Retinoid X Receptor β and Peroxisome Proliferator- Activated Receptor Activate an Estrogen Response Element
| Autor: | Walter Wahli, Hansjorg Keller Ken Wang, Keiko Ozato, James H. Segars, Susan B. Nunez, Jeffrey A. Medin |
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| Rok vydání: | 1995 |
| Předmět: |
Hormone response element
chemistry.chemical_classification Reporter gene Peroxisome proliferator-activated receptor Estrogen receptor Retinoid X receptor Biology Cell biology body regions Nuclear receptor chemistry Biochemistry embryonic structures lipids (amino acids peptides and proteins) Binding site Receptor hormones hormone substitutes and hormone antagonists |
| DOI: | 10.1016/b978-0-12-571150-0.50029-9 |
| Popis: | Publisher Summary This chapter discusses a study suggesting that an estrogen-responsive DNA element (ERE) can be specifically activated by cotransfection of the retinoid X receptor (RXR) and peroxisome proliferator-activated receptors (PPAR) in the absence of the estrogen receptor (ER). The specific nucleotide sequence of the ERE differs from the canonical RXR and PPAR element in the orientation and number of nucleotide spaces between half-sites of the element. The cotransfection of RXR and PPAR caused an augmentation of ERE-dependent reporter activity in the presence or absence of either 9-cis-RA or arachidonic acid. Transfection of either RXR or PPAR alone resulted in activation less than that observed when both expression vectors were introduced. The capacity of a single coregulator (RXR) to promote a discriminatory function in DNA site targeting suggested that binding site specificity is conferred both by RXR and the respective nuclear receptor partner. The activation of the ERE-dependent reporter gene by PPAR depends on the RXR as deletion of the DBD of RXR reduces the observed reporter activity. The finding of the experiment explained in the chapter that PPAR and RXR activate an estrogen-responsive element suggests that the two receptors are involved in a mechanism to generate diversity and tissue-specific regulation of estrogen-responsive genes. The concept that receptors other than the ER control estrogen responsive genes is supported by the presence of natural EREs such as in the rat oxytocin promoter, where the ER, TR, RAR and a COUP-like factor have been suggested to control expression of the gene. |
| Databáze: | OpenAIRE |
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