| pubmed-article:11029411 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11029411 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:11029411 | lifeskim:mentions | umls-concept:C0004595 | lld:lifeskim |
| pubmed-article:11029411 | lifeskim:mentions | umls-concept:C0035143 | lld:lifeskim |
| pubmed-article:11029411 | lifeskim:mentions | umls-concept:C0017787 | lld:lifeskim |
| pubmed-article:11029411 | lifeskim:mentions | umls-concept:C0028158 | lld:lifeskim |
| pubmed-article:11029411 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:11029411 | pubmed:issue | 21 | lld:pubmed |
| pubmed-article:11029411 | pubmed:dateCreated | 2000-11-24 | lld:pubmed |
| pubmed-article:11029411 | pubmed:abstractText | Synthesis of glutamate, the cell's major donor of nitrogen groups and principal anion, occupies a significant fraction of bacterial metabolism. In Bacillus subtilis, the gltAB operon, encoding glutamate synthase, requires a specific positive regulator, GltC, for its expression. In addition, the gltAB operon was shown to be repressed by TnrA, a regulator of several other genes of nitrogen metabolism and active under conditions of ammonium (nitrogen) limitation. TnrA was found to bind directly to a site immediately downstream of the gltAB promoter. As is true for other genes, the activity of TnrA at the gltAB promoter was antagonized by glutamine synthetase under certain growth conditions. | lld:pubmed |
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| pubmed-article:11029411 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11029411 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11029411 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11029411 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11029411 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11029411 | pubmed:issn | 0021-9193 | lld:pubmed |
| pubmed-article:11029411 | pubmed:author | pubmed-author:FisherS HSH | lld:pubmed |
| pubmed-article:11029411 | pubmed:author | pubmed-author:SonensheinA... | lld:pubmed |
| pubmed-article:11029411 | pubmed:author | pubmed-author:BohannonD EDE | lld:pubmed |
| pubmed-article:11029411 | pubmed:author | pubmed-author:WrayL VLVJr | lld:pubmed |
| pubmed-article:11029411 | pubmed:author | pubmed-author:BelitskyB RBR | lld:pubmed |
| pubmed-article:11029411 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11029411 | pubmed:volume | 182 | lld:pubmed |
| pubmed-article:11029411 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11029411 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11029411 | pubmed:pagination | 5939-47 | lld:pubmed |
| pubmed-article:11029411 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:11029411 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11029411 | pubmed:articleTitle | Role of TnrA in nitrogen source-dependent repression of Bacillus subtilis glutamate synthase gene expression. | lld:pubmed |
| pubmed-article:11029411 | pubmed:affiliation | Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA. | lld:pubmed |
| pubmed-article:11029411 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11029411 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11029411 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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