An essential function for the calcium-promoted Ras inactivator in Fcgamma receptor-mediated phagocytosis.
Fc receptor (FcR)- mediated phagocytosis requires activation of the Rho GTPases Cdc42 and Rac1, but how they are recruited to the FcR is unknown. Here we show that the calcium-promoted Ras inactivator (CAPRI), a Ras GTPase-activating protein, functions as an adaptor for Cdc42 and Rac1 during FcR-mediated phagocytosis. CAPRI-deficient macrophages had impaired FcgammaR-mediated phagocytosis and oxidative burst, as well as defective activation of Cdc42 and Rac1. CAPRI interacted constitutively with both Cdc42 and Rac1 and translocated to phagocytic cups during FcgammaR-mediated phagocytosis. CAPRI-deficient mice had an impaired innate immune response to bacterial infection. These results suggest that CAPRI provides a link between FcgammaR and Cdc42 and Rac1 and is essential for innate immune responses.[1]References
- An essential function for the calcium-promoted Ras inactivator in Fcgamma receptor-mediated phagocytosis. Zhang, J., Guo, J., Dzhagalov, I., He, Y.W. Nat. Immunol. (2005) [Pubmed]
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