| pubmed-article:16936639 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16936639 | lifeskim:mentions | umls-concept:C0108082 | lld:lifeskim |
| pubmed-article:16936639 | lifeskim:mentions | umls-concept:C0140283 | lld:lifeskim |
| pubmed-article:16936639 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:16936639 | lifeskim:mentions | umls-concept:C1621296 | lld:lifeskim |
| pubmed-article:16936639 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:16936639 | pubmed:dateCreated | 2006-10-3 | lld:pubmed |
| pubmed-article:16936639 | pubmed:abstractText | It is assumed that the retinoid X receptor (RXR) acts as a silent partner to the vitamin D receptor (VDR) with its only function to increase affinity of VDR/RXR to its DNA recognition site. In this study, we show that the RXR ligand 9-cis-retinoic acid (9-cis-RA) induces recruitment of coactivators by the DNA-bound heterodimer and potentiates vitamin D-dependent transcriptional responses. The presence of 9-cis-RA increases induction of cyp24 transcripts and differentiation of colon cancer cells by vitamin D, confers significant agonistic activity to a VDR ligand with very low agonistic activity and can even restore transcriptional activity of an AF-2 mutant VDR that causes hereditary rickets. This study shows that, in VDR/RXR heterodimers, allosteric communication triggered by the RXR ligand has a previously unrecognized role in vitamin D signalling, with important physiological and therapeutic implications. | lld:pubmed |
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| pubmed-article:16936639 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16936639 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16936639 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16936639 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:16936639 | pubmed:issn | 1469-221X | lld:pubmed |
| pubmed-article:16936639 | pubmed:author | pubmed-author:SteinmeyerAnd... | lld:pubmed |
| pubmed-article:16936639 | pubmed:author | pubmed-author:ArandaAnaA | lld:pubmed |
| pubmed-article:16936639 | pubmed:author | pubmed-author:CastilloAna... | lld:pubmed |
| pubmed-article:16936639 | pubmed:author | pubmed-author:Sánchez-Martí... | lld:pubmed |
| pubmed-article:16936639 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16936639 | pubmed:volume | 7 | lld:pubmed |
| pubmed-article:16936639 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16936639 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16936639 | pubmed:pagination | 1030-4 | lld:pubmed |
| pubmed-article:16936639 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16936639 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16936639 | pubmed:articleTitle | The retinoid X receptor ligand restores defective signalling by the vitamin D receptor. | lld:pubmed |
| pubmed-article:16936639 | pubmed:affiliation | Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, Arturo Duperier 4, Madrid 28029, Spain. | lld:pubmed |
| pubmed-article:16936639 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16936639 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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