ArticleNucleic acids research1993
Competition between transcription factors HNF1 and HNF3, and alternative cell-specific activation by DBP and C/EBP contribute to the regulation of the liver-specific aldolase B promoter.
Article in Nucleic acids research, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 63 citations in OpenAlex.
- Functional analyses of the mutation nt-128 T→G in the hepatocyte nuclear factor-1α promoter region in Chinese diabetes pedigrees.Diabetic medicine : a journal of the British Diabetic Association · 2012Article
- Mutations in the promoter region of the aldolase B gene that cause hereditary fructose intolerance.Journal of inherited metabolic disease · 2010Article
- Distinct regulation of hepatic nuclear factor 1alpha by NKX6.1 in pancreatic beta cells.The Journal of biological chemistry · 2010Article
- Environment-specific combinatorial cis-regulation in synthetic promoters.Molecular systems biology · 2009Article
- Kidney-specific activity of the bovine uromodulin promoter.Transgenic research · 2003Article
- Microarray analyses during adipogenesis: understanding the effects of Wnt signaling on adipogenesis and the roles of liver X receptor alpha in adipocyte metabolism.Molecular and cellular biology · 2002Article
- pha-4, an HNF-3 homolog, specifies pharyngeal organ identity in Caenorhabditis elegans.Genes & development · 1998Article
- Hereditary fructose intolerance.Journal of medical genetics · 1998Review
- A specific distal promoter controls gamma-glutamyl transpeptidase gene expression in undifferentiated rat transformed liver cells.The Biochemical journal · 1997Article
- C/EBPbeta is a negative regulator of human papillomavirus type 11 in keratinocytes.Journal of virology · 1996Article
- Role of the liver-enriched transcription factor hepatocyte nuclear factor 1 in transcriptional regulation of the factor V111 gene.Molecular and cellular biology · 1996Article
- Overproduction of a truncated hepatocyte nuclear factor 3 protein inhibits expression of liver-specific genes in hepatoma cells.Molecular and cellular biology · 1995Article
- Tissue-specific and ubiquitous factors binding next to the glucocorticoid receptor modulate transcription from the mouse mammary tumor virus promoter.Journal of virology · 1995Article
- Initiation zone of DNA replication at the aldolase B locus encompasses transcription promoter region.Nucleic acids research · 1994Article
- Genetic analysis of a transcriptional activation pathway by using hepatoma cell variants.Molecular and cellular biology · 1994Article
- Transcriptional control of genes that regulate glycolysis and gluconeogenesis in adult liver.The Biochemical journal · 1994Review
- Members of the CAAT/enhancer-binding protein, hepatocyte nuclear factor-1 and nuclear factor-1 families can differentially modulate the activities of the rat alpha-fetoprotein promoter and enhancer.The Biochemical journal · 1994Article
- Activity of the rat liver-specific aldolase B promoter is restrained by HNF3.Nucleic acids research · 1994Article
- Setting limits on homeotic gene function: restraint of Sex combs reduced activity by teashirt and other homeotic genes.The EMBO journal · 1994Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aldolase B proximal promoter is controlled by at least five elements spanning from -190 to -103 bp with respect to the start site of transcription. From 5' to 3', we found: a negative DE element, an activating C/EBP-DBP binding site, a CCAAT box binding NFY that seems to play a negative role, and an activating element consisting of two overlapping binding sites for HNF-1 and HNF-3. Contransfection experiments of aldolase B/CAT constructs and of expression vectors for different transcription factors were carried out in human hepatoma Hep G2 cells. We found that DBP and HNF-1 are strong transactivators of the aldolase B promoter while C/EBP and vHNF-1 are only weak activators and HNF-3 alone does not modify such activity. Deletion of the distal negative element results in a similar transactivation by C/EBP and DBP, enhanced for the former and reduced for the latter. In hepatocytes in primary culture, the strong transactivator is C/EBP while DBP is essentially inactive. This tissue-specificity of C/EBP and DBP action could depend on interaction with tissue-specific proteins bound to a neighbouring site, probably DE. Finally, HNF3 behaves as a very strong anti-activator of the aldolase B promoter. It competitively antagonizes transactivation by HNF-1 and non-competitively transactivation by DBP. This negative effect of HNF-3 and tissue-specificity of the transactivation potential of DBP and C/EBP are unique features of the aldolase B promoter.
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