pubmed-article:16179367 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0044602 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0285761 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C1368105 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C1451005 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C1705325 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0123771 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0597298 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C1514762 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C1150481 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0486379 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0205464 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C0683941 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C1554080 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C1706198 | lld:lifeskim |
pubmed-article:16179367 | lifeskim:mentions | umls-concept:C2346501 | lld:lifeskim |
pubmed-article:16179367 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:16179367 | pubmed:dateCreated | 2006-1-10 | lld:pubmed |
pubmed-article:16179367 | pubmed:abstractText | Mouse gene-targeting studies have documented a central role of the p110delta isoform of phosphoinositide 3-kinase (PI3K) in B-cell development and function. A defect in B-cell antigen receptor (BCR) signaling is key to this B-cell phenotype. Here we further characterize this signaling defect and report that a p110delta-selective small molecule inhibitor mirrors the effect of genetic inactivation of p110delta in BCR signaling. p110delta activity is indispensable for BCR-induced DNA synthesis and phosphorylation of Akt/protein kinase B (PKB), forkhead transcription factor/forkhead box O3a (FOXO3a), and p70 S6 kinase (p70 S6K), with modest effects on the phosphorylation of glycogen synthase kinase 3 alpha/beta (GSK3alpha/beta) and extracellular signal-regulated kinase (Erk). The PI3K-dependent component of intracellular calcium mobilization also completely relies on p110delta catalytic activity. Resting B cells with inactive p110delta fail to enter the cell cycle, correlating with an incapacity to up-regulate the expression of cyclins D2, A, and E, and to phosphorylate the retinoblastoma protein (Rb). p110delta is also critical for interleukin 4 (IL-4)-induced phosphorylation of Akt/PKB and FOXO3a, and protection from apoptosis. Taken together, these data show that defects observed in p110delta mutant mice are not merely a consequence of altered B-cell differentiation, and emphasize the potential utility of p110delta as a drug target in autoimmune diseases in which B cells play a crucial role. | lld:pubmed |
pubmed-article:16179367 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:language | eng | lld:pubmed |
pubmed-article:16179367 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16179367 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16179367 | pubmed:month | Jan | lld:pubmed |
pubmed-article:16179367 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:16179367 | pubmed:author | pubmed-author:Vanhaesebroec... | lld:pubmed |
pubmed-article:16179367 | pubmed:author | pubmed-author:OkkenhaugKlau... | lld:pubmed |
pubmed-article:16179367 | pubmed:author | pubmed-author:BilancioAnton... | lld:pubmed |
pubmed-article:16179367 | pubmed:author | pubmed-author:RommelChristi... | lld:pubmed |
pubmed-article:16179367 | pubmed:author | pubmed-author:RuckleThomasT | lld:pubmed |
pubmed-article:16179367 | pubmed:author | pubmed-author:CampsMontserr... | lld:pubmed |
pubmed-article:16179367 | pubmed:author | pubmed-author:EmeryJuliet... | lld:pubmed |
pubmed-article:16179367 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16179367 | pubmed:day | 15 | lld:pubmed |
pubmed-article:16179367 | pubmed:volume | 107 | lld:pubmed |
pubmed-article:16179367 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16179367 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16179367 | pubmed:pagination | 642-50 | lld:pubmed |
pubmed-article:16179367 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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pubmed-article:16179367 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16179367 | pubmed:articleTitle | Key role of the p110delta isoform of PI3K in B-cell antigen and IL-4 receptor signaling: comparative analysis of genetic and pharmacologic interference with p110delta function in B cells. | lld:pubmed |
pubmed-article:16179367 | pubmed:affiliation | Ludwig Institute for Cancer Research, 91 Riding House Street, London, W1W 7BS, United Kingdom. | lld:pubmed |
pubmed-article:16179367 | pubmed:publicationType | Journal Article | lld:pubmed |