| pubmed-article:16763553 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16763553 | lifeskim:mentions | umls-concept:C0008377 | lld:lifeskim |
| pubmed-article:16763553 | lifeskim:mentions | umls-concept:C0040845 | lld:lifeskim |
| pubmed-article:16763553 | lifeskim:mentions | umls-concept:C0073099 | lld:lifeskim |
| pubmed-article:16763553 | lifeskim:mentions | umls-concept:C0220781 | lld:lifeskim |
| pubmed-article:16763553 | lifeskim:mentions | umls-concept:C0870883 | lld:lifeskim |
| pubmed-article:16763553 | lifeskim:mentions | umls-concept:C1883254 | lld:lifeskim |
| pubmed-article:16763553 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:16763553 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:16763553 | pubmed:dateCreated | 2006-7-12 | lld:pubmed |
| pubmed-article:16763553 | pubmed:abstractText | Retinoic acid (RA) constitutes the major active ingredient of vitamin A and is required for various biological processes. The tissue RA level is maintained through a cascade of metabolic reactions where retinal dehydrogenases (RALDHs) catalyze the terminal reaction of RA biosynthesis from retinal, a rate-limiting step. We showed that dietary supplement of cholesterol enhanced the expression of RALDH1 and 2 genes and the cellular RA content in vital organs such as brain, kidney, liver and heart. Consistently, the cholesterol-lowering agent (pravastatin sodium) downregulated the expression of RALDH1 and 2 genes in several organs especially the liver and in cultured liver cells. Further, cholesterol metabolites, predominantly the oxysterols, the natural ligands for liver X receptor (LXR), induced these genes via upregulation of sterol regulatory element binding protein-1c (SREBP-1c) that bound to the regulatory regions of these genes. Knockdown of LXRalpha/beta or SREBP-1c downregulated the expression of RALDH genes, which could be rescued by re-expressing SREBP-1c, suggesting SREBP-1c as a direct positive regulator for these genes. This study uncovered a novel crosstalk between cholesterol and RA biosynthesis. | lld:pubmed |
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| pubmed-article:16763553 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16763553 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16763553 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16763553 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:16763553 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:16763553 | pubmed:author | pubmed-author:WeiLi-NaLN | lld:pubmed |
| pubmed-article:16763553 | pubmed:author | pubmed-author:GuptaPawanP | lld:pubmed |
| pubmed-article:16763553 | pubmed:author | pubmed-author:HuqM D... | lld:pubmed |
| pubmed-article:16763553 | pubmed:author | pubmed-author:TsaiNien-PeiN... | lld:pubmed |
| pubmed-article:16763553 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16763553 | pubmed:day | 12 | lld:pubmed |
| pubmed-article:16763553 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:16763553 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16763553 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16763553 | pubmed:pagination | 3203-13 | lld:pubmed |
| pubmed-article:16763553 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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