ArticleImmunology2010
Ectodomain shedding of Fcalpha receptor is mediated by ADAM10 and ADAM17.
Article in Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Alantolactone Activates the Extracellular Signal-Regulated Kinase Signaling Pathway to Promote Tumor Necrosis Factor Receptor 1 Ectodomain Shedding.Molecules (Basel, Switzerland) · 2026Article
- Metal binding site alignment enables network-driven discovery of recurrent geometries across sequence-divergent proteins and drug off-targets.PLoS computational biology · 2026Article
- Blockade of mTOR ameliorates IgA nephropathy by correcting CD89 and CD71 dysfunctions in humanized mice.PloS one · 2025Article
- Hypothesis: Efficacy of early treatments with some NSAIDs in COVID-19: Might it also depend on their direct and/or indirect zinc chelating ability?British journal of pharmacology · 2023Article
- Immune Responses to IAV Infection and the Roles of L-Selectin and ADAM17 in Lymphocyte Homing.Pathogens (Basel, Switzerland) · 2022Review
- Immunomodulatory role of metalloproteinase ADAM17 in tumor development.Frontiers in immunology · 2022Review
- Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Thiosemicarbazones suppress expression of the c-Met oncogene by mechanisms involving lysosomal degradation and intracellular shedding.The Journal of biological chemistry · 2020Article
- Serum Soluble CD89-IgA Complexes Are Elevated in IgA Nephropathy without Immunosuppressant History.Disease markers · 2020Article
- FcαRI binding at the IgA1 CProceedings of the National Academy of Sciences of the United States of America · 2018Article
- SheddomeDB: the ectodomain shedding database for membrane-bound shed markers.BMC bioinformatics · 2017Review
- Recent Advances in ADAM17 Research: A Promising Target for Cancer and Inflammation.Mediators of inflammation · 2017Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FcalphaR (CD89) plays important roles in immunoglobulin A (IgA)-mediated immune responses. Soluble forms of FcalphaR (sFcalphaR) are found in the culture supernatants of FcalphaR-expressing cells, in human serum and in the serum of FcalphaR transgenic mice, and have been suggested to be produced through a proteolytic process. However, little is known about the mechanism involved in the proteolytic release of sFcalphaR. In this study, we investigated the shedding mechanism of FcalphaR and determined the nature of the proteinase involved in FcalphaR shedding. In chemical inhibitor assays, shedding of FcalphaR was dramatically inhibited by EDTA, EGTA and a broad-spectrum metalloproteinase inhibitor, GM6001, suggesting that a metalloproteinase was responsible for FcalphaR shedding. Overexpression of dominant-negative mutants of ADAM (a disintegrin and metalloproteinase) 10 and ADAM17 markedly inhibited the production of sFcalphaR. Finally, knockdown of both endogenous ADAM10 and endogenous ADAM17 inhibited FcalphaR shedding, demonstrating that ADAM10 and ADAM17 were involved in the shedding of FcalphaR. The characterization of ADAM10 and ADAM17 as sFcalphaR-releasing enzymes provides a novel insight into the molecular mechanism of sFcalphaR production and will help in further elucidation of the physiological and pathological roles of sFcalphaR.
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Registered trials
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