| pubmed-article:2498806 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2498806 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
| pubmed-article:2498806 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:2498806 | lifeskim:mentions | umls-concept:C0013081 | lld:lifeskim |
| pubmed-article:2498806 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:2498806 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:2498806 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:2498806 | pubmed:dateCreated | 1989-7-6 | lld:pubmed |
| pubmed-article:2498806 | pubmed:abstractText | The low basal expression of Fos and the rapid and effective turn-off of serum induced Fos transcription is due to autoregulation. Fos and Jun/AP-1 protein cooperate in the repression mechanism. Overexpressions of Fos and Jun decrease basal and induced transcription from Fos-CAT constructs and from the endogenous gene in NIH3T3 cells. The introduction into cells of either antisense Fos or antisense Jun sequences leads to elevated basal Fos promoter activity. Gel retardation experiments with synthetic oligonucleotides define two target sequences in the Fos promoter which bind Fos-Jun/AP-1 (centering at about -296 and -60). In vivo competition with these oligonucleotides relieves repression. | lld:pubmed |
| pubmed-article:2498806 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2498806 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2498806 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2498806 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2498806 | pubmed:month | May | lld:pubmed |
| pubmed-article:2498806 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:HattoriKK | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:HerrlichPP | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:RahmsdorfH... | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:PontaHH | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:KarinMM | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:SchönthalAA | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:ChiuRR | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:AngerVV | lld:pubmed |
| pubmed-article:2498806 | pubmed:author | pubmed-author:BüscherMM | lld:pubmed |
| pubmed-article:2498806 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2498806 | pubmed:volume | 4 | lld:pubmed |
| pubmed-article:2498806 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2498806 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2498806 | pubmed:pagination | 629-36 | lld:pubmed |
| pubmed-article:2498806 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:2498806 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2498806 | pubmed:articleTitle | The Fos and Jun/AP-1 proteins are involved in the downregulation of Fos transcription. | lld:pubmed |
| pubmed-article:2498806 | pubmed:affiliation | Kernforschungszentrum Karlsruhe, Institut für Genetik und Toxikologie, Federal Republic of Germany. | lld:pubmed |
| pubmed-article:2498806 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2498806 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:2498806 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2498806 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:2498806 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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