ArticleCellular signalling2008
Formyl peptide receptor-mediated ERK1/2 activation occurs through G(i) and is not dependent on beta-arrestin1/2.
Article in Cellular signalling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Investigation into ligand selectivity and bias at the formyl peptide receptor family.The Journal of pharmacology and experimental therapeutics · 2026Article
- Mucosal acidosis elicits a unique molecular signature in epithelia and intestinal tissue mediated by GPR31-induced CREB phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Deficiency of FAM3D (Family With Sequence Similarity 3, Member D), A Novel Chemokine, Attenuates Neutrophil Recruitment and Ameliorates Abdominal Aortic Aneurysm Development.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Orthosteric and allosteric action of the C5a receptor antagonists.Nature structural & molecular biology · 2018Article
- The natural sesquiterpene lactones arglabin, grosheimin, agracin, parthenolide, and estafiatin inhibit T cell receptor (TCR) activation.Phytochemistry · 2018Article
- β-Arrestin 1-dependent regulation of Rap2 is required for fMLP-stimulated chemotaxis in neutrophil-like HL-60 cells.Journal of leukocyte biology · 2017Article
- Anethole and eugenol reduce in vitro and in vivo leukocyte migration induced by fMLP, LTB4, and carrageenan.Journal of natural medicines · 2014Article
- Article
- Activated human hydroxy-carboxylic acid receptor-3 signals to MAP kinase cascades via the PLC-dependent PKC and MMP-mediated EGFR pathways.British journal of pharmacology · 2012Article
- Anti-inflammatory role of the murine formyl-peptide receptor 2: ligand-specific effects on leukocyte responses and experimental inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- International Union of Basic and Clinical Pharmacology. LXXIII. Nomenclature for the formyl peptide receptor (FPR) family.Pharmacological reviews · 2009Review
- Anti-inflammatory cannabinoids in diet: Towards a better understanding of CB(2) receptor action?Communicative & integrative biology · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Formyl peptide receptor (FPR) and C5a receptor (C5aR) are chemoattractant G protein-coupled receptors (GPCRs) involved in the innate immune response against bacterial infections and tissue injury. Like other GPCRs, they recruit beta-arrestin1/2 to the plasma membrane and activate the extracellular signal-regulated kinases 1 and 2 (ERK1/2). Previous studies with several GPCRs have suggested that beta-arrestins play an important role as signal transducers by scaffolding signaling molecules such as ERK1/2. This function of the beta-arrestins was not discovered until several years after their role in desensitization and endocytosis had been reported. In this study, we investigated the role of the beta-arrestins in the activation of ERK1/2 and receptor endocytosis. We took advantage of previously described mutants of FPR that have defects in G(i) coupling or beta-arrestin recruitment. The results obtained with the mutant FPRs, as well as experiments using an inhibitor of G(i) and cells overexpressing beta-arrestin2, showed that activation of ERK1/2 takes place through G(i) and is not affected by beta-arrestins. However, overexpression of beta-arrestin2 does enhance FPR sequestration from the cell surface, suggesting a role in desensitization, as shown for many other GPCRs. Experiments with CHO C5aR cells showed similar sensitivity to the G(i) inhibitor as CHO FPR cells, suggesting that the predominant activation of ERK1/2 through G protein may be a common characteristic among chemoattractant receptors.
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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.