pubmed-article:2578447 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2578447 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
pubmed-article:2578447 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
pubmed-article:2578447 | lifeskim:mentions | umls-concept:C0061493 | lld:lifeskim |
pubmed-article:2578447 | lifeskim:mentions | umls-concept:C0680582 | lld:lifeskim |
pubmed-article:2578447 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:2578447 | pubmed:dateCreated | 1985-3-1 | lld:pubmed |
pubmed-article:2578447 | pubmed:abstractText | We studied the regulation of in vivo expression of Escherichia coli glutaminyl-tRNA synthetase at the transcriptional and translational level by analysis of glnS mRNA and glutaminyl-tRNA synthetase levels under a variety of growth conditions. In addition, strains carrying fusions of the beta-galactosidase structural gene and the glnS promoter were constructed and subsequently used for glnS regulatory studies. The level of glutaminyl-tRNA synthetase increases with the increasing growth rate, with a concomitant though much larger increase in glnS mRNA levels. Thus, transcriptional control appears to mediate metabolic regulation. It is known that glnR5, a regulatory mutation unlinked to glnS, causes overproduction of glutaminyl-tRNA synthetase. Here we showed that the glnR5 product enhances transcription of glnS 10- to 15-fold. The glnR5 mutation does not affect metabolic control. Thus, glnS appears to be regulated by two different control systems affecting transcription. Furthermore, our results suggest post-transcriptional regulation of glutaminyl-tRNA synthetase. | lld:pubmed |
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pubmed-article:2578447 | pubmed:language | eng | lld:pubmed |
pubmed-article:2578447 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2578447 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2578447 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:2578447 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2578447 | pubmed:month | Jan | lld:pubmed |
pubmed-article:2578447 | pubmed:issn | 0021-9193 | lld:pubmed |
pubmed-article:2578447 | pubmed:author | pubmed-author:SöllDD | lld:pubmed |
pubmed-article:2578447 | pubmed:author | pubmed-author:WatsonLL | lld:pubmed |
pubmed-article:2578447 | pubmed:author | pubmed-author:CheungA YAY | lld:pubmed |
pubmed-article:2578447 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2578447 | pubmed:volume | 161 | lld:pubmed |
pubmed-article:2578447 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2578447 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2578447 | pubmed:pagination | 212-8 | lld:pubmed |
pubmed-article:2578447 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:2578447 | pubmed:year | 1985 | lld:pubmed |
pubmed-article:2578447 | pubmed:articleTitle | Two control systems modulate the level of glutaminyl-tRNA synthetase in Escherichia coli. | lld:pubmed |
pubmed-article:2578447 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2578447 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
entrez-gene:945310 | entrezgene:pubmed | pubmed-article:2578447 | lld:entrezgene |
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