| pubmed-article:20705244 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20705244 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:20705244 | lifeskim:mentions | umls-concept:C0812230 | lld:lifeskim |
| pubmed-article:20705244 | lifeskim:mentions | umls-concept:C1334123 | lld:lifeskim |
| pubmed-article:20705244 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:20705244 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:20705244 | pubmed:dateCreated | 2010-8-13 | lld:pubmed |
| pubmed-article:20705244 | pubmed:abstractText | Mammalian target of rapamycin (mTOR) is an important mediator of phosphoinositol-3-kinase (PI3K) signaling. PI3K signaling regulates B cell development, homeostasis, and immune responses. However, the function and molecular mechanism of mTOR-mediated PI3K signaling in B cells has not been fully elucidated. Here we show that Sin1, an essential component of mTOR complex 2 (mTORC2), regulates B cell development. Sin1 deficiency results in increased IL-7 receptor (il7r) and RAG recombinase (rag1 and rag2) gene expression, leading to enhanced pro-B cell survival and augmented V(D)J recombinase activity. We further show that Akt2 specifically mediates the Sin1-mTORC2 dependent suppression of il7r and rag gene expression in B cells by regulating FoxO1 phosphorylation. Finally, we demonstrate that the mTOR inhibitor rapamycin induces rag expression and promotes V(D)J recombination in B cells. Our study reveals that the Sin1/mTORC2-Akt2 signaling axis is a key regulator of FoxO1 transcriptional activity in B cells. | lld:pubmed |
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| pubmed-article:20705244 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20705244 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20705244 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20705244 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20705244 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20705244 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20705244 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:20705244 | pubmed:issn | 1097-4164 | lld:pubmed |
| pubmed-article:20705244 | pubmed:author | pubmed-author:LeeG WGW | lld:pubmed |
| pubmed-article:20705244 | pubmed:author | pubmed-author:SessaWilliam... | lld:pubmed |
| pubmed-article:20705244 | pubmed:author | pubmed-author:SuBingB | lld:pubmed |
| pubmed-article:20705244 | pubmed:author | pubmed-author:SchatzDavid... | lld:pubmed |
| pubmed-article:20705244 | pubmed:author | pubmed-author:FacchinettiVa... | lld:pubmed |
| pubmed-article:20705244 | pubmed:author | pubmed-author:Di... | lld:pubmed |
| pubmed-article:20705244 | pubmed:author | pubmed-author:LazorchakAdam... | lld:pubmed |
| pubmed-article:20705244 | pubmed:copyrightInfo | Copyright 2010 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:20705244 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20705244 | pubmed:day | 13 | lld:pubmed |
| pubmed-article:20705244 | pubmed:volume | 39 | lld:pubmed |
| pubmed-article:20705244 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20705244 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20705244 | pubmed:pagination | 433-43 | lld:pubmed |
| pubmed-article:20705244 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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