Signaling cross-talk between peroxisome proliferator-activated receptor/retinoid X receptor and estrogen receptor through estrogen response elements.

Details

Serval ID
serval:BIB_7B3DEF62D5F6
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Signaling cross-talk between peroxisome proliferator-activated receptor/retinoid X receptor and estrogen receptor through estrogen response elements.
Journal
Molecular Endocrinology
Author(s)
Keller H., Givel F., Perroud M., Wahli W.
ISSN
0888-8809[print], 0888-8809[linking]
Publication state
Published
Issued date
07/1995
Volume
9
Number
7
Pages
794-804
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
Peroxisome proliferator-activated receptors (PPARs) and retinoid X receptors (RXRs) are nuclear hormone receptors that are activated by fatty acids and 9-cis-retinoic acid, respectively. PPARs and RXRs form heterodimers that activate transcription by binding to PPAR response elements (PPREs) in the promoter of target genes. The PPREs described thus far consist of a direct tandem repeat of the AGGTCA core element with one intervening nucleotide. We show here that the vitellogenin A2 estrogen response element (ERE) can also function as a PPRE and is bound by a PPAR/RXR heterodimer. Although this heterodimer can bind to several other ERE-related palindromic response elements containing AGGTCA half-sites, only the ERE is able to confer transactivation of test reporter plasmids, when the ERE is placed either close to or at a distance from the transcription initiation site. Examination of natural ERE-containing promoters, including the pS2, very-low-density apolipoprotein II and vitellogenin A2 genes, revealed considerable differences in the binding of PPAR/RXR heterodimers to these EREs. In their natural promoter context, these EREs did not allow transcriptional activation by PPARs/RXRs. Analysis of this lack of stimulation of the vitellogenin A2 promoter demonstrated that PPARs/RXRs bind to the ERE but cannot transactivate due to a nonpermissive promoter structure. As a consequence, PPARs/RXRs inhibit transactivation by the estrogen receptor through competition for ERE binding. This is the first example of signaling cross-talk between PPAR/RXR and estrogen receptor.
Keywords
Base Sequence, Chromosome Mapping, Estrogens/metabolism, Fatty Acids/metabolism, Hela Cells, Humans, Molecular Sequence Data, Promoter Regions, Genetic/genetics, Receptors, Cytoplasmic and Nuclear/metabolism, Receptors, Estrogen/metabolism, Receptors, Retinoic Acid/metabolism, Retinoid X Receptors, Signal Transduction, Transcription Factors/metabolism, Transcriptional Activation, Tretinoin/metabolism, Vitellogenins/genetics, Vitellogenins/metabolism
Pubmed
Web of science
Create date
24/01/2008 16:04
Last modification date
20/08/2019 14:37
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