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| http://purl.uniprot.org/citations/7615825 | http://www.w3.org/2000/01/rdf-schema#comment | "We have used apolipoprotein genes to investigate the signal transduction mechanisms involved in the control of intestinal specific gene expression. The human apoAI, apoCIII, and apoAIV genes are tandemly organized within a 15-kb DNA segment and are expressed predominantly in the liver and intestine. Transient transfection of various human apoAI gene plasmid constructs into human hepatoma (HepG2) and colon carcinoma (Caco-2) cells showed that apoAI gene transcription is under the control of two separate and distinct cell-specific promoters. The region between nucleotides -192 and -41 is essential for expression in HepG2 cells, whereas the region from -595 to -192 is essential for expression in Caco-2 cells. A third 0.6 kb DNA fragment in the apoCIII gene promoter region, approximately 5 kb down-stream from the human apoAI gene, enhances transcription mediated by either of these two tissue-specific apoAI promoters. In Caco-2 cells, expression of the apoAI gene and activation by the distal enhancer required the presence of a nuclear hormone receptor response element (NHRRE) located in the -214 to -192 apoAI promoter region. Overexpression of the orphan receptor hepatocyte nuclear factor 4 (HNF-4), which binds to the NHRRE, dramatically stimulates apoAI gene expression in Caco-2 cells but not in HepG2 cells. Maximal stimulation of transcription by HNF-4 in Caco-2 cells required the presence of both the intestinal specific promoter, the NHRRE, and distal enhancer elements. Transactivation by HNF-4 thus appears to result from functional synergy between the NHRRE binding HNF-4 and distal DNA elements containing intestinal-specific DNA binding activities. The apoAI gene provides a model system to define the mechanism(s) governing intestinal cell specific gene regulation and the role of nuclear hormone receptors in the establishment and regulation of enterocytic gene transcription."xsd:string |
| http://purl.uniprot.org/citations/7615825 | http://purl.org/dc/terms/identifier | "doi:10.1172/jci118065"xsd:string |
| http://purl.uniprot.org/citations/7615825 | http://purl.uniprot.org/core/author | "Karathanasis S.K."xsd:string |
| http://purl.uniprot.org/citations/7615825 | http://purl.uniprot.org/core/author | "Ginsburg G.S."xsd:string |
| http://purl.uniprot.org/citations/7615825 | http://purl.uniprot.org/core/author | "Ozer J."xsd:string |
| http://purl.uniprot.org/citations/7615825 | http://purl.uniprot.org/core/date | "1995"xsd:gYear |
| http://purl.uniprot.org/citations/7615825 | http://purl.uniprot.org/core/name | "J Clin Invest"xsd:string |
| http://purl.uniprot.org/citations/7615825 | http://purl.uniprot.org/core/pages | "528-538"xsd:string |
| http://purl.uniprot.org/citations/7615825 | http://purl.uniprot.org/core/title | "Intestinal apolipoprotein AI gene transcription is regulated by multiple distinct DNA elements and is synergistically activated by the orphan nuclear receptor, hepatocyte nuclear factor 4."xsd:string |
| http://purl.uniprot.org/citations/7615825 | http://purl.uniprot.org/core/volume | "96"xsd:string |
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