| pubmed-article:16186825 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16186825 | lifeskim:mentions | umls-concept:C0031727 | lld:lifeskim |
| pubmed-article:16186825 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:16186825 | lifeskim:mentions | umls-concept:C1749719 | lld:lifeskim |
| pubmed-article:16186825 | lifeskim:mentions | umls-concept:C1417830 | lld:lifeskim |
| pubmed-article:16186825 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:16186825 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:16186825 | pubmed:dateCreated | 2005-10-21 | lld:pubmed |
| pubmed-article:16186825 | pubmed:abstractText | Transforming growth factor-beta-activated kinase 1 (TAK1) has been linked to interleukin 1 receptor and tumor necrosis factor receptor signaling. Here we generated mouse strains with conditional expression of a Map3k7 allele encoding part of TAK1. TAK1-deficient embryonic fibroblasts demonstrated loss of responses to interleukin 1beta and tumor necrosis factor. Studies of mice with B cell-specific TAK1 deficiency showed that TAK1 was indispensable for cellular responses to Toll-like receptor ligands, CD40 and B cell receptor crosslinking. In addition, antigen-induced immune responses were considerably impaired in mice with B cell-specific TAK1 deficiency. TAK1-deficient cells failed to activate transcription factor NF-kappaB and mitogen-activated protein kinases in response to interleukin 1beta, tumor necrosis factor and Toll-like receptor ligands. However, TAK1-deficient B cells were able to activate NF-kappaB but not the kinase Jnk in response to B cell receptor stimulation. These results collectively indicate that TAK1 is key in the cellular response to a variety of stimuli. | lld:pubmed |
| pubmed-article:16186825 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16186825 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16186825 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16186825 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16186825 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:16186825 | pubmed:issn | 1529-2908 | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:TakedaKiyoshi... | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:Ninomiya-Tsuj... | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:MatsumotoKuni... | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:AkiraShizuoS | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:YamamotoMasah... | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:TakeuchiOsamu... | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:SatoShintaroS | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:SanjoHidekiH | lld:pubmed |
| pubmed-article:16186825 | pubmed:author | pubmed-author:KawaiTaroT | lld:pubmed |
| pubmed-article:16186825 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16186825 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:16186825 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16186825 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16186825 | pubmed:pagination | 1087-95 | lld:pubmed |
| pubmed-article:16186825 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:16186825 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16186825 | pubmed:articleTitle | Essential function for the kinase TAK1 in innate and adaptive immune responses. | lld:pubmed |
| pubmed-article:16186825 | pubmed:affiliation | Akira Innate Immunity Project, Exploratory Research for Advanced Technology, Japan Science and Technology Agency. | lld:pubmed |
| pubmed-article:16186825 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16186825 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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