ArticleThe Journal of experimental medicine2004
WIP regulates signaling via the high affinity receptor for immunoglobulin E in mast cells.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Cytoskeletal Transport, Reorganization, and Fusion Regulation in Mast Cell-Stimulus Secretion Coupling.Frontiers in cell and developmental biology · 2021Review
- The Disordered Cellular Multi-Tasker WIP and Its Protein-Protein Interactions: A Structural View.Biomolecules · 2020Review
- Crosstalk between WIP and Rho family GTPases.Small GTPases · 2020Review
- Cutting Edge: Drebrin-Regulated Actin Dynamics Regulate IgE-Dependent Mast Cell Activation and Allergic Responses.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- PIP kinases define PI4,5P₂signaling specificity by association with effectors.Biochimica et biophysica acta · 2015Review
- DOCK5 functions as a key signaling adaptor that links FcεRI signals to microtubule dynamics during mast cell degranulation.The Journal of experimental medicine · 2014Article
- Stem cell factor programs the mast cell activation phenotype.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- WIP remodeling actin behind the scenes: how WIP reshapes immune and other functions.International journal of molecular sciences · 2012Review
- Cytoskeleton in mast cell signaling.Frontiers in immunology · 2012Article
- Loss of TRPC1-mediated Ca2+ influx contributes to impaired degranulation in Fyn-deficient mouse bone marrow-derived mast cells.Journal of leukocyte biology · 2010Article
- Immune pathology associated with altered actin cytoskeleton regulation.Autoimmunity · 2010Review
- Article
- Pivotal role of mast cells in pruritogenesis in patients with myeloproliferative disorders.Blood · 2009Article
- Article
- IL-21R is essential for epicutaneous sensitization and allergic skin inflammation in humans and mice.The Journal of clinical investigation · 2009Article
- Recent advances in the biology of WASP and WIP.Immunologic research · 2009Review
- WIP is essential for lytic granule polarization and NK cell cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Structure-function analysis of the WIP role in T cell receptor-stimulated NFAT activation: evidence that WIP-WASP dissociation is not required and that the WIP NH2 terminus is inhibitory.The Journal of biological chemistry · 2007Article
- WIP is a chaperone for Wiskott-Aldrich syndrome protein (WASP).Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Decoding IgE Fc receptors.Immunologic research · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Wiskott-Aldrich syndrome protein-interacting protein (WIP) stabilizes actin filaments and is important for immunoreceptor-mediated signal transduction leading to actin cytoskeleton rearrangement in T and B cells. Here we report a role for WIP in signaling pathways downstream of the high affinity receptor for immunoglobulin (Ig)E (FcepsilonRI) in mast cells. WIP-deficient bone marrow-derived mast cells (BMMCs) were impaired in their capacity to degranulate and secrete interleukin 6 after FcepsilonRI ligation. Calcium mobilization, phosphorylation of Syk, phospholipase C-g2, and c-Jun NH2-terminal kinase were markedly decreased in WIP-deficient BMMCs. WIP was found to associate with Syk after FcepsilonRI ligation and to inhibit Syk degradation as evidenced by markedly diminished Syk levels in WIP-deficient BMMCs. WIP-deficient BMMCs exhibited no apparent defect in their subcortical actin network and were normal in their ability to form protrusions when exposed to an IgE-coated surface. However, the kinetics of actin changes and the cell shape changes that follow FcepsilonRI signaling were altered in WIP-deficient BMMCs. These results suggest that WIP regulates FcepsilonRI-mediated mast cell activation by regulating Syk levels and actin cytoskeleton rearrangement.
Indexed as
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What OpenQuestion holds
Registered trials
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.