6533b870fe1ef96bd12cf2bc

RESEARCH PRODUCT

The analysis of modified peroxisome proliferator responsive elements of the peroxisomal bifunctional enzyme in transfected HepG2 cells reveals two regulatory motifs

Olivier BardotNorbert LatruffeMarie Claude ClemencetPatricia Passilly

subject

Peroxisome proliferator-activated receptor gammaReceptors Retinoic AcidSteroid hormone receptorMolecular Sequence DataResponse elementBiophysicsReceptors Cytoplasmic and NuclearPeroxisome proliferator-activated receptorchemical and pharmacologic phenomenaIn Vitro TechniquesRegulatory Sequences Nucleic AcidRetinoid X receptorBiologyPeroxisomal Bifunctional EnzymeTransfectionMicrobodiesBiochemistryGene Expression Regulation EnzymologicTranscriptional activationPeroxisomal Bifunctional EnzymeMultienzyme ComplexesStructural BiologyPeroxisome proliferator response element9-cis Retinoic acid receptor alphaTumor Cells CulturedGeneticsHumansRNA MessengerIsomerasesEnoyl-CoA HydrataseMolecular Biologychemistry.chemical_classificationBinding SitesBase Sequence3-Hydroxyacyl CoA DehydrogenasesPeroxisome proliferator-activated receptorCell BiologyDNA-Binding ProteinsRetinoic acid receptorRetinoid X ReceptorsLiverOligodeoxyribonucleotidesBiochemistrychemistryRat peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenaseEnzyme InductionPeroxisome proliferator-activated receptor alphaTranscription Factors

description

AbstractPeroxisome proliferators (PPs) are non-genotoxic carcinogens in rodents. They can induce the expression of numerous genes via the heterodimerization of two members of the steroid hormone receptor superfamily, called the peroxisome proliferator-activated receptor (PPAR) and the 9-cis retinoic acid receptor (RXR). Many of the PP responsive genes possess a peroxisome proliferator response element (PPRE) formed by two TGACCT-related motifs. The bifunctional enzyme (HD) PPRE contains 3 such motifs, creating DR1 and DR2 sequences. PPAR and RXR regulate transcription via the DR1 element while DR2 modulates the expression of the gene via auxiliary factors in HepG2 cells.

yearjournalcountryeditionlanguage
1995-02-27FEBS Letters
https://doi.org/10.1016/0014-5793(95)00097-s