pubmed-article:10542180 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10542180 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
pubmed-article:10542180 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:10542180 | lifeskim:mentions | umls-concept:C0029073 | lld:lifeskim |
pubmed-article:10542180 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:10542180 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
pubmed-article:10542180 | pubmed:issue | 21 | lld:pubmed |
pubmed-article:10542180 | pubmed:dateCreated | 1999-12-6 | lld:pubmed |
pubmed-article:10542180 | pubmed:abstractText | In Escherichia coli, the CpxRA two-component signal transduction system senses and responds to aggregated and misfolded proteins in the bacterial envelope. We show that CpxR-P (the phosphorylated form of the cognate response regulator) activates cpxRA expression in conjunction with RpoS, suggesting an involvement of the Cpx system in stationary-phase survival. Engagement of the CpxRA system in functions beyond protein management is indicated by several putative targets identified after a genomic screening for the CpxR-P recognition consensus sequence. Direct negative control of the newly identified targets motABcheAW (specifying motility and chemotaxis) and tsr (encoding the serine chemoreceptor) by CpxR-P was shown by electrophoretic mobility shift analysis and Northern hybridization. The results suggest that the CpxRA system plays a core role in an extensive stress response network in which the coordination of protein turnover and energy conservation may be the unifying element. | lld:pubmed |
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pubmed-article:10542180 | pubmed:language | eng | lld:pubmed |
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pubmed-article:10542180 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:10542180 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10542180 | pubmed:month | Nov | lld:pubmed |
pubmed-article:10542180 | pubmed:issn | 0021-9193 | lld:pubmed |
pubmed-article:10542180 | pubmed:author | pubmed-author:LinE CEC | lld:pubmed |
pubmed-article:10542180 | pubmed:author | pubmed-author:KwohAA | lld:pubmed |
pubmed-article:10542180 | pubmed:author | pubmed-author:De WulfPP | lld:pubmed |
pubmed-article:10542180 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10542180 | pubmed:volume | 181 | lld:pubmed |
pubmed-article:10542180 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10542180 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10542180 | pubmed:pagination | 6772-8 | lld:pubmed |
pubmed-article:10542180 | pubmed:dateRevised | 2010-9-10 | lld:pubmed |
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pubmed-article:10542180 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10542180 | pubmed:articleTitle | The CpxRA signal transduction system of Escherichia coli: growth-related autoactivation and control of unanticipated target operons. | lld:pubmed |
pubmed-article:10542180 | pubmed:affiliation | Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. | lld:pubmed |
pubmed-article:10542180 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10542180 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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