An essential function for the calcium-promoted Ras inactivator in Fcγ receptor-mediated phagocytosis

Jun Zhang, Jian Guo, Ivan Dzhagalov, You Wen He*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

40 Scopus citations

Abstract

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 FcγR-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 FcγR-mediated phagocytosis. CAPRI-deficient mice had an impaired innate immune response to bacterial infection. These results suggest that CAPRI provides a link between FcγR and Cdc42 and Rac1 and is essential for innate immune responses.

Original languageEnglish
Pages (from-to)911-919
Number of pages9
JournalNature Immunology
Volume6
Issue number9
DOIs
StatePublished - Sep 2005

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