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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0013879,
umls-concept:C0017337,
umls-concept:C0040649,
umls-concept:C0085201,
umls-concept:C0086418,
umls-concept:C0086860,
umls-concept:C0182953,
umls-concept:C0185027,
umls-concept:C0205054,
umls-concept:C0205145,
umls-concept:C0205160,
umls-concept:C1145667,
umls-concept:C1314939,
umls-concept:C1446409,
umls-concept:C1521761
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pubmed:issue |
9
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pubmed:dateCreated |
1991-4-23
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pubmed:abstractText |
DNase I footprinting analysis of the proximal apoA-I promoter sequences with rat liver nuclear extracts identified four protected regions: A, -22 to +17; B, -128 to -77; C, -175 to -148; and D, -220 to -190. Region D (-220 to -190) binds at least two distinct activities, designated AID1 and AID2, respectively, which can be separated by ion exchange chromatography. Region C (-175 to -148) forms five DNA protein complexes. Three of the complexes (2, 4, and 5) originate from the binding of more than one heat-stable nuclear factor, and two (1 and 3), from the binding of two heat-labile factors. The heat-stable factors bind in the -175 to -148 region and can be distinguished from C/EBP, which recognizes the same region, with DNA binding gel electrophoretic assays. Both factors 1 and 3 bind in the -168 to -148 apoA-I region. Despite the lack of a CCAAT motif in this region, the binding of factor 1 is competed out by oligonucleotides containing the binding sites of NFY and NFY*. Mutagenesis of the promoter region showed that mutations in the -171 to -166 and -158 to -153 regions diminished the binding of the heat-stable factors and reduced hepatic transcription to 14 and 8% of control, respectively. In contrast, a mutation in the -164 to -159 region abolished the binding of factor 1 and was associated with a 4.6-fold increase in hepatic transcription. These findings suggest that the heat-stable factors act as positive regulators, whereas factor 1 acts as a negative regulator in apoA-I gene transcription.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
266
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5790-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:1900840-Animals,
pubmed-meshheading:1900840-Apolipoprotein A-I,
pubmed-meshheading:1900840-Apolipoproteins A,
pubmed-meshheading:1900840-Binding, Competitive,
pubmed-meshheading:1900840-Chloramphenicol O-Acetyltransferase,
pubmed-meshheading:1900840-DNA Fingerprinting,
pubmed-meshheading:1900840-Electrophoresis, Agar Gel,
pubmed-meshheading:1900840-Humans,
pubmed-meshheading:1900840-Liver,
pubmed-meshheading:1900840-Molecular Sequence Data,
pubmed-meshheading:1900840-Mutagenesis,
pubmed-meshheading:1900840-Plasmids,
pubmed-meshheading:1900840-Promoter Regions, Genetic,
pubmed-meshheading:1900840-Rats,
pubmed-meshheading:1900840-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:1900840-Transcription, Genetic,
pubmed-meshheading:1900840-Tumor Cells, Cultured
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pubmed:year |
1991
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pubmed:articleTitle |
Promoter elements and factors involved in hepatic transcription of the human ApoA-I gene positive and negative regulators bind to overlapping sites.
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pubmed:affiliation |
University of Crete Medical School, Greece.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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