ArticleBlood2006
FcgammaR-induced production of superoxide and inflammatory cytokines is differentially regulated by SHIP through its influence on PI3K and/or Ras/Erk pathways.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 38 citations in OpenAlex.
- SHIP-1 adapter functions mediate recruitment of FCRL1 to the BCR and inhibition of ERK.ImmunoHorizons · 2026Article
- Proteomics-driven screening of artemisinin-based combination ratios and mechanistic insights intoFrontiers in immunology · 2025Article
- Bortezomib Sustains T Cell Function by Inducing miR-155-Mediated Downregulation of SOCS1 and SHIP1.Frontiers in immunology · 2021Article
- Granulocyte-CSF links destructive inflammation and comorbidities in obstructive lung disease.The Journal of clinical investigation · 2018Article
- Fc gamma receptors are expressed in the developing rat brain and activate downstream signaling molecules upon cross-linking with immune complex.Journal of neuroinflammation · 2018Article
- The Transcription Factor T-Bet Is Regulated by MicroRNA-155 in Murine Anti-Viral CD8Frontiers in immunology · 2017Article
- Analysis of the Effects of the Bruton's tyrosine kinase (Btk) Inhibitor Ibrutinib on Monocyte Fcγ Receptor (FcγR) Function.The Journal of biological chemistry · 2016Article
- Article
- Dendritic cell c-kit signaling and adaptive immunity: implications for the upper airways.Current opinion in allergy and clinical immunology · 2014Review
- Phosphoinositide lipid phosphatase SHIP1 and PTEN coordinate to regulate cell migration and adhesion.Molecular biology of the cell · 2012Article
- Glycodelin-A protein interacts with Siglec-6 protein to suppress trophoblast invasiveness by down-regulating extracellular signal-regulated kinase (ERK)/c-Jun signaling pathway.The Journal of biological chemistry · 2011Article
- LyGDI, a novel SHIP-interacting protein, is a negative regulator of FcγR-mediated phagocytosis.PloS one · 2011Article
- Inhibitor and activator: dual functions for SHIP in immunity and cancer.Annals of the New York Academy of Sciences · 2011Review
- Article
- Signaling of c-kit in dendritic cells influences adaptive immunity.Annals of the New York Academy of Sciences · 2010Review
- Differential requirement of lipid rafts for FcγRIIA mediated effector activities.Cellular immunology · 2010Article
- Adaptor protein SLAT modulates Fcgamma receptor-mediated phagocytosis in murine macrophages.The Journal of biological chemistry · 2009Article
- PI3K limits TNF-alpha production in CD16-activated monocytes.European journal of immunology · 2009Article
- SHIP-1 increases early oxidative burst and regulates phagosome maturation in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Fcgamma receptor signaling in phagocytes.International journal of hematology · 2006Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Phagocytosis of IgG-coated particles via FcgammaR is accompanied by the generation of superoxide and inflammatory cytokines, which can cause collateral tissue damage in the absence of regulation. Molecular mechanisms regulating these phagocytosis-associated events are not known. SHIP is an inositol phosphatase that downregulates PI3K-mediated activation events. Here, we have examined the role of SHIP in FcgammaR-induced production of superoxide and inflammatory cytokines. We report that primary SHIP-deficient bone marrow macrophages produce elevated levels of superoxide upon FcgammaR clustering. Analysis of the molecular mechanism revealed that SHIP regulates upstream Rac-GTP binding, an obligatory event for superoxide production. Likewise, SHIP-deficient macrophages displayed enhanced IL-1beta and IL-6 production in response to FcgammaR clustering. Interestingly, whereas IL-6 production required activation of both PI3K and Ras/Erk pathways, IL-1beta production was dependent only on Ras/Erk activation, suggesting that SHIP may also regulate the Ras/Erk pathway in macrophages. Consistently, SHIP-deficient macrophages displayed enhanced activation of Erk upon FcgammaR clustering. Inhibition of Ras/Erk or PI3K suppressed the enhanced production of IL-6 in SHIP-deficient macrophages. In contrast, inhibition of Ras/Erk, but not PI3K, suppressed IL-1beta production in these cells. Together, these data demonstrate that SHIP regulates phagocytosis-associated events through the inhibition of PI3K and Ras/Erk pathways.
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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 Socratic graph.