| pubmed-article:1509265 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1509265 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
| pubmed-article:1509265 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:1509265 | lifeskim:mentions | umls-concept:C0206120 | lld:lifeskim |
| pubmed-article:1509265 | lifeskim:mentions | umls-concept:C0040624 | lld:lifeskim |
| pubmed-article:1509265 | lifeskim:mentions | umls-concept:C1513403 | lld:lifeskim |
| pubmed-article:1509265 | pubmed:issue | 5073 | lld:pubmed |
| pubmed-article:1509265 | pubmed:dateCreated | 1992-9-23 | lld:pubmed |
| pubmed-article:1509265 | pubmed:abstractText | Anergy is a mechanism of T lymphocyte tolerance induced by antigen receptor stimulation in the absence of co-stimulation. Anergic T cells were shown to have a defect in antigen-induced transcription of the interleukin-2 gene. Analysis of the promoter indicated that the transcription factor AP-1 and its corresponding cis element were specifically down-regulated. Exposure of anergic T cells to interleukin-2 restored both antigen responsiveness and activity of the AP-1 element. | lld:pubmed |
| pubmed-article:1509265 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1509265 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1509265 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1509265 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:1509265 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1509265 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:1509265 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:1509265 | pubmed:author | pubmed-author:SchwartzR HRH | lld:pubmed |
| pubmed-article:1509265 | pubmed:author | pubmed-author:KangS MSM | lld:pubmed |
| pubmed-article:1509265 | pubmed:author | pubmed-author:LenardoM JMJ | lld:pubmed |
| pubmed-article:1509265 | pubmed:author | pubmed-author:BeverlyBB | lld:pubmed |
| pubmed-article:1509265 | pubmed:author | pubmed-author:BrorsonKK | lld:pubmed |
| pubmed-article:1509265 | pubmed:author | pubmed-author:TranA CAC | lld:pubmed |
| pubmed-article:1509265 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1509265 | pubmed:day | 21 | lld:pubmed |
| pubmed-article:1509265 | pubmed:volume | 257 | lld:pubmed |
| pubmed-article:1509265 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1509265 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1509265 | pubmed:pagination | 1134-8 | lld:pubmed |
| pubmed-article:1509265 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:1509265 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1509265 | pubmed:articleTitle | Transactivation by AP-1 is a molecular target of T cell clonal anergy. | lld:pubmed |
| pubmed-article:1509265 | pubmed:affiliation | Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. | lld:pubmed |
| pubmed-article:1509265 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1509265 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1509265 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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