ArticleJournal of immunology (Baltimore, Md. : 1950)2012
The adaptor 3BP2 is required for early and late events in FcεRI signaling in human mast cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 20 citations in OpenAlex.
- KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST.Cell communication and signaling : CCS · 2024Review
- MRGPRX2 signaling involves the Lysyl-tRNA synthetase and MITF pathway.Frontiers in immunology · 2023Article
- KIT as a master regulator of the mast cell lineage.The Journal of allergy and clinical immunology · 2022Review
- MYO1F Regulates IgE and MRGPRX2-Dependent Mast Cell Exocytosis.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Long-Tailed Unconventional Class I Myosins in Health and Disease.International journal of molecular sciences · 2020Review
- Alveolar Bone Protection by Targeting the SH3BP2-SYK Axis in Osteoclasts.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- Myo1f, an Unconventional Long-Tailed Myosin, Is a New Partner for the Adaptor 3BP2 Involved in Mast Cell Migration.Frontiers in immunology · 2019Article
- MRGPRX2-mediated mast cell response to drugs used in perioperative procedures and anaesthesia.Scientific reports · 2018Article
- Silencing of adaptor protein SH3BP2 reduces KIT/PDGFRA receptors expression and impairs gastrointestinal stromal tumors growth.Molecular oncology · 2018Article
- Timed Regulation of 3BP2 Induction Is Critical for Sustaining CD8Cell reports · 2018Article
- Syk-dependent tyrosine phosphorylation of 3BP2 is required for optimal FcRγ-mediated phagocytosis and chemokine expression in U937 cells.Scientific reports · 2017Article
- The adaptor 3BP2 is required for KIT receptor expression and human mast cell survival.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Loss of SH3 domain-binding protein 2 function suppresses bone destruction in tumor necrosis factor-driven and collagen-induced arthritis in mice.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Article
- SH3BP2 cherubism mutation potentiates TNF-α-induced osteoclastogenesis via NFATc1 and TNF-α-mediated inflammatory bone loss.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014Article
- Prostaglandin E2 prevents hyperosmolar-induced human mast cell activation through prostanoid receptors EP2 and EP4.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Adaptor molecules are essential in organizing signaling molecules and in coordinating and compartmentalizing their activity. SH3-binding protein 2 (3BP2) is a cytoplasmic adaptor protein mainly expressed by hematopoietic cells that has been shown to act as a positive regulator in T, B, and NK cell signal transduction. 3BP2 is an important regulator of cytotoxic granule release in NK cells. Mast cells (MCs) similarly degranulate following Ag-dependent aggregation of the FcεRI on the cell surface. Activation of these cells induces the release of preformed inflammatory mediators and the de novo synthesis and secretion of cytokines and chemokines. Thus, MCs participate in both innate and acquired responses. We observed that 3BP2 is expressed in human MCs (huMCs) from diverse origins. Moreover, 3BP2 coimmunoprecipitates with essential MC signaling mediators such as Lyn, Syk, and phospholipase C γ; thus, a role for this adaptor in MC function was postulated. In the present work, we used the short hairpin RNA lentiviral targeting approach to silence 3BP2 expression in huMCs. Our findings point to a requirement for 3BP2 in optimal immediate and late MCs responses such as degranulation and IL-8 or GM-CSF secretion. 3BP2 was determined to be necessary for optimal phosphorylation of Syk, linker for activation of T cells, and phospholipase C γ(1), critical signals for calcium release from intracellular stores. Taken together, our results show that by participating in FcεRI- mediated signal transduction 3BP2 is an important regulator of huMC activation. Thus, 3BP2 could be a potential therapeutic target for IgE-dependent MC-mediated inflammatory disease.
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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.