| First Author | Zhang J | Year | 2005 |
| Journal | Nat Immunol | Volume | 6 |
| Issue | 9 | Pages | 911-9 |
| PubMed ID | 16041389 | Mgi Jnum | J:100455 |
| Mgi Id | MGI:3588589 | Doi | 10.1038/ni1232 |
| Citation | Zhang J, et al. (2005) An essential function for the calcium-promoted Ras inactivator in Fcgamma receptor-mediated phagocytosis. Nat Immunol 6(9):911-9 |
| abstractText | 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. |
