| pubmed-article:16849466 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16849466 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:16849466 | lifeskim:mentions | umls-concept:C0034789 | lld:lifeskim |
| pubmed-article:16849466 | lifeskim:mentions | umls-concept:C0079004 | lld:lifeskim |
| pubmed-article:16849466 | lifeskim:mentions | umls-concept:C1514762 | lld:lifeskim |
| pubmed-article:16849466 | lifeskim:mentions | umls-concept:C0022702 | lld:lifeskim |
| pubmed-article:16849466 | lifeskim:mentions | umls-concept:C0016263 | lld:lifeskim |
| pubmed-article:16849466 | lifeskim:mentions | umls-concept:C0024779 | lld:lifeskim |
| pubmed-article:16849466 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16849466 | pubmed:dateCreated | 2006-7-19 | lld:pubmed |
| pubmed-article:16849466 | pubmed:abstractText | Differences in BCR signaling may govern outcomes as diverse as proliferation and cell death. We profiled BCR signaling kinetics in subsets of primary human B cells using flow cytometry. In the predominant population expressing IgM, BCR cross-linking led to a quick burst of Syk, ERK1/2, and p38 signaling. In contrast, IgG B cells sustained higher per-cell ERK1/2 phosphorylation over time. This dichotomy suggested a mechanism for dampening signals transmitted by IgM. Regulatory phosphatase activity in IgM B cells was BCR-mediated and initiated more slowly than kinase activity. This BCR-mediated phosphatase activity was sensitive to inhibition by H(2)O(2) and required to attenuate IgM BCR signaling. These results provide the first kinetic maps of BCR signaling in primary human B cell subsets and enable new studies of signaling in B cell disorders, such as autoimmunity and cancer. | lld:pubmed |
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| pubmed-article:16849466 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16849466 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16849466 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16849466 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16849466 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:16849466 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:16849466 | pubmed:author | pubmed-author:NolanGarry... | lld:pubmed |
| pubmed-article:16849466 | pubmed:author | pubmed-author:LevyRonaldR | lld:pubmed |
| pubmed-article:16849466 | pubmed:author | pubmed-author:CzerwinskiDeb... | lld:pubmed |
| pubmed-article:16849466 | pubmed:author | pubmed-author:IrishJonathan... | lld:pubmed |
| pubmed-article:16849466 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16849466 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16849466 | pubmed:volume | 177 | lld:pubmed |
| pubmed-article:16849466 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16849466 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16849466 | pubmed:pagination | 1581-9 | lld:pubmed |
| pubmed-article:16849466 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:16849466 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16849466 | pubmed:articleTitle | Kinetics of B cell receptor signaling in human B cell subsets mapped by phosphospecific flow cytometry. | lld:pubmed |
| pubmed-article:16849466 | pubmed:affiliation | Department of Medicine, Oncology Division, Stanford University, Stanford, CA 94305, USA. | lld:pubmed |
| pubmed-article:16849466 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16849466 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:16849466 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16849466 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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