| pubmed-article:10759542 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10759542 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:10759542 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
| pubmed-article:10759542 | lifeskim:mentions | umls-concept:C0038323 | lld:lifeskim |
| pubmed-article:10759542 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:10759542 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:10759542 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:10759542 | lifeskim:mentions | umls-concept:C1871899 | lld:lifeskim |
| pubmed-article:10759542 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:10759542 | pubmed:dateCreated | 2000-5-17 | lld:pubmed |
| pubmed-article:10759542 | pubmed:abstractText | To understand cholesterol-mediated regulation of human fatty acid synthase promoter I, we tested various 5'-deletion constructs of promoter I-luciferase reporter gene constructs in HepG2 cells. The reporter gene constructs that contained only the Sp-1-binding site (nucleotides -82 to -74) and the two tandem sterol regulatory elements (SREs; nucleotides -63 to -46) did not respond to cholesterol. Only the reporter gene constructs containing a nuclear factor-Y (NF-Y) sequence, the CCAAT sequence (nucleotides -90 to -86), an Sp-1 sequence, and the two tandem SREs responded to cholesterol. The NF-Y-binding site, therefore, is essential for cholesterol response. Mutating the SREs or the NF-Y site and inserting 4 bp between the Sp-1- and NF-Y-binding sites both resulted in a minimal cholesterol response of the reporter genes. Electrophoretic mobility-shift assays using anti-SRE-binding protein (SREBP) and anti-NF-Ya antibodies confirmed that these SREs and the NF-Y site bind the respective factors. We also identified a second Sp-1 site located between nucleotides -40 and -30 that can substitute for the mutated Sp-1 site located between nucleotides -82 and -74. The reporter gene expression of the wild-type promoter and the Sp-1 site (nucleotides -82 to -74) mutant promoter was similar when SREBP1a [the N-terminal domain of SREBP (amino acids 1-520)] was constitutively overexpressed, suggesting that Sp-1 recruits SREBP to the SREs. Under the same conditions, an NF-Y site mutation resulted in significant loss of reporter gene expression, suggesting that NF-Y is required to activate the cholesterol response. | lld:pubmed |
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| pubmed-article:10759542 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10759542 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10759542 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10759542 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10759542 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10759542 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10759542 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10759542 | pubmed:author | pubmed-author:WakilS JSJ | lld:pubmed |
| pubmed-article:10759542 | pubmed:author | pubmed-author:ChiralaS SSS | lld:pubmed |
| pubmed-article:10759542 | pubmed:author | pubmed-author:XiongSS | lld:pubmed |
| pubmed-article:10759542 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10759542 | pubmed:day | 11 | lld:pubmed |
| pubmed-article:10759542 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:10759542 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10759542 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10759542 | pubmed:pagination | 3948-53 | lld:pubmed |
| pubmed-article:10759542 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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