Formylpeptide receptors in GtoPdb v.2021.2

The formylpeptide receptors (nomenclature agreed by the NC-IUPHAR Subcommittee on the formylpeptide receptor family [196]) respond to exogenous ligands such as the bacterial product fMet-Leu-Phe (fMLP) and endogenous ligands such as lipoxin A4 (LXA4), 15-epi-lipoxin A4, annexin I , cathepsin G, amyloid β42, serum amyloid A and spinorphin, derived from β-haemoglobin. FPR1 also serves as a plague receptor for selective destruction of human immune cells by Y. pestis [135]. The FPR1/2 agonists 'compound 17b' and 'compound 43' have shown cardiac protective functions [149, 64].

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Formylpeptide receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

IUPHAR/BPS Guide to Pharmacology CITE ◽

10.2218/gtopdb/f23/2019.4 ◽

2019 ◽

Vol 2019 (4) ◽

Author(s):

Magnus Bäck ◽

François Boulay ◽

Nan Chiang ◽

Sven-Erik Dahlén ◽

Claes Dahlgren ◽

...

Keyword(s):

Serum Amyloid A ◽

Serum Amyloid ◽

Cathepsin G ◽

Bacterial Product ◽

Endogenous Ligands ◽

Amyloid A ◽

Annexin I ◽

Exogenous Ligands ◽

Receptor Family ◽

Formylpeptide Receptor

The formylpeptide receptors (nomenclature agreed by the NC-IUPHAR Subcommittee on the formylpeptide receptor family [185]) respond to exogenous ligands such as the bacterial product fMet-Leu-Phe (fMLP) and endogenous ligands such as annexin I , cathepsin G, amyloid β42, serum amyloid A and spinorphin, derived from β-haemoglobin.

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Serum amyloid A opposes lipoxin A4 to mediate glucocorticoid refractory lung inflammation in chronic obstructive pulmonary disease

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1109382109 ◽

2012 ◽

Vol 109 (3) ◽

pp. 935-940 ◽

Cited By ~ 99

Author(s):

S. Bozinovski ◽

M. Uddin ◽

R. Vlahos ◽

M. Thompson ◽

J. L. McQualter ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Pulmonary Disease ◽

Lung Inflammation ◽

Serum Amyloid A ◽

Serum Amyloid ◽

Chronic Obstructive ◽

Lipoxin A4 ◽

Obstructive Pulmonary Disease ◽

Amyloid A

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Serum amyloid A induces IL-8 secretion through a G protein–coupled receptor, FPRL1/LXA4R

Blood ◽

10.1182/blood-2002-05-1431 ◽

2003 ◽

Vol 101 (4) ◽

pp. 1572-1581 ◽

Cited By ~ 227

Author(s):

Rong He ◽

Hairong Sang ◽

Richard D. Ye

Keyword(s):

Serum Amyloid A ◽

Acute Phase Proteins ◽

Inflammatory Diseases ◽

Nuclear Factor Κb ◽

Serum Amyloid ◽

Human Neutrophils ◽

Lipoxin A4 ◽

Amyloid A ◽

Mitogen Activated Protein ◽

Factor Α

Host response to injury and infection is accompanied by a rapid rise in the blood of acute-phase proteins such as serum amyloid A (SAA). Although SAA has been used as a marker for inflammatory diseases, its role in the modulation of inflammation and immunity has not been defined. Human neutrophils respond to SAA with secretion of the proinflammatory cytokines interleukin 8 (IL-8) and, to a lesser extent, tumor necrosis factor α (TNF-α). The induction of IL-8 secretion by SAA involves both transcription and translation and correlates with activation of nuclear factor κB (NF-κB). The proximal signaling events induced by SAA include mobilization of intracellular Ca2+ and activation of the mitogen-activated protein kinases ERK1/2 and p38, both required for the induced IL-8 secretion. Pertussis toxin effectively blocks SAA-induced IL-8 secretion indicating involvement of a Gi-coupled receptor. Overexpression of FPRL1/LXA4R in HeLa cells results in a significant increase of the expression of NF-κB and IL-8 luciferase reporters by SAA, and an antibody against the N-terminal domain of FPRL1/LXA4R inhibits IL-8 secretion. Lipoxin A4, which binds to FPRL1/LXA4R specifically, decreases SAA-induced IL-8 secretion significantly. Collectively, these results indicate that the cytokine-like property of SAA is manifested through activation of the Gi-coupled FPRL1/LXA4R, which has been known to mediate the anti-inflammatory effects of lipoxin A4. The ability of FPRL1/LXA4R to mediate 2 drastically different and opposite functions suggests that it plays a role in the modulation of inflammatory and immune responses.

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