| pubmed-article:3287326 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3287326 | lifeskim:mentions | umls-concept:C0008155 | lld:lifeskim |
| pubmed-article:3287326 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:3287326 | lifeskim:mentions | umls-concept:C0008266 | lld:lifeskim |
| pubmed-article:3287326 | lifeskim:mentions | umls-concept:C0284965 | lld:lifeskim |
| pubmed-article:3287326 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:3287326 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:3287326 | pubmed:dateCreated | 1988-6-30 | lld:pubmed |
| pubmed-article:3287326 | pubmed:abstractText | We show that in E. coli, a Chlamydomonas chloroplast promoter, PA, is repressed by Integration Host Factor (IHF). The himA 42 mutation, altering the alpha-subunit of E. coli IHF, leads to over-accumulation of PA transcripts in vivo. This effect requires upstream chloroplast DNA sequences. DNAase I and methylation protection experiments show that IHF binds in vitro to a site within PA and band-retardation shows that IHF inhibits formation of PA-E. coli RNA polymerase open complexes. We interpret these results, together with our previous deletion analyses, to mean that in E. coli, repression of PA by IHF minimally requires both binding of IHF to a site overlapping PA and binding of one or more additional proteins, perhaps including IHF itself, to sequences upstream of PA. | lld:pubmed |
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| pubmed-article:3287326 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3287326 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3287326 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3287326 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3287326 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:3287326 | pubmed:issn | 0305-1048 | lld:pubmed |
| pubmed-article:3287326 | pubmed:author | pubmed-author:ThompsonR JRJ | lld:pubmed |
| pubmed-article:3287326 | pubmed:author | pubmed-author:MosigGG | lld:pubmed |
| pubmed-article:3287326 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3287326 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:3287326 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:3287326 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3287326 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3287326 | pubmed:pagination | 3313-26 | lld:pubmed |
| pubmed-article:3287326 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3287326 | pubmed:meshHeading | pubmed-meshheading:3287326-... | lld:pubmed |
| pubmed-article:3287326 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:3287326 | pubmed:articleTitle | Integration host factor (IHF) represses a Chlamydomonas chloroplast promoter in E. coli. | lld:pubmed |
| pubmed-article:3287326 | pubmed:affiliation | Department of Molecular Biology, Vanderbilt University, Nashville, TN 37235. | lld:pubmed |
| pubmed-article:3287326 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3287326 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:3287326 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:3287326 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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