| pubmed-article:17028587 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17028587 | lifeskim:mentions | umls-concept:C1819882 | lld:lifeskim |
| pubmed-article:17028587 | lifeskim:mentions | umls-concept:C1158320 | lld:lifeskim |
| pubmed-article:17028587 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:17028587 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:17028587 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:17028587 | pubmed:dateCreated | 2006-10-20 | lld:pubmed |
| pubmed-article:17028587 | pubmed:abstractText | Anergic T cells have altered diacylglycerol metabolism, but whether that altered metabolism has a causative function in the induction of T cell anergy is not apparent. To test the importance of diacylglycerol metabolism in T cell anergy, we manipulated diacylglycerol kinases (DGKs), which are enzymes that terminate diacylglycerol-dependent signaling. Overexpression of DGK-alpha resulted in a defect in T cell receptor signaling that is characteristic of anergy. We generated DGK-alpha-deficient mice and found that DGK-alpha-deficient T cells had more diacylglycerol-dependent T cell receptor signaling. In vivo anergy induction was impaired in DGK-alpha-deficient mice. When stimulated in anergy-producing conditions, T cells lacking DGK-alpha or DGK-zeta proliferated and produced interleukin 2. Pharmacological inhibition of DGK-alpha activity in DGK-zeta-deficient T cells that received an anergizing stimulus proliferated similarly to wild-type T cells that received CD28 costimulation and prevented anergy induction. Our findings suggest that regulation of diacylglycerol metabolism is critical in determining whether activation or anergy ensues after T cell receptor stimulation. | lld:pubmed |
| pubmed-article:17028587 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17028587 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17028587 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17028587 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17028587 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17028587 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17028587 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17028587 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17028587 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17028587 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:17028587 | pubmed:issn | 1529-2908 | lld:pubmed |
| pubmed-article:17028587 | pubmed:author | pubmed-author:KoretzkyGary... | lld:pubmed |
| pubmed-article:17028587 | pubmed:author | pubmed-author:TophamMatthew... | lld:pubmed |
| pubmed-article:17028587 | pubmed:author | pubmed-author:ZhongXiao-Pin... | lld:pubmed |
| pubmed-article:17028587 | pubmed:author | pubmed-author:OlenchockBenj... | lld:pubmed |
| pubmed-article:17028587 | pubmed:author | pubmed-author:JordanMarthaM | lld:pubmed |
| pubmed-article:17028587 | pubmed:author | pubmed-author:GuoRishuR | lld:pubmed |
| pubmed-article:17028587 | pubmed:author | pubmed-author:CarpenterJeff... | lld:pubmed |
| pubmed-article:17028587 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17028587 | pubmed:volume | 7 | lld:pubmed |
| pubmed-article:17028587 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17028587 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17028587 | pubmed:pagination | 1174-81 | lld:pubmed |
| pubmed-article:17028587 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:17028587 | pubmed:meshHeading | pubmed-meshheading:17028587... | lld:pubmed |
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| pubmed-article:17028587 | pubmed:meshHeading | pubmed-meshheading:17028587... | lld:pubmed |
| pubmed-article:17028587 | pubmed:meshHeading | pubmed-meshheading:17028587... | lld:pubmed |
| pubmed-article:17028587 | pubmed:meshHeading | pubmed-meshheading:17028587... | lld:pubmed |
| pubmed-article:17028587 | pubmed:meshHeading | pubmed-meshheading:17028587... | lld:pubmed |
| pubmed-article:17028587 | pubmed:meshHeading | pubmed-meshheading:17028587... | lld:pubmed |
| pubmed-article:17028587 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:17028587 | pubmed:articleTitle | Disruption of diacylglycerol metabolism impairs the induction of T cell anergy. | lld:pubmed |
| pubmed-article:17028587 | pubmed:affiliation | Signal Transduction Program, Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA. | lld:pubmed |
| pubmed-article:17028587 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17028587 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:17028587 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17028587 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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