Evidence map›Paper›PMID 18188450›Full record

ArticleThe Journal of clinical investigation2008

Role of Gas6 in erythropoiesis and anemia in mice.

Anne Angelillo-Scherrer, Laurent Burnier, Diether Lambrechts, Richard J Fish, Marc Tjwa, Stéphane Plaisance, Rocco Sugamele, Maria DeMol, Eduardo Martinez-Soria, Patrick H Maxwell and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Recent advances in TAM mechanisms in lung diseases.Journal of translational medicine · 2025
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  3. AXL signaling in cancer: from molecular insights to targeted therapies.Signal transduction and targeted therapy · 2025
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  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Targeting of TAM Receptors Ameliorates Fibrotic Mechanisms in Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2018
    Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review
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

20 authors at 5 institutions in 2 countries.

Anne Angelillo-ScherrerService and Central Laboratory of Hematology, Centre Hospitalier Universitaire Vaudois, University Hospital Center, University of Lausanne, Lausanne, Switzerland. Anne.Angellilo-Scherrer@chuv.ch
Laurent Burnier
Diether Lambrechts
Richard J Fish
Marc Tjwa
Stéphane Plaisance
Rocco Sugamele
Maria DeMol
Eduardo Martinez-Soria
Patrick H Maxwell
Greg Lemke
Stephen P Goff
Glenn K Matsushima
H Shelton Earp
Marc Chanson
Désiré Collen
Shozo Izui
Marc Schapira
Edward M Conway
Peter Carmeliet
Center for Neurosciences · USColumbia University Irving Medical Center · USSalk Institute for Biological Studies · USUniversity Hospital of Lausanne · CHUniversity of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many patients with anemia fail to respond to treatment with erythropoietin (Epo), a commonly used hormone that stimulates erythroid progenitor production and maturation by human BM or by murine spleen. The protein product of growth arrest-specific gene 6 (Gas6) is important for cell survival across several cell types, but its precise physiological role remains largely enigmatic. Here, we report that murine erythroblasts released Gas6 in response to Epo and that Gas6 enhanced Epo receptor signaling by activating the serine-threonine kinase Akt in these cells. In the absence of Gas6, erythroid progenitors and erythroblasts were hyporesponsive to the survival activity of Epo and failed to restore hematocrit levels in response to anemia. In addition, Gas6 may influence erythropoiesis via paracrine erythroblast-independent mechanisms involving macrophages. When mice with acute anemia were treated with Gas6, the protein normalized hematocrit levels without causing undesired erythrocytosis. In a transgenic mouse model of chronic anemia caused by insufficient Epo production, Gas6 synergized with Epo in restoring hematocrit levels. These findings may have implications for the treatment of patients with anemia who fail to adequately respond to Epo.

Indexed as

AnemiaAnimalsAxl Receptor Tyrosine KinaseCell AdhesionCell Survivalc-Mer Tyrosine KinaseDisease Models, AnimalDrug ResistanceErythroblastsErythropoiesisErythropoietinGrowth Arrest-Specific Protein 6HumansIntercellular Signaling Peptides and ProteinsMiceMice, Mutant StrainsAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseErythropoietinGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsMertk protein, mouseOncogene ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptor Protein-Tyrosine KinasesReceptors, ErythropoietinRecombinant ProteinsTyro3 protein, mouse

Identifiers

PMID18188450
PMCPMC2176185
OpenAlexW2162451892

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.