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. Author manuscript; available in PMC: 2013 Nov 1.
Published in final edited form as: Int Immunopharmacol. 2012 Aug 2;14(3):283–288. doi: 10.1016/j.intimp.2012.07.015

Figure 1. FPR1-mediated phagocyte activation.

Figure 1

On agonist binding, trimeric Gi-proteins coupled to FPR1 are uncoupled and a series of signaling events result in rapid phagocyte activation, including Ca2+ mobilization, F-actin-dependent chemotaxis, NADPH-mediated superoxide production and NF-κB translocation leading to cytokine gene transcription. PLC: phospholipase C, PI3K: phosphatidylinositol 3-kinase, PIP2: phosphatidylinositol 4,5–biphosphate, PIP3: phosphatidylinositol 3,4,5-triphosphate, IP3: inositol triphosphate, DAG: diacylglycerol, PTX: pertussis toxin, Erk: extracellular signal-regulated kinase, NF-κB: nuclear factor-κB.