| http://purl.uniprot.org/citations/24819304 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24819304 | http://www.w3.org/2000/01/rdf-schema#comment | "CYP26A1 expression is very highly induced by retinoic acid (RA) in the liver, compared to most other tissues, suggesting that a liver-enriched factor may be required for its physiological transcriptional response. HNF4α is a highly conserved liver-specific/enriched member of nuclear receptor superfamily. In this study, we hypothesized that HNF4α and RARs may cooperate in an RA-dependent manner to induce a high level of CYP26A1 expression in liver cells. Partial inhibition of endogenous HNF4α by siRNA reduced the level of RA-induced CYP26A1 mRNA in HepG2 cells. Cotransfection of HNF4α, with or without RARs, demonstrated RA-dependent activation of a human CYP26A1 promoter-luciferase construct. Analysis of a 2.5-kbp putative CYP26A1 promoter sequence identified five potential HNF4α DNA response elements: H1 located in a proximal region overlapping with an RAR element-1 (RARE1 or R1); H2 and H3 in the distal region, close to RARE2 (R2) and RARE3 (R3); and H4 and H5 in intermediary regions. In EMSA and ChIP analyses HNF4α and RARs binding in the proximal and distal CYP26A1 promoter regions was significantly higher in RA-treated cells. Mutational analysis of the individual HNF4α DNA-response elements identified H1 as the major site for HNF4α binding because mutation of H1 inhibited the promoter activity by ~90%, followed by H2 mutation with less than 40% inhibition. Our results indicate that HNF4α coordinates with RARs in an RA-dependent manner to strongly induce CYP26A1 gene expression in the liver, which may explain the high level of response to RA observed in vivo."xsd:string |
| http://purl.uniprot.org/citations/24819304 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcb.24839"xsd:string |
| http://purl.uniprot.org/citations/24819304 | http://purl.uniprot.org/core/author | "Ross A.C."xsd:string |
| http://purl.uniprot.org/citations/24819304 | http://purl.uniprot.org/core/author | "Zolfaghari R."xsd:string |
| http://purl.uniprot.org/citations/24819304 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24819304 | http://purl.uniprot.org/core/name | "J Cell Biochem"xsd:string |
| http://purl.uniprot.org/citations/24819304 | http://purl.uniprot.org/core/pages | "1740-1751"xsd:string |
| http://purl.uniprot.org/citations/24819304 | http://purl.uniprot.org/core/title | "Hepatocyte nuclear factor 4alpha (HNF4alpha) in coordination with retinoic acid receptors increases all-trans-retinoic acid-dependent CYP26A1 gene expression in HepG2 human hepatocytes."xsd:string |
| http://purl.uniprot.org/citations/24819304 | http://purl.uniprot.org/core/volume | "115"xsd:string |
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