ArticleMolecular and cellular biology1991
Synergistic interactions between transcription factors control expression of the apolipoprotein AI gene in liver cells.
Article in Molecular and cellular biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 126 citations in OpenAlex.
- NKX2.2 and KLF4 cooperate to regulate α-cell identity.Genes & development · 2025Article
- FOXO1 and LXRα downregulate the apolipoprotein A-I gene expression during hydrogen peroxide-induced oxidative stress in HepG2 cells.Cell stress & chaperones · 2017Article
- The nuclear receptors COUP-TF: a long-lasting experience in forebrain assembly.Cellular and molecular life sciences : CMLS · 2014Review
- Pioglitazone increases apolipoprotein A-I production by directly enhancing PPRE-dependent transcription in HepG2 cells.Journal of lipid research · 2010Article
- Proteomics reveals a physical and functional link between hepatocyte nuclear factor 4alpha and transcription factor IID.The Journal of biological chemistry · 2009Article
- High density lipoprotein, apolipoprotein A-I, and coronary artery disease.Molecular and cellular biochemistry · 2000Review
- Mechanism of action of niacin on lipoprotein metabolism.Current atherosclerosis reports · 2000Review
- The full induction of human apoprotein A-I gene expression by the experimental nephrotic syndrome in transgenic mice depends on cis-acting elements in the proximal 256 base-pair promoter region and the trans-acting factor early growth response factor 1.The Journal of clinical investigation · 1998Article
- E1A represses apolipoprotein AI enhancer activity in liver cells through a pRb- and CBP-independent pathway.Nucleic acids research · 1998Article
- Functional domains of the human orphan receptor ARP-1/COUP-TFII involved in active repression and transrepression.Molecular and cellular biology · 1997Article
- Identification of a cis-acting regulatory element conferring inducibility of the atrial natriuretic factor gene in acute pressure overload.The Journal of clinical investigation · 1997Article
- Modification of apolipoprotein(a) lysine binding site reduces atherosclerosis in transgenic mice.The Journal of clinical investigation · 1997Article
- Intestinal transcription and synthesis of apolipoprotein AI is regulated by five natural polymorphisms upstream of the apolipoprotein CIII gene.The Journal of clinical investigation · 1997Article
- Opposite regulation of human versus mouse apolipoprotein A-I by fibrates in human apolipoprotein A-I transgenic mice.The Journal of clinical investigation · 1996Article
- Article
- Intestinal apolipoprotein AI gene transcription is regulated by multiple distinct DNA elements and is synergistically activated by the orphan nuclear receptor, hepatocyte nuclear factor 4.The Journal of clinical investigation · 1995Article
- Transcriptional activation by the orphan nuclear receptor ARP-1.Nucleic acids research · 1995Article
- Transcription factors as drug targets: opportunities for therapeutic selectivity.Gene expression · 1995Review
- Transcriptional regulation of the apoAI gene by hepatic nuclear factor 4 in yeast.Nucleic acids research · 1994Article
- Transactivation and repression of the alpha-fetoprotein gene promoter by retinoid X receptor and chicken ovalbumin upstream promoter transcription factor.Nucleic acids research · 1994Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The gene coding for apolipoprotein AI (apoAI), a plasma protein involved in the transport of cholesterol and other lipids in the plasma, is expressed predominantly in liver and intestine. Previous work in our laboratory has shown that different cis-acting elements in the 5'-flanking region of the human apoAI gene control its expression in human hepatoma (HepG2) and colon carcinoma (Caco-2) cells. Hepatocyte-specific expression is mediated by elements within the -256 to -41 DNA region relative to the apoAI gene transcription start site (+1). In this study it was found that the -222 to -110 apoAI gene region is necessary and sufficient for expression in HepG2 cells. It was also found that this DNA region functions as a powerful hepatocyte-specific transcriptional enhancer. Gel retardation and DNase I protection experiments showed that HepG2 cells contain proteins that bind to specific sites, sites A (-214 to -192), B (-169 to -146), and C (-134 to -119), within this enhancer. Site-directed mutagenesis that prevents binding of these proteins to individual or different combinations of these sites followed by functional analysis of these mutants in HepG2 cells revealed that protein binding to any one of these sites in the absence of binding to the others was not sufficient for expression. Binding to any two of these sites in any combination was sufficient for only low levels of expression. Binding to all three sites was essential for maximal expression. These results indicate that the transcriptional activity of the apoAI gene in liver cells is dependent on synergistic interactions between transcription factors bound to its enhancer.
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