Proposed model for PMNL signaling through the MAP kinase pathway during FcR-mediated phagocytosis.

Receptor ligation directly or indirectly initiates tyrosine phosphorylation, followed by activation of phospholipase D. Phosphatidic phosphohydrolase generates diglyceride, a cofactor for PKC. PKCδ and Raf-1 are known to translocate to the plasma membrane during phagocytosis, and the MEK–MAP kinase pathway is activated. In this study we show that activation of ERK2 leads to activation of MLCK, which then phosphorylates myosin, and myosin ATPase activation is required for phagocytosis.