| pubmed-article:8683110 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8683110 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:8683110 | lifeskim:mentions | umls-concept:C0162508 | lld:lifeskim |
| pubmed-article:8683110 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:8683110 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:8683110 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:8683110 | lifeskim:mentions | umls-concept:C0162493 | lld:lifeskim |
| pubmed-article:8683110 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:8683110 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:8683110 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:8683110 | pubmed:dateCreated | 1996-8-16 | lld:pubmed |
| pubmed-article:8683110 | pubmed:abstractText | Sublethal levels of oxidative stress are well known to alter T cell functional responses, but the underlying mechanisms are unknown. The current study examined the effects of oxidative stress on transcriptional activities mediated by c-Fos/c-Jun AP-1 and the nuclear factor of activated T cells (NF-AT). The present results show that Jurkat T cells acutely exposed to micromolar concentrations of H2O2 exhibit substantial increases in AP-1 binding activity and the expression of c-jun but not c-fos mRNA. The preferential induction of c-jun by H2O2 did not represent redox stabilization of mRNA transcripts, and oxidative signals closely resembled PHA/PMA stimulation by effectively transactivating the full length c-jun promoter via the proximal jun1 tumor promoter-responsive element (TRE)-like promoter element. Similarly, the complexes binding the consensus AP-1 TRE and jun TRE-like motifs in cells exposed to oxidative signals or PHA/PMA were indistinguishable, being composed of c-Fos, c-Jun, and JunD. However, PHA/PMA but not oxidative signals induced the coordinate activation of reporter constructs containing the AP-1-TRE, NF-AT, and IL-2 promoter regions along with IL-2 mRNA expression. Furthermore, sublethal levels of H2O2 actively suppressed the transcriptional activation of NF-AT and IL-2 reporters as well as the expression of IL-2 mRNA in cells stimulated with PHA/PMA. Gel shift analysis revealed that oxidative suppression of NF-AT represented inhibition in the early generation of NFAT complexes rather than the binding of preformed NF-AT complexes. These results suggest that oxidative signals can positively and negatively regulate T cell transcriptional events and that changes in cellular redox can uncouple AP-1 regulation of c-jun from transcriptional up-regulation of IL-2 via NF-AT. | lld:pubmed |
| pubmed-article:8683110 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8683110 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8683110 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8683110 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:8683110 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:8683110 | pubmed:author | pubmed-author:ChenMM | lld:pubmed |
| pubmed-article:8683110 | pubmed:author | pubmed-author:WhislerR LRL | lld:pubmed |
| pubmed-article:8683110 | pubmed:author | pubmed-author:BeiqingLL | lld:pubmed |
| pubmed-article:8683110 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8683110 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:8683110 | pubmed:volume | 157 | lld:pubmed |
| pubmed-article:8683110 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8683110 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8683110 | pubmed:pagination | 160-9 | lld:pubmed |
| pubmed-article:8683110 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:8683110 | pubmed:meshHeading | pubmed-meshheading:8683110-... | lld:pubmed |
| pubmed-article:8683110 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8683110 | pubmed:articleTitle | Sublethal levels of oxidative stress stimulate transcriptional activation of c-jun and suppress IL-2 promoter activation in Jurkat T cells. | lld:pubmed |
| pubmed-article:8683110 | pubmed:affiliation | Department of Medical Biochemistry, William H. Davis Medical Research Center, Ohio State University, Columbus 43210, USA. | lld:pubmed |
| pubmed-article:8683110 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8683110 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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