pubmed-article:7928983 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7928983 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
pubmed-article:7928983 | lifeskim:mentions | umls-concept:C0205147 | lld:lifeskim |
pubmed-article:7928983 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:7928983 | lifeskim:mentions | umls-concept:C1880022 | lld:lifeskim |
pubmed-article:7928983 | pubmed:issue | 20 | lld:pubmed |
pubmed-article:7928983 | pubmed:dateCreated | 1994-11-10 | lld:pubmed |
pubmed-article:7928983 | pubmed:abstractText | We constructed a set of deletions upstream of the gcv promoter and analyzed the effects of the deletions on expression of a gcvT-lacZ gene fusion. A deletion that ends at position -313 upstream of the transcription initiation site (+1) results in reduced levels of gcvT-lacZ expression, but the fusion is still inducible by glycine and repressible by purines. A deletion that ends at position -169 results in loss of both GcvA- and Lrp-mediated activation of the gcvT-lacZ fusion. The endpoints of delta -313 and delta -169 also define a site that down-regulates gcvT-lacZ expression two- to threefold. A deletion that ends at position -89 upstream from the transcription initiation site still shows PurR-mediated repression, suggesting that PurR-mediated repression is not by direct interference with the GcvA- and Lrp-mediated regulatory mechanism(s). Gel mobility shift assays and DNase I footprinting showed that Lrp protein binds to multiple sites upstream of the gcv promoter, from about bp -92 to bp -229. The results suggest that the gcv regulatory region is complex, with numerous cis-acting sites that are required for normal gcv expression. | lld:pubmed |
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pubmed-article:7928983 | pubmed:language | eng | lld:pubmed |
pubmed-article:7928983 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7928983 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:7928983 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7928983 | pubmed:month | Oct | lld:pubmed |
pubmed-article:7928983 | pubmed:issn | 0021-9193 | lld:pubmed |
pubmed-article:7928983 | pubmed:author | pubmed-author:StaufferG VGV | lld:pubmed |
pubmed-article:7928983 | pubmed:author | pubmed-author:StaufferL TLT | lld:pubmed |
pubmed-article:7928983 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7928983 | pubmed:volume | 176 | lld:pubmed |
pubmed-article:7928983 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7928983 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7928983 | pubmed:pagination | 6159-64 | lld:pubmed |
pubmed-article:7928983 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:7928983 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7928983 | pubmed:articleTitle | Characterization of the gcv control region from Escherichia coli. | lld:pubmed |
pubmed-article:7928983 | pubmed:affiliation | Department of Microbiology, University of Iowa, Iowa City 52242. | lld:pubmed |
pubmed-article:7928983 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7928983 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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