Evidence map›Paper›PMID 21926349›Full record

ArticleBlood2011

PTEN deficiency in mast cells causes a mastocytosis-like proliferative disease that heightens allergic responses and vascular permeability.

Yasuko Furumoto, Nicolas Charles, Ana Olivera, Wai Hang Leung, Sandra Dillahunt, Jennifer L Sargent, Kevin Tinsley, Sandra Odom, Eric Scott, Todd M Wilson and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Signal transduction and chemotaxis in mast cells.European journal of pharmacology · 2016
    Review
  7. Review
  8. Phosphatidylinositol-3,4,5-triphosphate and cellular signaling: implications for obesity and diabetes.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015
    Review
  9. Review
  10. Review
  11. Article
  12. Article
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  15. 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

16 authors at 5 institutions in 2 countries.

Yasuko FurumotoLaboratory of Molecular Immunogenetics, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA.
Nicolas Charles
Ana Olivera
Wai Hang Leung
Sandra Dillahunt
Jennifer L Sargent
Kevin Tinsley
Sandra Odom
Eric Scott
Todd M Wilson
Kamran Ghoreschi
Manfred Kneilling
Mei Chen
David M Lee
Silvia Bolland
Juan Rivera
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USHarvard University · USImmungenetics (Germany) · DENational Institute of Allergy and Infectious Diseases · USUniversity of Tübingen · DE

Funding

Genetic Modifiers Of Autoimmune Disease In FcgammaRIIB Mutant MiceZIAAI000912 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BOLLAND, SILVIA · 2009 to 2025
$27.0M
Intracellular Signaling By The Cell Surface Receptor For IgEZIAAR041101 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI RIVERA, JUAN · 2009 to 2013
$4.8M
Intramural NIH HHS
6 · The paper itself

Abstract

Kit regulation of mast cell proliferation and differentiation has been intimately linked to the activation of phosphatidylinositol 3-OH kinase (PI3K). The activating D816V mutation of Kit, seen in the majority of mastocytosis patients, causes a robust activation of PI3K signals. However, whether increased PI3K signaling in mast cells is a key element for their in vivo hyperplasia remains unknown. Here we report that dysregulation of PI3K signaling in mice by deletion of the phosphatase and tensin homolog (Pten) gene (which regulates the levels of the PI3K product, phosphatidylinositol 3,4,5-trisphosphate) caused mast cell hyperplasia and increased numbers in various organs. Selective deletion of Pten in the mast cell compartment revealed that the hyperplasia was intrinsic to the mast cell. Enhanced STAT5 phosphorylation and increased expression of survival factors, such as Bcl-XL, were observed in PTEN-deficient mast cells, and these were further enhanced by stem cell factor stimulation. Mice carrying PTEN-deficient mast cells also showed increased hypersensitivity as well as increased vascular permeability. Thus, Pten deletion in the mast cell compartment results in a mast cell proliferative phenotype in mice, demonstrating that dysregulation of PI3K signals is vital to the observed mast cell hyperplasia.

Indexed as

Adoptive TransferAnimalsBone Marrow CellsCapillary PermeabilityCell DegranulationCell DivisionCells, CulturedCell SurvivalDisease Models, AnimalHypersensitivityMast CellsMastocytosisMiceMice, Mutant StrainsPhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID21926349
PMCPMC3217349
OpenAlexW1993501111

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.