| pubmed-article:16115887 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C0015576 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C1704928 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C0034805 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:16115887 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:16115887 | pubmed:issue | 42 | lld:pubmed |
| pubmed-article:16115887 | pubmed:dateCreated | 2005-10-17 | lld:pubmed |
| pubmed-article:16115887 | pubmed:abstractText | The inhibitory Fc receptors function to regulate the antigen-driven activation and expansion of lymphocytes. In B cells, the Fc gammaRIIB1 is a potent inhibitor of B cell antigen receptor (BCR) signaling when coligated to the BCR by engagement of antigen-containing immune complexes. Inhibition is mediated by the recruitment of the inositol phosphatase, SHIP, to the Fc gammaRIIB1 phosphorylated tyrosine-based inhibitory motif (ITIM). Here we show that BCR-independent aggregation of the Fc gammaRIIB1 transduces an ITIM- and SHIP-independent proapoptotic signal that is dependent on members of the c-Abl tyrosine kinase family. These results define a novel Abl family kinase-dependent Fc gammaRIIB1 signaling pathway that functions independently of the BCR in controlling antigen-driven B cell responses. | lld:pubmed |
| pubmed-article:16115887 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16115887 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16115887 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16115887 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:16115887 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:16115887 | pubmed:author | pubmed-author:InabeKazunori... | lld:pubmed |
| pubmed-article:16115887 | pubmed:author | pubmed-author:KurosakiTomoh... | lld:pubmed |
| pubmed-article:16115887 | pubmed:author | pubmed-author:PierceSusan... | lld:pubmed |
| pubmed-article:16115887 | pubmed:author | pubmed-author:BollandSilvia... | lld:pubmed |
| pubmed-article:16115887 | pubmed:author | pubmed-author:TzengShiang-J... | lld:pubmed |
| pubmed-article:16115887 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16115887 | pubmed:day | 21 | lld:pubmed |
| pubmed-article:16115887 | pubmed:volume | 280 | lld:pubmed |
| pubmed-article:16115887 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16115887 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16115887 | pubmed:pagination | 35247-54 | lld:pubmed |
| pubmed-article:16115887 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16115887 | pubmed:meshHeading | pubmed-meshheading:16115887... | lld:pubmed |
| pubmed-article:16115887 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16115887 | pubmed:articleTitle | The B cell inhibitory Fc receptor triggers apoptosis by a novel c-Abl family kinase-dependent pathway. | lld:pubmed |
| pubmed-article:16115887 | pubmed:affiliation | Laboratory of Immunogenetics, NIAID, National Institutes of Health, Rockville, Maryland 20852, USA. | lld:pubmed |
| pubmed-article:16115887 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16115887 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
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