| pubmed-article:15749857 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0034789 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0034793 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0056184 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0425152 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0056185 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15749857 | lifeskim:mentions | umls-concept:C0205296 | lld:lifeskim |
| pubmed-article:15749857 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:15749857 | pubmed:dateCreated | 2005-3-7 | lld:pubmed |
| pubmed-article:15749857 | pubmed:abstractText | C3dg is a cleavage product of the C3 component of complement that can facilitate the coligation of the complement receptor 2 (CR2/CD21) with the BCR via C3dg/Ag complexes. This interaction can greatly amplify BCR-mediated signaling events and acts to lower the threshold for B cell activation. Although previous studies have used anti-CR2 Abs or used chimeric Ags in the context of BCR transgenic mice as surrogate C3d-containing ligands, we have used a physiological form of C3d to study signaling in B cells from wild-type C57BL/6 mice. We find that while CR2-enhanced BCR signaling causes intracellular Ca2+ mobilization and total pTyr phosphorylation of an intensity comparable to optimal BCR ligation using anti-IgM Abs, it does so with limited activation of inhibitory effectors (such as CD22, Src homology region 2 domain containing phosphatase 1, and SHIP-1) and without substantial receptor cross-linking. In summary, we demonstrate that CR2-enhanced BCR signaling may proceed not only through the previously described amplification of positive signaling pathways, but is potentially augmented by a lack of normal inhibitory/feedback signaling. | lld:pubmed |
| pubmed-article:15749857 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15749857 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15749857 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15749857 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:15749857 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15749857 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15749857 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15749857 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:15749857 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:15749857 | pubmed:author | pubmed-author:HolersV... | lld:pubmed |
| pubmed-article:15749857 | pubmed:author | pubmed-author:CambierJohn... | lld:pubmed |
| pubmed-article:15749857 | pubmed:author | pubmed-author:LyubchenkoTar... | lld:pubmed |
| pubmed-article:15749857 | pubmed:author | pubmed-author:dal PortoJoeJ | lld:pubmed |
| pubmed-article:15749857 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15749857 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:15749857 | pubmed:volume | 174 | lld:pubmed |
| pubmed-article:15749857 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15749857 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15749857 | pubmed:pagination | 3264-72 | lld:pubmed |
| pubmed-article:15749857 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15749857 | pubmed:meshHeading | pubmed-meshheading:15749857... | lld:pubmed |
| pubmed-article:15749857 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15749857 | pubmed:articleTitle | Coligation of the B cell receptor with complement receptor type 2 (CR2/CD21) using its natural ligand C3dg: activation without engagement of an inhibitory signaling pathway. | lld:pubmed |
| pubmed-article:15749857 | pubmed:affiliation | Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80220, USA. Taras.Lyubchenko@UCHSC.edu | lld:pubmed |
| pubmed-article:15749857 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15749857 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:15749857 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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