| pubmed-article:16990604 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16990604 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:16990604 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
| pubmed-article:16990604 | lifeskim:mentions | umls-concept:C0598934 | lld:lifeskim |
| pubmed-article:16990604 | lifeskim:mentions | umls-concept:C0060105 | lld:lifeskim |
| pubmed-article:16990604 | lifeskim:mentions | umls-concept:C0108796 | lld:lifeskim |
| pubmed-article:16990604 | lifeskim:mentions | umls-concept:C1521889 | lld:lifeskim |
| pubmed-article:16990604 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:16990604 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16990604 | pubmed:dateCreated | 2006-12-27 | lld:pubmed |
| pubmed-article:16990604 | pubmed:abstractText | The IgA Fc receptor (FcalphaRI) has dual proinflammatory and anti-inflammatory functions that are transmitted through the immunoreceptor tyrosine-based activation motifs (ITAMs) of the associated FcRgamma subunit. Whereas the involvement of FcalphaRI in inflammation is well documented, little is known of its anti-inflammatory mechanisms. Here we show that monomeric targeting of FcalphaRI by anti-FcalphaRI Fab or serum IgA triggers apoptosis in human monocytes, monocytic cell lines, and FcalphaRI+ transfectants. However, the physiologic ligand IgA induced apoptosis only when cells were cultured in low serum conditions, indicating differences with induction of anti-inflammatory signaling. Apoptosis signaling required the FcRgamma ITAM, as cells transfected with FcalphaRI or with a chimeric FcalphaRI-FcRgamma responded to death-activating signals, whereas cells expressing a mutated FcalphaRI(R209L) unable to associate with FcRgamma, or an ITAM-mutated chimeric FcalphaRI-FcRgamma, did not respond. FcalphaRI-mediated apoptosis signals were blocked by treatment with the pan-caspase inhibitor zVAD-fmk, involved proteolysis of procaspase-3, and correlated negatively with SHP-1 concentration. Anti-FcalphaRI Fab treatment of nude mice injected subcutaneously with FcalphaRI+ mast-cell transfectants prevented tumor development and halted the growth of established tumors. These findings demonstrate that, on monomeric targeting, FcalphaRI functions as an FcRgamma ITAM-dependent apoptotic module that may be fundamental for controlling inflammation and tumor growth. | lld:pubmed |
| pubmed-article:16990604 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16990604 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16990604 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16990604 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16990604 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:16990604 | pubmed:author | pubmed-author:BlankUlrichU | lld:pubmed |
| pubmed-article:16990604 | pubmed:author | pubmed-author:MonteiroRenat... | lld:pubmed |
| pubmed-article:16990604 | pubmed:author | pubmed-author:KanamaruYutak... | lld:pubmed |
| pubmed-article:16990604 | pubmed:author | pubmed-author:PretolaniMari... | lld:pubmed |
| pubmed-article:16990604 | pubmed:author | pubmed-author:Guérin-Marcha... | lld:pubmed |
| pubmed-article:16990604 | pubmed:author | pubmed-author:PfirschSéveri... | lld:pubmed |
| pubmed-article:16990604 | pubmed:author | pubmed-author:TamouzaHoudaH | lld:pubmed |
| pubmed-article:16990604 | pubmed:author | pubmed-author:El-MehdiDelph... | lld:pubmed |
| pubmed-article:16990604 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16990604 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16990604 | pubmed:volume | 109 | lld:pubmed |
| pubmed-article:16990604 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16990604 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16990604 | pubmed:pagination | 203-11 | lld:pubmed |
| pubmed-article:16990604 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:meshHeading | pubmed-meshheading:16990604... | lld:pubmed |
| pubmed-article:16990604 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:16990604 | pubmed:articleTitle | IgA Fc receptor I signals apoptosis through the FcRgamma ITAM and affects tumor growth. | lld:pubmed |
| pubmed-article:16990604 | pubmed:affiliation | Institut National de la Santé et de la Recherche Médicale (INSERM) U699, Paris, France. | lld:pubmed |
| pubmed-article:16990604 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16990604 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:2204 | entrezgene:pubmed | pubmed-article:16990604 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:16990604 | lld:entrezgene |
| lhgdn:association:41480 | lhgdn:found_in | pubmed-article:16990604 | lld:lhgdn |
| lhgdn:association:41481 | lhgdn:found_in | pubmed-article:16990604 | lld:lhgdn |
