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| pubmed-article:8416900 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:8416900 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:8416900 | lifeskim:mentions | umls-concept:C1336789 | lld:lifeskim |
| pubmed-article:8416900 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:8416900 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:8416900 | lifeskim:mentions | umls-concept:C0560013 | lld:lifeskim |
| pubmed-article:8416900 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:8416900 | pubmed:dateCreated | 1993-1-27 | lld:pubmed |
| pubmed-article:8416900 | pubmed:abstractText | Two regulatory proteins, Gal repressor and isorepressor, control the expression of the gal and mgl operons in Escherichia coli. The transcription start sites for galR and galS, the genes for the repressor and isorepressor, were determined by primer extension of in vivo transcripts. Study of the promoter-lacZ gene fusions introduced into the chromosome indicated that galS expression was elevated in cells in which the normal galS gene was interrupted, but not in cells in which the galR gene was deleted. When both genes were disrupted, galS expression was further elevated. Expression from the galS promoter was stimulated by the addition of D-fucose, repressed by glucose, and dependent on cyclic AMP receptor protein (CRP). Expression of a similar gene fusion of the galR promoter to lacZ was unregulated. Both galR and galS genes contain two potential operator sites (OE and OI) and a CRP-binding site. The arrangement of OE, OI, and the CRP-binding site in the galS gene is analogous to the arrangement in the gal and mgl promoters, but the arrangement in galR is atypical. The increased concentration of the isorepressor when inducer is present may facilitate early shutoff of the isorepressor-regulated genes of the gal regulon when inducer (substrate) concentration falls. | lld:pubmed |
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| pubmed-article:8416900 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8416900 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8416900 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8416900 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:8416900 | pubmed:issn | 0021-9193 | lld:pubmed |
| pubmed-article:8416900 | pubmed:author | pubmed-author:AdhyaSS | lld:pubmed |
| pubmed-article:8416900 | pubmed:author | pubmed-author:WeickertM JMJ | lld:pubmed |
| pubmed-article:8416900 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8416900 | pubmed:volume | 175 | lld:pubmed |
| pubmed-article:8416900 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8416900 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8416900 | pubmed:pagination | 251-8 | lld:pubmed |
| pubmed-article:8416900 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8416900 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8416900 | pubmed:articleTitle | Control of transcription of gal repressor and isorepressor genes in Escherichia coli. | lld:pubmed |
| pubmed-article:8416900 | pubmed:affiliation | Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. | lld:pubmed |
| pubmed-article:8416900 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8416900 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:8416900 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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