P-Rex1 controls phagocytosis and the killing of bacteria by murine neutrophils independently of its catalytic activity

Abstract

Using catalytic-dead and knockout mouse models, this study shows that P-Rex1 supports neutrophil migration, ROS production, and NET formation through its Rac-GEF activity, but drives bacterial killing and phagocytosis through a separate catalytic-independent mechanism. The work identifies P-Rex1 as a regulator of bactericidal activity and Fc receptor-dependent phagocytosis in neutrophils.