Figure 5.

Signalling pathways of neutrophil Rac‐GEFs. The Rac‐GEF P‐Rex1, which mediates signalling through GPCRs, E‐selectin and TLR4 (not all shown here for simplicity), is activated by the lipid second messenger PIP ₃ and by the Gβγ subunits of heterotrimeric G proteins. The Vav family Rac‐GEFs, which are activated by tyrosine phosphorylation, are important in integrin and FcR signalling, but they also couple to TLR4 and GPCRs. It is currently unknown, which mechanisms control Tiam2 in neutrophils, except that this GEF controls chemoattractant‐induced responses. DOCK2 also signals upon GPCR stimulation. It is activated by RhoG and recruited to the plasma membrane by PIP ₃ and phosphatidic acid (PA). The preferred Rac substrate of each Rac‐GEF is shown here, but usually, the GEFs can activate both Rac1 and Rac2 to some extent. P‐Rex1 can also activate RhoG and may thus signal in sequence with DOCK2 in some pathways. The list of cell responses regulated by each neutrophil Rac‐GEF is likely to grow with further study