ArticleThe Journal of experimental medicine2000
A dual role for Src homology 2 domain-containing inositol-5-phosphatase (SHIP) in immunity: aberrant development and enhanced function of b lymphocytes in ship -/- mice.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 151 citations in OpenAlex.
- Lyn governs the establishment and maintenance of B cell anergy by suppressing PI3K signaling.Nature communications · 2026Article
- SH2 domain-containing inositol 5-phosphatases support the survival of Burkitt lymphoma cells by promoting energy metabolism.Haematologica · 2024Article
- Obesity control by SHIP inhibition requires pan-paralog inhibition and an intact eosinophil compartment.iScience · 2023Article
- Role of inhibitory signaling in peripheral B cell tolerance.Immunological reviews · 2022Review
- The Lupus-Associated Fcγ Receptor IIb-I232T Polymorphism Results in Impairment in the Negative Selection of Low-Affinity Germinal Center B Cells Via c-Abl in Mice.Arthritis & rheumatology (Hoboken, N.J.) · 2018Article
- Role of SHIP1 in Invariant NKT Cell Development and Functions.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Signaling mechanisms regulating B-lymphocyte activation and tolerance.Journal of molecular medicine (Berlin, Germany) · 2015Review
- SHIP-1 deficiency in the myeloid compartment is insufficient to induce myeloid expansion or chronic inflammation.Genes and immunity · 2014Article
- Pathogenic microRNA's in myeloid malignancies.Frontiers in genetics · 2014Review
- Deletion of microRNA-155 reduces autoantibody responses and alleviates lupus-like disease in the Fas(lpr) mouse.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Phosphatase regulation of immunoreceptor signaling in T cells, B cells and mast cells.Current opinion in immunology · 2013Review
- Aberrant antibody affinity selection in SHIP-deficient B cells.European journal of immunology · 2013Article
- Article
- Carabin deficiency in B cells increases BCR-TLR9 costimulation-induced autoimmunity.EMBO molecular medicine · 2012Article
- Lineage extrinsic and intrinsic control of immunoregulatory cell numbers by SHIP.European journal of immunology · 2012Article
- The phosphoinositide 3-kinase signaling pathway in normal and malignant B cells: activation mechanisms, regulation and impact on cellular functions.Frontiers in immunology · 2012Article
- Pharmacological targeting of phosphoinositide lipid kinases and phosphatases in the immune system: success, disappointment, and new opportunities.Frontiers in immunology · 2012Article
- CIN85 interacting proteins in B cells-specific role for SHIP-1.Molecular & cellular proteomics : MCP · 2011Article
- Review
- Inhibitor and activator: dual functions for SHIP in immunity and cancer.Annals of the New York Academy of Sciences · 2011Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this report, we demonstrate that the Src homology 2 domain-containing inositol-5-phosphatase (SHIP) plays a critical role in regulating both B cell development and responsiveness to antigen stimulation. SHIP(-/-) mice exhibit a transplantable alteration in B lymphoid development that results in reduced numbers of precursor B (fraction C) and immature B cells in the bone marrow. In vitro, purified SHIP(-/)- B cells exhibit enhanced proliferation in response to B cell receptor stimulation in both the presence and absence of Fcgamma receptor IIB coligation. This enhancement is associated with increased phosphorylation of both mitogen-activated protein kinase and Akt, as well as with increased survival and cell cycling. SHIP(-/)- mice manifest elevated serum immunoglobulin (Ig) levels and an exaggerated IgG response to the T cell-independent type 2 antigen trinitrophenyl Ficoll. However, only altered B cell development was apparent upon transplantation into nonobese diabetic-severe combined immunodeficient (NOD/SCID) mice. The in vitro hyperresponsiveness, together with the in vivo findings, suggests that SHIP regulates B lymphoid development and antigen responsiveness by both intrinsic and extrinsic mechanisms.
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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.