Figure 2.

Intracellular signaling events after FPR1 receptor activation. After binding of ligand to formyl peptide receptor 1 (FPR1), conversion of guanosine diphosphate to guanosine triphosphate induces dissociation of the α from the βγ subunits. These trigger a range of intracellular kinase pathways, resulting in the induction of a variety of cell functions, including neutrophil chemotaxis, degranulation, superoxide anion production, and transcriptional activity. The predominant signaling pathways are those of phosphoinositide-3 kinase (PI3K), mitogen-activated protein kinase (MAPK), and phospholipase C. The latter triggers release of intracellular calcium from the endoplasmic reticulum to activate protein kinase C (PKC) and subsequent reactive oxygen species production, whereas PI3K triggers protein kinase B (alias Akt)-mediated and phosphoinositol-3,4,5-trisphosphate (PIP₃)-mediated signaling, with a variety of cellular effects. With PI3K pulled toward the plasma membrane by the β and γ G-protein subunits (Gβ and Gγ), activation of Ras family proteins and MAPK further contributes to oxidative burst and chemotaxis. CDC, cell division control protein; DAG, diacyl glycerol; Gα, G-protein α; GEF, guanine nucleotide exchange factor; Grb, growth factor receptor–bound protein; IP₃, inositol trisphosphate; MEKK, mitogen-activated protein kinase kinase; PA, phosphatidic acid; PLCβ, phospholipase Cβ; PLD, phospholipase D; RAF, rapidly accelerated fibrosarcoma; Sos, son of sevenless; WASP, Wiskott-Aldrich syndrome protein.