pubmed-article:19011223 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19011223 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
pubmed-article:19011223 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
pubmed-article:19011223 | lifeskim:mentions | umls-concept:C1705633 | lld:lifeskim |
pubmed-article:19011223 | lifeskim:mentions | umls-concept:C1819433 | lld:lifeskim |
pubmed-article:19011223 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:19011223 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
pubmed-article:19011223 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
pubmed-article:19011223 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:19011223 | pubmed:dateCreated | 2009-3-6 | lld:pubmed |
pubmed-article:19011223 | pubmed:abstractText | T cells possess a p38 activation alternative pathway in which stimulation via the antigen receptor (T-cell receptor [TCR]) induces phosphorylation of p38alpha and beta on Tyr323. To assess the contribution of this pathway to normal T-cell function, we generated p38alpha knockin mice in which Tyr323 was replaced with Phe (p38alpha(Y323F)). TCR-mediated stimulation failed to activate p38alpha(Y323F) as measured by phosphorylation of the Thr-Glu-Tyr activation motif and p38alpha catalytic activity. Cell-cycle entry was delayed in TCR-stimulated p38alpha(Y323F) T cells, which also produced less interferon (IFN)-gamma than wild-type T cells in response to TCR-mediated but not TCR-independent stimuli. p38alpha(Y323F) mice immunized with T-helper 1 (Th1)-inducing antigens generated normal Th1 effector cells, but these cells produced less IFN-gamma than wild-type cells when stimulated through the TCR. Thus, the Tyr323-dependent pathway and not the classic mitogen-activated protein (MAP) kinase cascade is the physiologic means of p38alpha activation through the TCR and is necessary for normal Th1 function but not Th1 generation. | lld:pubmed |
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pubmed-article:19011223 | pubmed:language | eng | lld:pubmed |
pubmed-article:19011223 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19011223 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:19011223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19011223 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19011223 | pubmed:month | Mar | lld:pubmed |
pubmed-article:19011223 | pubmed:issn | 1528-0020 | lld:pubmed |
pubmed-article:19011223 | pubmed:author | pubmed-author:JankovicDraga... | lld:pubmed |
pubmed-article:19011223 | pubmed:author | pubmed-author:AshwellJonath... | lld:pubmed |
pubmed-article:19011223 | pubmed:author | pubmed-author:MittelstadtPa... | lld:pubmed |
pubmed-article:19011223 | pubmed:author | pubmed-author:JirmanovaLudm... | lld:pubmed |
pubmed-article:19011223 | pubmed:author | pubmed-author:SarmaDandapan... | lld:pubmed |
pubmed-article:19011223 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19011223 | pubmed:day | 5 | lld:pubmed |
pubmed-article:19011223 | pubmed:volume | 113 | lld:pubmed |
pubmed-article:19011223 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19011223 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19011223 | pubmed:pagination | 2229-37 | lld:pubmed |
pubmed-article:19011223 | pubmed:dateRevised | 2010-9-23 | lld:pubmed |
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pubmed-article:19011223 | pubmed:year | 2009 | lld:pubmed |