| pubmed-article:14517301 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14517301 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:14517301 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:14517301 | lifeskim:mentions | umls-concept:C0031671 | lld:lifeskim |
| pubmed-article:14517301 | lifeskim:mentions | umls-concept:C1514762 | lld:lifeskim |
| pubmed-article:14517301 | lifeskim:mentions | umls-concept:C1149836 | lld:lifeskim |
| pubmed-article:14517301 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:14517301 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:14517301 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:14517301 | pubmed:dateCreated | 2003-9-30 | lld:pubmed |
| pubmed-article:14517301 | pubmed:abstractText | Phospholipase C (PLC) plays important roles in phosphoinositide turnover by regulating the calcium-protein kinase C signaling pathway. PLC-L2 is a novel PLC-like protein which lacks PLC activity, although it is very homologous with PLC delta. PLC-L2 is expressed in hematopoietic cells, but its physiological roles and intracellular functions in the immune system have not yet been clarified. To elucidate the physiological function of PLC-L2, we generated mice which had a genetic PLC-L2 deficiency. PLC-L2-deficient mice grew with no apparent abnormalities. However, mature B cells from PLC-L2-deficient mice were hyperproliferative in response to B-cell receptor (BCR) cross-linking, although B2 cell development appeared to be normal. Molecular biological analysis revealed that calcium influx and NFATc accumulation in nuclei were increased in PLC-L2-deficient B cells. Extracellular signal-regulated kinase activity was also enhanced in PLC-L2-deficient B cells. These mice had a stronger T-cell-independent antigen response. These results indicate that PLC-L2 is a novel negative regulator of BCR signaling and immune responses. | lld:pubmed |
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| pubmed-article:14517301 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14517301 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14517301 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14517301 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14517301 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14517301 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14517301 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14517301 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:14517301 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:TakenawaTadao... | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:YoshidaNobuak... | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:NishikawaShin... | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:NakamuraYoshi... | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:FukamiKiyokoK | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:WadaMikaM | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:KataokaYukiY | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:TsujiKohichir... | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:OtsukiMakikoM | lld:pubmed |
| pubmed-article:14517301 | pubmed:author | pubmed-author:TakenakaKeiK | lld:pubmed |
| pubmed-article:14517301 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14517301 | pubmed:volume | 23 | lld:pubmed |
| pubmed-article:14517301 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14517301 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14517301 | pubmed:pagination | 7329-38 | lld:pubmed |
| pubmed-article:14517301 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:14517301 | pubmed:year | 2003 | lld:pubmed |
