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Fig. 6. Pathway of T. gondii-induced PKB and ERK1/2 activation in MØs. T. gondii infection activated PI 3-kinase through Gi-protein-coupled receptor signaling. In turn, PI 3-kinase stimulates PKB activation and MEK1/2 phosphorylation leading to ERK1/2 activation. Pertussis toxin, which uncouples Gi-protein signaling, and wortmannin and LY294002, which inhibit PI 3-kinase activation, block PKB/Akt and ERK1/2 activation. PTx, pertussis toxin; WM, wortmannin; Ly, LY294002.
