The proximal element of the human apolipoprotein A-II promoter increases the enhancer activity of the distal region
Autor: | Philippe Cardot, Esther Fourniat, Agnès Ribeiro, Danièle Pastier, Jean Chambaz, Jean-Marc Lacorte |
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Rok vydání: | 1996 |
Předmět: |
Chloramphenicol O-Acetyltransferase
Transcriptional Activation Transcription Genetic Recombinant Fusion Proteins TATA box Response element Enhancer RNAs Biology Transfection Polymerase Chain Reaction Biochemistry Gene Expression Regulation Enzymologic Transcription (biology) Chlorocebus aethiops Animals Humans Binding site Promoter Regions Genetic Enhancer Molecular Biology DNA Primers Orphan receptor Binding Sites Base Sequence Basic Helix-Loop-Helix Leucine Zipper Transcription Factors Cell Biology Phosphoproteins TATA Box Molecular biology DNA-Binding Proteins Enhancer Elements Genetic Hepatocyte Nuclear Factor 4 Hepatocyte nuclear factor 4 COS Cells Mutagenesis Site-Directed lipids (amino acids peptides and proteins) Apolipoprotein A-II Transcription Factors Research Article |
Zdroj: | ResearcherID |
ISSN: | 1470-8728 0264-6021 |
DOI: | 10.1042/bj3180681 |
Popis: | We have previously shown that human apolipoprotein A-II (apoA-II) transcription is controlled by a complex set of regulatory elements. In this study, we demonstrate that the distal region of the apoA-II promoter (-911/-614) acts as an enhancer and results in a 6-fold increase in activity when the proximal AB element is inserted between this enhancer and a TATA box. The AB element alone does not display any transcriptional activity. The combination of the proximal AB element and the enhancer is sufficient to activate transcription to the same level as that achieved with the full-length promoter. DNA binding and competition assays, and binding interference experiments allowed us to identify two adjacent binding sites within the AB element. These bind activities designated CIIIB1 and AIIAB3/4, respectively. Mutation on each of these sites showed that the binding site of CIIIB1 within the AB element played a major role in the interaction with the enhancer. Whereas transcriptional activation of other apolipoprotein genes involves the binding of the liver-enriched hepatocyte nuclear factor 4 (HNF4) on their proximal promoter, the present study demonstrates that neither HNF4 nor ApoA-I regulatory protein 1, its antagonistic orphan receptor, was able to bind the AB element. Instead, apoA-II transcription was driven by the interaction of apoA-II enhancer with proximal AB element, which involves an unidentified activity, CIIIB1. |
Databáze: | OpenAIRE |
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