, RICHARD J · 1998 to 2003
$753k
NHLBI NIH HHS R01 HL060657NHLBI NIH HHS R01 HL60657
6 · The paper itself

Abstract

Granulocyte/macrophage colony-stimulating factor promotes growth, survival, differentiation, and activation of normal myeloid cells and plays an important role in myeloid leukemias. The GM-CSF receptor (GMR) shares a signaling subunit, beta(c), with interleukin-3 and interleukin-5 receptors and has recently been shown to induce activation of Janus kinase 2 (JAK2) and downstream signaling via formation of a unique dodecameric receptor complex. In this study we use 2 activated beta(c) mutants that display distinct signaling capacity and have differential requirements for the GMR alpha-subunit (GMR-alpha) to dissect the signaling pathways associated with the GM-CSF response. The V449E transmembrane mutant selectively activates JAK2/signal transducer and activator of transcription 5 and extracellular signal-regulated kinase (ERK) pathways, resulting in a high level of sensitivity to JAK and ERK inhibitors, whereas the extracellular mutant (FIDelta) selectively activates the phosphoinositide 3-kinase/Akt and IkappaKbeta/nuclear factorkappaB pathways. We also demonstrate a novel and direct interaction between the SH3 domains of Lyn and Src with a conserved proline-rich motif in GMR-alpha and show a selective requirement for Src family kinases by the FIDelta mutant. We relate the nonoverlapping nature of signaling by the activated mutants to the structure of the unique GMR complex and propose alternative modes of receptor activation acting synergistically in the mature liganded receptor complex.

Indexed as

AnimalsBlotting, WesternCell LineEnzyme ActivationFlow CytometryImmunoprecipitationLeukemia, Myeloid, AcuteMiceMicroscopy, FluorescenceMutationReceptors, Granulocyte-Macrophage Colony-Stimulating FactorSignal TransductionReceptors, Granulocyte-Macrophage Colony-Stimulating Factor

Identifiers

PMID20173116
PMCPMC2858480
OpenAlexW2075433335

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.