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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Zhang, J; Guo, J; Dzhagalov, I; He, Y-W

Published Date

  • September 2005

Published In

Volume / Issue

  • 6 / 9

Start / End Page

  • 911 - 919

PubMed ID

  • 16041389

Pubmed Central ID

  • 16041389

International Standard Serial Number (ISSN)

  • 1529-2908

Digital Object Identifier (DOI)

  • 10.1038/ni1232

Language

  • eng

Conference Location

  • United States