| pubmed-article:16041389 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16041389 | lifeskim:mentions | umls-concept:C0031308 | lld:lifeskim |
| pubmed-article:16041389 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:16041389 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:16041389 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:16041389 | pubmed:dateCreated | 2005-8-23 | lld:pubmed |
| pubmed-article:16041389 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16041389 | pubmed: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. | lld:pubmed |
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| pubmed-article:16041389 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16041389 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16041389 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16041389 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16041389 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:16041389 | pubmed:issn | 1529-2908 | lld:pubmed |
| pubmed-article:16041389 | pubmed:author | pubmed-author:ZhangJunJ | lld:pubmed |
| pubmed-article:16041389 | pubmed:author | pubmed-author:GuoJianJ | lld:pubmed |
| pubmed-article:16041389 | pubmed:author | pubmed-author:HeYou-WenYW | lld:pubmed |
| pubmed-article:16041389 | pubmed:author | pubmed-author:DzhagalovIvan... | lld:pubmed |
| pubmed-article:16041389 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16041389 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:16041389 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16041389 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16041389 | pubmed:pagination | 911-9 | lld:pubmed |
| pubmed-article:16041389 | pubmed:dateRevised | 2011-1-7 | lld:pubmed |
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| pubmed-article:16041389 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16041389 | pubmed:articleTitle | An essential function for the calcium-promoted Ras inactivator in Fcgamma receptor-mediated phagocytosis. | lld:pubmed |
| pubmed-article:16041389 | pubmed:affiliation | Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA. | lld:pubmed |
| pubmed-article:16041389 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16041389 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:16041389 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16041389 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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