ArticleMolecular and cellular biology1993
Functional characterization of the L-type pyruvate kinase gene glucose response complex.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 113 citations in OpenAlex.
- Modulating glucocorticoid receptor actions in physiology and pathology: Insights from coregulators.Pharmacology & therapeutics · 2023Review
- HNF4α isoforms: the fraternal twin master regulators of liver function.Frontiers in endocrinology · 2023Review
- Article
- Deletion of hepatic carbohydrate response element binding protein (ChREBP) impairs glucose homeostasis and hepatic insulin sensitivity in mice.Molecular metabolism · 2017Article
- Identification of HNF-4α as a key transcription factor to promote ChREBP expression in response to glucose.Scientific reports · 2016Article
- Transcriptional regulation of hepatic lipogenesis.Nature reviews. Molecular cell biology · 2015Review
- Acute exercise reduces hepatic glucose production through inhibition of the Foxo1/HNF-4alpha pathway in insulin resistant mice.The Journal of physiology · 2010Article
- Monosaccharide-induced lipogenesis regulates the human hepatic sex hormone-binding globulin gene.The Journal of clinical investigation · 2007Article
- Polyunsaturated fatty acids suppress glycolytic and lipogenic genes through the inhibition of ChREBP nuclear protein translocation.The Journal of clinical investigation · 2005Article
- Glucose mediates transcriptional repression of the human angiotensin type-1 receptor gene: role for a novel cis-acting element.Molecular biology of the cell · 2004Article
- New perspectives in the regulation of hepatic glycolytic and lipogenic genes by insulin and glucose: a role for the transcription factor sterol regulatory element binding protein-1c.The Biochemical journal · 2002Review
- Activation of glucokinase gene expression by hepatic nuclear factor 4alpha in primary hepatocytes.The Biochemical journal · 2002Article
- Promoter I of the ovine acetyl-CoA carboxylase-alpha gene: an E-box motif at -114 in the proximal promoter binds upstream stimulatory factor (USF)-1 and USF-2 and acts as an insulin-response sequence in differentiating adipocytes.The Biochemical journal · 2001Article
- Spot 14 protein interacts and co-operates with chicken ovalbumin upstream promoter-transcription factor 1 in the transcription of the L-type pyruvate kinase gene through a specificity protein 1 (Sp1) binding site.The Biochemical journal · 2001Article
- An indirect role for upstream stimulatory factor in glucose-mediated induction of pyruvate kinase and S14 gene expression.Molecular and cellular biochemistry · 2000Article
- Upstream stimulatory factor regulates Pdx-1 gene expression in differentiated pancreatic beta-cells.The Biochemical journal · 1999Article
- Nutrient and hormonal regulation of pyruvate kinase gene expression.The Biochemical journal · 1999Review
- Two HNF-1 binding sites govern the glucose repression of the human sucrase-isomaltase promoter.The Biochemical journal · 1998Article
- Identification of upstream stimulatory factor as transcriptional activator of the liver promoter of the glucokinase gene.The Biochemical journal · 1998Article
- Multiple parameters determine the specificity of transcriptional response by nuclear receptors HNF-4, ARP-1, PPAR, RAR and RXR through common response elements.Nucleic acids research · 1998Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
L-type pyruvate kinase (L-PK) gene expression is modulated by hormonal and nutritional conditions. We have previously shown that the glucose/insulin response element (GlRE) of the L-PK gene is built around two noncanonical E boxes (element L4) that cooperate closely with a contiguous binding site (element L3). We present in this report the identification of proteins that interact with both elements. The L3 site binds hepatocyte nuclear factor 4 (HNF4)- and COUP/TF-related proteins. In fibroblasts, the overexpression of HNF4 transactivates the L-PK promoter. On the contrary, COUP/TF strongly inhibits the active promoter in hepatocytes. The L4 site binds the major late transcription factor (MLTF) in vitro and ex vivo; mutations that suppress this binding activity also inactivated the GlRE function. Mutations transforming one or two noncanonical E boxes of element L4 into consensus MLTF/USF binding sites strongly increase the affinity for MLTF/USF and do not impair the glucose responsiveness. However, merely the ability to bind MLTF/USF does not seem to be sufficient to confer a GlRE activity: those elements in which one E box has been destroyed and the other has been transformed into a consensus MLTF/USF sequence bind MLTF/USF efficiently but do not confer a high glucose responsiveness on the L-PK gene promoter. Consequently, the full activity of the L-PK GlRE seems to require the cooperation between two putative MLTF/USF binding sites located in the vicinity of an HNF4 binding site.
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