pubmed-article:3517853 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3517853 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:3517853 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:3517853 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:3517853 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
pubmed-article:3517853 | lifeskim:mentions | umls-concept:C0205160 | lld:lifeskim |
pubmed-article:3517853 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:3517853 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:3517853 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:3517853 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:3517853 | pubmed:dateCreated | 1986-6-23 | lld:pubmed |
pubmed-article:3517853 | pubmed:abstractText | Two cis-acting elements, the enhancer and the promoter, independently contribute to the cell-specific expression of the rat insulin 1 gene. The activities of these elements are presumably mediated by trans-acting factors. We have performed intracellular competition experiments that suggest the presence of a negative factor(s) that represses the enhancer activity in cells that do not express the insulin gene. In these experiments fibroblast cells (COS-7) were transfected with two plasmids: a test plasmid containing the gene for chloramphenicol acetyltransferase under the control of the thymidine kinase promoter and the insulin enhancer; and a competitor plasmid containing insulin enhancer sequences and the simian virus 40 origin of replication to permit its replication in the recipient cells. The presence of the competitor plasmid led to a 5- to 6-fold increase in chloramphenicol acetyltransferase activity as compared with the activity detected when insulin enhancer was absent from either the competitor or the test plasmid. A 5-fold increase in chloramphenicol acetyltransferase activity was also seen when the rat amylase enhancer was present on the competitor plasmid; in contrast the simian virus 40 enhancer exerted no effect. Efficient derepression required additional sequences downstream from those essential for enhancer activity. We propose that the activity of the rat insulin 1 enhancer is modulated by a negative trans-acting factor(s) that is active in cells not expressing insulin but is overridden by the dominant positive trans-acting factor(s) present in insulin-producing cells. | lld:pubmed |
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pubmed-article:3517853 | pubmed:language | eng | lld:pubmed |
pubmed-article:3517853 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3517853 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:3517853 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3517853 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3517853 | pubmed:month | May | lld:pubmed |
pubmed-article:3517853 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:3517853 | pubmed:author | pubmed-author:RutterW JWJ | lld:pubmed |
pubmed-article:3517853 | pubmed:author | pubmed-author:NivYY | lld:pubmed |
pubmed-article:3517853 | pubmed:author | pubmed-author:WalkerM DMD | lld:pubmed |
pubmed-article:3517853 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3517853 | pubmed:volume | 83 | lld:pubmed |
pubmed-article:3517853 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3517853 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3517853 | pubmed:pagination | 3180-4 | lld:pubmed |
pubmed-article:3517853 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:3517853 | pubmed:year | 1986 | lld:pubmed |
pubmed-article:3517853 | pubmed:articleTitle | Regulation of rat insulin 1 gene expression: evidence for negative regulation in nonpancreatic cells. | lld:pubmed |
pubmed-article:3517853 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:3517853 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:3517853 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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