ArticlePloS one2012
Shp2 activates Fyn and Ras to regulate RBL-2H3 mast cell activation following FcεRI aggregation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting Shp2 as a therapeutic strategy for neurodegenerative diseases.Translational psychiatry · 2025Review
- Inhibiting Isoprenylation Suppresses FcεRI-Mediated Mast Cell Function and Allergic Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Review
- Deficiency of the Src homology phosphatase 2 in podocytes is associated with renoprotective effects in mice under hyperglycemia.Cellular and molecular life sciences : CMLS · 2022Article
- ShcA Adaptor Protein Promotes Nephrin Endocytosis and Is Upregulated in Proteinuric Nephropathies.Journal of the American Society of Nephrology : JASN · 2018Article
- Nephrin Signaling in the Podocyte: An Updated View of Signal Regulation at the Slit Diaphragm and Beyond.Frontiers in endocrinology · 2018Review
- THEMIS enhances TCR signaling and enables positive selection by selective inhibition of the phosphatase SHP-1.Nature immunology · 2017Article
- Cell-based phenotypic screening of mast cell degranulation unveils kinetic perturbations of agents targeting phosphorylation.Scientific reports · 2016Article
- T cell activation is reduced by the catalytically inactive form of protein tyrosine phosphatase SHP-2.International journal of clinical and experimental medicine · 2015Article
- Transmembrane adaptor protein PAG/CBP is involved in both positive and negative regulation of mast cell signaling.Molecular and cellular biology · 2014Article
- Phosphatase regulation of immunoreceptor signaling in T cells, B cells and mast cells.Current opinion in immunology · 2013Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protein-tyrosine phosphatase (PTP) Shp2 has been implicated in many immunoreceptor signaling pathways, but its role in immunoreceptor FcεRI signaling, which leads to the activation of mast cells and blood basophils, is still largely undefined. Using Shp2 knockdown RBL-2H3 (RBL) mast cells, we here reported that Shp2 is required for the activation of RBL cells induced by FcεRI. FcεRΙ-evoked degranulation, calcium mobilization, and synthesis of cytokine transcripts (IL-1β, IL-10, and monocyte chemoattractant protein 1 (MCP-1)) were reduced in Shp2 knockdown RBL cells. Signaling regulatory mechanism investigation using immunoblotting, immunoprecipitation, and GST pull-down assay reveals that the down-regulation of Shp2 expression in RBL cells leads to decreased activities of Fyn, PLCγ, JNK, p38MAPK, and Ras/Erk1/2 after FcεRΙ aggregation. Further studies suggest that Paxillin phosphoryaltion was also impaired, but PAG phosphorylation was normal after FcεRΙ stimulation as a consequence of the inhibition of Shp2 expression in RBL cells. Collectively, our data strongly indicate that Shp2 is essential for the activation of RBL cells in response to FcεRΙ aggregation. Shp2 regulates this process through Fyn and Ras with no involvement of PAG. In addition, we identify Paxillin as an indirect substrate of Shp2 in FcεRΙ-initiated signaling of RBL cells.
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