| pubmed-article:8637901 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8637901 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:8637901 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:8637901 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:8637901 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:8637901 | lifeskim:mentions | umls-concept:C0205360 | lld:lifeskim |
| pubmed-article:8637901 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:8637901 | lifeskim:mentions | umls-concept:C1704735 | lld:lifeskim |
| pubmed-article:8637901 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:8637901 | pubmed:dateCreated | 1996-7-10 | lld:pubmed |
| pubmed-article:8637901 | pubmed:abstractText | In Escherichia coli, the sigma factor, RpoS, is a central regulator in stationary-phase cells. We have identified a gene, sprE (stationary-phase regulator), as essential for the negative regulation of rpoS expression. SprE negatively regulates the rpoS gene product at the level of protein stability, perhaps in response to nutrient availability. The ability of SprE to destabilize RpoS is dependent on the ClpX/ClpP protease. Based on homology, SprE is a member of the response regulator family of proteins. SprE is the first response regulator identified that is implicated in the control of protein stability. Moreover, SprE is the first reported protein that appears to regulate rpoS in response to a specific environmental parameter. | lld:pubmed |
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| pubmed-article:8637901 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8637901 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8637901 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8637901 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:8637901 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8637901 | pubmed:author | pubmed-author:SilhavyT JTJ | lld:pubmed |
| pubmed-article:8637901 | pubmed:author | pubmed-author:PrattL ALA | lld:pubmed |
| pubmed-article:8637901 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8637901 | pubmed:day | 19 | lld:pubmed |
| pubmed-article:8637901 | pubmed:volume | 93 | lld:pubmed |
| pubmed-article:8637901 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8637901 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8637901 | pubmed:pagination | 2488-92 | lld:pubmed |
| pubmed-article:8637901 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8637901 | pubmed:meshHeading | pubmed-meshheading:8637901-... | lld:pubmed |
| pubmed-article:8637901 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8637901 | pubmed:articleTitle | The response regulator SprE controls the stability of RpoS. | lld:pubmed |
| pubmed-article:8637901 | pubmed:affiliation | Department of Molecular Biology, Princeton University, New Jersey 08544, USA. | lld:pubmed |
| pubmed-article:8637901 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8637901 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8637901 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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