Evidence map›Paper›PMID 20587594›Full record

ArticleJournal of cell science2010

Btk-dependent Rac activation and actin rearrangement following FcepsilonRI aggregation promotes enhanced chemotactic responses of mast cells.

Hye Sun Kuehn, Madeleine Rådinger, Jared M Brown, Khaled Ali, Bart Vanhaesebroeck, Michael A Beaven, Dean D Metcalfe, Alasdair M Gilfillan

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. RIPK1 ubiquitination regulates its kinase-independent function in development and inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  5. Article
  6. Article
  7. Review
  8. Platelets Independently Recruit into Asthmatic Lungs and Models of Allergic Inflammation via CCR3.American journal of respiratory cell and molecular biology · 2021
    Article
  9. Review
  10. The deleterious role of the prostaglandin EAmerican journal of physiology. Heart and circulatory physiology · 2020
    Article
  11. Article
  12. Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Signal transduction and chemotaxis in mast cells.European journal of pharmacology · 2016
    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

8 authors at 3 institutions in 1 country.

Hye Sun KuehnLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892-1881, USA.
Madeleine Rådinger
Jared M Brown
Khaled Ali
Bart Vanhaesebroeck
Michael A Beaven
Dean D Metcalfe
Alasdair M Gilfillan
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · USNational Heart Lung and Blood Institute · US

Funding

Integrated Signaling Pathways for the Enhancement of Mast Cell ActivationZIAAI000965 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI METCALFE, DEAN D · 2009 to 2018
$5.3M
Generation Of Cytokines And Arachidonic Acid In Mast CellsZIAHL000990 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BEAVEN, MICHAEL A · 2009 to 2010
$885k
Intramural NIH HHS
6 · The paper itself

Abstract

Mast cells infiltrate the sites of inflammation associated with chronic atopic disease and during helminth and bacterial infection. This process requires receptor-mediated cell chemotaxis across a concentration gradient of their chemotactic ligands. In vivo, mast cells are likely to be exposed to several such agents, which can cooperate in a synergistic manner to regulate mast cell homing. Here, we report that chemotaxis of mouse bone-marrow-derived mast cells (BMMCs) in response to the chemoattractants stem-cell factor (SCF) and prostaglandin (PG)E(2), is substantially enhanced following antigen-dependent ligation of the high-affinity receptor for IgE (FcεRI). These responses were associated with enhanced activation of phosphoinositide 3-kinase (PI3K), and downstream activation of the tyrosine protein kinase Btk, with subsequent enhanced phospholipase (PL)Cγ-mediated Ca(2+) mobilization, Rac activation and F-actin rearrangement. Antigen-induced chemotaxis, and the ability of antigen to amplify responses mediated by SCF, adenosine and PGE(2) were suppressed following inhibition of PI3K, and were impaired in BMMCs derived from Btk(-/-) mice. There were corresponding decreases in the PLCγ-mediated Ca(2+) signal, Rac activation and F-actin rearrangement, which, as they are essential for BMMC chemotaxis, accounts for the impaired migration of Btk-deficient cells. Taken together, these data demonstrate that, by regulating signaling pathways that control F-actin rearrangement, Btk is crucial for the ability of antigen to amplify mast-cell chemotactic responses.

Indexed as

ActinsAgammaglobulinaemia Tyrosine KinaseAnimalsBone Marrow CellsCalciumCells, CulturedChemotaxisDinoprostoneFlow CytometryImmunoblottingMast CellsMiceMice, Inbred C57BLMice, Mutant StrainsMicroscopy, FluorescencePhospholipase C gammaActinsAgammaglobulinaemia Tyrosine KinaseCalciumDinoprostonePhospholipase C gammaProtein-Tyrosine Kinasesrac GTP-Binding ProteinsStem Cell Factor

Identifiers

PMID20587594
PMCPMC2908047
OpenAlexW2131697342

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.