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| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1332420 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1135629 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1550548 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1555714 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1705654 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:11274146 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:11274146 | pubmed:issue | 23 | lld:pubmed |
| pubmed-article:11274146 | pubmed:dateCreated | 2001-6-4 | lld:pubmed |
| pubmed-article:11274146 | pubmed:abstractText | B lymphocytes lacking the adaptor protein B cell linker (BLNK) do not proliferate in response to B cell antigen receptor (BCR) engagement. We demonstrate here that BCR-activated BLNK(-)/- B cells fail to enter the cell cycle, and this is due to their inability to induce the expression of the cell cycle regulatory proteins such as cyclin D2 and cyclin-dependent kinase 4. BCR-stimulated BLNK(-)/- B cells also do not up-regulate the cell survival protein Bcl-x(L), which may be necessary for the cells to complete the cell cycle. In addition, BLNK(-)/- B cells exhibit a high rate of spontaneous apoptosis in culture. Examination of the various BCR-activated signaling pathways in mouse BLNK(-)/- B cells reveals the intact activation of Akt and mitogen-activated protein kinases but the impaired activation of nuclear factor (NF)-kappaB that is known to regulate genes involved in cell proliferation and survival. The inability to activate NF-kappaB in BCR-stimulated BLNK(-)/- B cells is due to a failure to induce the degradation of the inhibitory kappaB protein. In all these aspects, BLNK(-)/- B cells resemble xid B cells that have a mutation in Bruton's tyrosine kinase (Btk). Recently, phospholipase C (PLC)-gamma2 has also been demonstrated to be essential for NF-kappaB activation. Since BLNK has been shown separately to interact with both Btk and PLC-gamma2, our finding of normal Btk but impaired PLC-gamma2 activation in BCR-stimulated BLNK(-)/- B cells strongly suggests that BLNK orchestrates the formation of a Btk-PLC-gamma2 signaling axis that regulates NF-kappaB activation. Taken together, the NF-kappaB activation defect may be sufficient to explain the similar defects in BCR-induced B cell proliferation and T cell-independent immune responses in BLNK(-)/-, Btk(-)/-, and PLC-gamma2(-)/- mice. | lld:pubmed |
| pubmed-article:11274146 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11274146 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11274146 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11274146 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11274146 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:11274146 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:11274146 | pubmed:author | pubmed-author:KimH DHD | lld:pubmed |
| pubmed-article:11274146 | pubmed:author | pubmed-author:WongS CSC | lld:pubmed |
| pubmed-article:11274146 | pubmed:author | pubmed-author:GAYJ GJG | lld:pubmed |
| pubmed-article:11274146 | pubmed:author | pubmed-author:GanS KSK | lld:pubmed |
| pubmed-article:11274146 | pubmed:author | pubmed-author:FoxW JWJ | lld:pubmed |
| pubmed-article:11274146 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11274146 | pubmed:day | 8 | lld:pubmed |
| pubmed-article:11274146 | pubmed:volume | 276 | lld:pubmed |
| pubmed-article:11274146 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11274146 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11274146 | pubmed:pagination | 20055-63 | lld:pubmed |
| pubmed-article:11274146 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:11274146 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11274146 | pubmed:articleTitle | The adaptor protein BLNK is required for b cell antigen receptor-induced activation of nuclear factor-kappa B and cell cycle entry and survival of B lymphocytes. | lld:pubmed |
| pubmed-article:11274146 | pubmed:affiliation | Institute of Molecular and Cell Biology, 30 Medical Drive, Singapore 117609, Singapore. | lld:pubmed |
| pubmed-article:11274146 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11274146 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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