ArticleThe Journal of experimental medicine1998
The inositol polyphosphate 5-phosphatase ship is a crucial negative regulator of B cell antigen receptor signaling.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
70 citing papers in PubMed, 205 citations in OpenAlex.
- SHIP-1 regulates the differentiation and function of Tregs via inhibiting mTORC1 activity.Cellular and molecular life sciences : CMLS · 2024Article
- Fc-FcγR interactions during infections: From neutralizing antibodies to antibody-dependent enhancement.Immunological reviews · 2024Review
- Enzyme Is the Name-Adapter Is the Game.Cells · 2024Review
- LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155.BMC pulmonary medicine · 2021Article
- Selective deletion of SHIP-1 in hematopoietic cells in mice leads to severe lung inflammation involving ILC2 cells.Scientific reports · 2021Article
- Ectopic Expression of Hematopoietic SHIP1 in Human Colorectal Cancer.Biomedicines · 2020Article
- CD5 signalosome coordinates antagonist TCR signals to control the generation of Treg cells induced by foreign antigens.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Preclinical Evaluation of a Novel SHIP1 Phosphatase Activator for Inhibition of PI3K Signaling in Malignant B Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- SHIP-1, a target of miR-155, regulates endothelial cell responses in lung fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The regulators of BCR signaling during B cell activation.Blood science (Baltimore, Md.) · 2019Review
- Active PI3K abrogates central tolerance in high-avidity autoreactive B cells.The Journal of experimental medicine · 2019Article
- Recombinant factor VIII Fc fusion protein drives regulatory macrophage polarization.Blood advances · 2018Article
- Activated PIK3CD drives innate B cell expansion yet limits B cell-intrinsic immune responses.The Journal of experimental medicine · 2018Article
- Granulocyte-CSF links destructive inflammation and comorbidities in obstructive lung disease.The Journal of clinical investigation · 2018Article
- AQX-1125, small molecule SHIP1 activator inhibits bleomycin-induced pulmonary fibrosis.British journal of pharmacology · 2017Article
- Continuous inhibitory signaling by both SHP-1 and SHIP-1 pathways is required to maintain unresponsiveness of anergic B cells.The Journal of experimental medicine · 2016Article
- The Role of the Transcription Factor Ets1 in Lupus and Other Autoimmune Diseases.Critical reviews in immunology · 2016Article
- Physiological roles of miR-155.Immunology · 2015Review
- SHIP1 intrinsically regulates NK cell signaling and education, resulting in tolerance of an MHC class I-mismatched bone marrow graft in mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- SHIP-1 deficiency in the myeloid compartment is insufficient to induce myeloid expansion or chronic inflammation.Genes and immunity · 2014Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ship is an Src homology 2 domain containing inositol polyphosphate 5-phosphatase which has been implicated as an important signaling molecule in hematopoietic cells. In B cells, Ship becomes associated with Fcgamma receptor IIB (FcgammaRIIB), a low affinity receptor for the Fc portion of immunoglobulin (Ig)G, and is rapidly tyrosine phosphorylated upon B cell antigen receptor (BCR)-FcgammaRIIB coligation. The function of Ship in lymphocytes was investigated in Ship-/- recombination-activating gene (Rag)-/- chimeric mice generated from gene-targeted Ship-/- embryonic stem cells. Ship-/-Rag-/- chimeras showed reduced numbers of B cells and an overall increase in basal serum Ig. Ship-/- splenic B cells displayed prolonged Ca2+ influx, increased proliferation in vitro, and enhanced mitogen-activated protein kinase (MAPK) activation in response to BCR-FcgammaRIIB coligation. These results demonstrate that Ship plays an essential role in FcgammaRIIB-mediated inhibition of BCR signaling, and that Ship is a crucial negative regulator of Ca2+ flux and MAPK activation.
Indexed as
Identifiers
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.