ArticleMolecular and cellular biology1997
Recruitment and phosphorylation of SH2-containing inositol phosphatase and Shc to the B-cell Fc gamma immunoreceptor tyrosine-based inhibition motif peptide motif.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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Who cites it
25 citing papers in PubMed, 121 citations in OpenAlex.
- The Inositol-5-Phosphatase SHIP1: Expression, Regulation and Role in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Review
- Increased levels of a pro-inflammatory IgG receptor in the midbrain of people with schizophrenia.Journal of neuroinflammation · 2022Article
- Beyond the Cell Surface: Targeting Intracellular Negative Regulators to Enhance T cell Anti-Tumor Activity.International journal of molecular sciences · 2019Review
- A physical interaction between the adaptor proteins DOK3 and DAP12 is required to inhibit lipopolysaccharide signaling in macrophages.Science signaling · 2013Article
- The phosphoinositide 3-kinase signaling pathway in normal and malignant B cells: activation mechanisms, regulation and impact on cellular functions.Frontiers in immunology · 2012Article
- Inhibitor and activator: dual functions for SHIP in immunity and cancer.Annals of the New York Academy of Sciences · 2011Review
- TREM2- and DAP12-dependent activation of PI3K requires DAP10 and is inhibited by SHIP1.Science signaling · 2010Article
- Differential roles for the inositol phosphatase SHIP in the regulation of macrophages and lymphocytes.Immunologic research · 2009Review
- Regulation of hematopoietic cell function by inhibitory immunoglobulin G receptors and their inositol lipid phosphatase effectors.Immunological reviews · 2008Review
- SHIP-1 increases early oxidative burst and regulates phagosome maturation in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Differential association of phosphatidylinositol 3-kinase, SHIP-1, and PTEN with forming phagosomes.Molecular biology of the cell · 2007Article
- Fcgamma receptor signaling in phagocytes.International journal of hematology · 2006Review
- Article
- Macrophage pro-inflammatory response to Francisella novicida infection is regulated by SHIP.PLoS pathogens · 2006Article
- Vav activation and function as a rac guanine nucleotide exchange factor in macrophage colony-stimulating factor-induced macrophage chemotaxis.Molecular and cellular biology · 2005Article
- Fc receptors and their role in immune regulation and autoimmunity.Journal of clinical immunology · 2005Review
- Src homology 2-containing 5-inositol phosphatase (SHIP) suppresses an early stage of lymphoid cell development through elevated interleukin-6 production by myeloid cells in bone marrow.The Journal of experimental medicine · 2004Article
- Roles of Fc receptors in autoimmunity.Nature reviews. Immunology · 2002Review
- Visualization of negative signaling in B cells by quantitative confocal microscopy.Molecular and cellular biology · 2001Article
- Vav-2 controls NFAT-dependent transcription in B- but not T-lymphocytes.The EMBO journal · 2000Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Recently, we and others have demonstrated that negative signaling in B cells selectively induces the tyrosine phosphorylation of a novel inositol polyphosphate phosphatase, p145SHIP. In this study, we present data indicating that p145SHIP binds directly a phosphorylated motif, immunoreceptor tyrosine-based inhibition motif (ITIM), present in the cytoplasmic domain of Fc gammaRIIB1. Using recombinant SH2 domains, we show that binding is mediated via the Src homology region 2 (SH2)-containing inositol phosphatase (SHIP) SH2 domain. SHIP also bound to a phosphopeptide derived from CD22, raising the possibility that SHIP contributes to negative signaling by this receptor as well as Fc gammaRIIB1. The association of SHIP with the ITIM phosphopeptide was activation independent, while coassociation with Shc was activation dependent. Furthermore, experiments with Fc gammaRIIB1-deficient B cells demonstrated a genetic requirement for expression of Fc gammaRIIB1 in the induction of SHIP phosphorylation and its interaction with Shc. Based on these results, we propose a model of negative signaling in which co-cross-linking of surface immunoglobulin and Fc gammaRIIB1 results in sequential tyrosine phosphorylation of the ITIM, recruitment and phosphorylation of p145SHIP, and subsequent binding of Shc.
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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.