pubmed-article:8051409 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8051409 | lifeskim:mentions | umls-concept:C0162508 | lld:lifeskim |
pubmed-article:8051409 | lifeskim:mentions | umls-concept:C0288011 | lld:lifeskim |
pubmed-article:8051409 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:8051409 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
pubmed-article:8051409 | lifeskim:mentions | umls-concept:C1512032 | lld:lifeskim |
pubmed-article:8051409 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
pubmed-article:8051409 | lifeskim:mentions | umls-concept:C0879590 | lld:lifeskim |
pubmed-article:8051409 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
pubmed-article:8051409 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:8051409 | pubmed:dateCreated | 1994-9-6 | lld:pubmed |
pubmed-article:8051409 | pubmed:abstractText | Expression of the transcription complex AP-1, composed of Jun and Fos family members, can be induced by a variety of stimuli. In lymphocytes, AP-1 transcriptional activity increases after TCR ligation and plays an important role in T cell activation events such as lymphokine secretion. To explore the requirements for AP-1 in IL-2 production, the AP-1 complex was targeted with a dominant negative mutant c-Jun protein, TAM-67, from which the transactivation domain has been deleted. In transient transfections of Jurkat cells, TAM-67 efficiently inhibited endogenous AP-1 transcriptional activity and blocked the activity of a reporter construct containing the 5' regulatory region of the IL-2 gene. TAM-67 also inhibited the transcriptional activity of nuclear factor-AT (NF-AT), whereas the NF-kappa B, NF-IL-2A, and the proximal TRE-like sites were relatively unaffected. The use of this dominant negative transcription factor suggests that: 1) transactivation-defective nuclear factors represent a novel approach to study the functional consequences of nuclear protein interactions on gene transcription; 2) the proximal TRE-like site from the IL-2 promoter is different from the consensus TRE; and 3) AP-1 plays an important role in the transcriptional activation mediated by the NF-AT binding complex. | lld:pubmed |
pubmed-article:8051409 | pubmed:language | eng | lld:pubmed |
pubmed-article:8051409 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8051409 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:8051409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8051409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8051409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8051409 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8051409 | pubmed:month | Sep | lld:pubmed |
pubmed-article:8051409 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:8051409 | pubmed:author | pubmed-author:ZacharchukC... | lld:pubmed |
pubmed-article:8051409 | pubmed:author | pubmed-author:AshwellJ DJD | lld:pubmed |
pubmed-article:8051409 | pubmed:author | pubmed-author:BirrerM JMJ | lld:pubmed |
pubmed-article:8051409 | pubmed:author | pubmed-author:MehraI VIV | lld:pubmed |
pubmed-article:8051409 | pubmed:author | pubmed-author:PetrakDD | lld:pubmed |
pubmed-article:8051409 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8051409 | pubmed:day | 1 | lld:pubmed |
pubmed-article:8051409 | pubmed:volume | 153 | lld:pubmed |
pubmed-article:8051409 | pubmed:geneSymbol | c-jun | lld:pubmed |
pubmed-article:8051409 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8051409 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8051409 | pubmed:pagination | 2046-51 | lld:pubmed |
pubmed-article:8051409 | pubmed:dateRevised | 2005-11-17 | lld:pubmed |
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pubmed-article:8051409 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:8051409 | pubmed:articleTitle | Dominant negative mutant of c-Jun inhibits NF-AT transcriptional activity and prevents IL-2 gene transcription. | lld:pubmed |
pubmed-article:8051409 | pubmed:affiliation | Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. | lld:pubmed |
pubmed-article:8051409 | pubmed:publicationType | Journal Article | lld:pubmed |
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