pubmed-article:1694265 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1694265 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
pubmed-article:1694265 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
pubmed-article:1694265 | lifeskim:mentions | umls-concept:C0034788 | lld:lifeskim |
pubmed-article:1694265 | lifeskim:mentions | umls-concept:C1519726 | lld:lifeskim |
pubmed-article:1694265 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
pubmed-article:1694265 | pubmed:issue | 6278 | lld:pubmed |
pubmed-article:1694265 | pubmed:dateCreated | 1990-8-2 | lld:pubmed |
pubmed-article:1694265 | pubmed:abstractText | Signalling by membrane immunoglobulin, the B-lymphocyte antigen receptor, regulates B-cell maturation and activation. Crosslinking of membrane immunoglobulin by antigen or by anti-immunoglobulin antibodies inactivates immature B cells, eliminating many of the B cells capable of producing auto-antibodies. By contrast, crosslinking of membrane immunoglobulin promotes activation of mature B cells for clonal expansion and antibody production against foreign antigens. Crosslinking membrane IgM on the immature B-cell line WEHI-231 induces growth arrest. This response may be analogous to the deletion or inactivation of immature B cells that is induced by antigen or anti-IgM antibodies. Membrane immunoglobulin crosslinking stimulates phosphoinositide hydrolysis, which leads to increases in intracellular calcium and activation of protein kinase C. The induced phosphoinositide breakdown is important for inhibiting WEHI-231 growth (ref. 7 and D. Page, M.R.G., K. Fahey, L. Matsuuchi and A.L.D., manuscript submitted for publication), but may not be sufficient, as agents that elevate calcium and activate protein kinase C cause only partial growth arrest. We now show that in both mature splenic B cells and the immature B-cell line WEHI-231 crosslinking membrane immunoglobulin also stimulates phosphorylation of protein tyrosine, a reaction that has been implicated as a key regulator of cell growth. Most of these phosphorylations were not a consequence of the phosphoinositide pathway. Thus, tyrosine phosphorylation is a second mode of transmembrane signalling by membrane immunoglobulin. | lld:pubmed |
pubmed-article:1694265 | pubmed:language | eng | lld:pubmed |
pubmed-article:1694265 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1694265 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1694265 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1694265 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1694265 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1694265 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1694265 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1694265 | pubmed:month | Jun | lld:pubmed |
pubmed-article:1694265 | pubmed:issn | 0028-0836 | lld:pubmed |
pubmed-article:1694265 | pubmed:author | pubmed-author:DeFrancoA LAL | lld:pubmed |
pubmed-article:1694265 | pubmed:author | pubmed-author:GoldM RMR | lld:pubmed |
pubmed-article:1694265 | pubmed:author | pubmed-author:LauD CDC | lld:pubmed |
pubmed-article:1694265 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1694265 | pubmed:day | 28 | lld:pubmed |
pubmed-article:1694265 | pubmed:volume | 345 | lld:pubmed |
pubmed-article:1694265 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1694265 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1694265 | pubmed:pagination | 810-3 | lld:pubmed |
pubmed-article:1694265 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:1694265 | pubmed:meshHeading | pubmed-meshheading:1694265-... | lld:pubmed |
pubmed-article:1694265 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:1694265 | pubmed:articleTitle | Stimulation of protein tyrosine phosphorylation by the B-lymphocyte antigen receptor. | lld:pubmed |
pubmed-article:1694265 | pubmed:affiliation | George Williams Hooper Foundation, University of California, San Francisco 94143-0552. | lld:pubmed |
pubmed-article:1694265 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1694265 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:1694265 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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