ArticleMolecular and cellular biology2000
Elevated levels of hepatocyte nuclear factor 3beta in mouse hepatocytes influence expression of genes involved in bile acid and glucose homeostasis.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 102 citations in OpenAlex.
- Spermatogonial Gene Networks Selectively Couple to Glutathione and Pentose Phosphate Metabolism but Not Cysteine Biosynthesis.iScience · 2021Article
- The extracellular sulfatase SULF2 promotes liver tumorigenesis by stimulating assembly of a promoter-looping GLI1-STAT3 transcriptional complex.The Journal of biological chemistry · 2020Article
- FOXA2 alleviates CClScientific reports · 2017Article
- Transcription factor binding site enrichment analysis predicts drivers of altered gene expression in nonalcoholic steatohepatitis.Biochemical pharmacology · 2016Article
- Clinical application of transcriptional activators of bile salt transporters.Molecular aspects of medicine · 2014Review
- Foxa1 reduces lipid accumulation in human hepatocytes and is down-regulated in nonalcoholic fatty liver.PloS one · 2012Article
- Genetic predictors of interindividual variability in hepatic CYP3A4 expression.The Journal of pharmacology and experimental therapeutics · 2010Article
- Transcriptional regulation of glucose sensors in pancreatic β-cells and liver: an update.Sensors (Basel, Switzerland) · 2010Review
- Bile acid transporters.Journal of lipid research · 2009Review
- Growth hormone-activated STAT5 may indirectly stimulate IGF-I gene transcription through HNF-3{gamma}.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Global analysis of in vivo Foxa2-binding sites in mouse adult liver using massively parallel sequencing.Nucleic acids research · 2008Article
- Transcriptional activation by growth hormone of HNF-6-regulated hepatic genes, a potential mechanism for improved liver repair during biliary injury in mice.American journal of physiology. Gastrointestinal and liver physiology · 2008Article
- Hepatocyte-specific ablation of Foxa2 alters bile acid homeostasis and results in endoplasmic reticulum stress.Nature medicine · 2008Article
- Bile acid transporters in health and disease.Xenobiotica; the fate of foreign compounds in biological systems · 2008Review
- BRE is an antiapoptotic protein in vivo and overexpressed in human hepatocellular carcinoma.Oncogene · 2008Article
- Farnesoid X receptor, hepatocyte nuclear factors 1alpha and 3beta are essential for transcriptional activation of the liver-specific organic anion transporter-2 gene.Journal of gastroenterology · 2006Article
- Increased expression of hepatocyte nuclear factor 6 stimulates hepatocyte proliferation during mouse liver regeneration.Gastroenterology · 2006Article
- C/EBPalpha and HNF6 protein complex formation stimulates HNF6-dependent transcription by CBP coactivator recruitment in HepG2 cells.Hepatology (Baltimore, Md.) · 2006Article
- Transgenic rescue of insulin receptor-deficient mice.The Journal of clinical investigation · 2004Article
- Foxm1b transcription factor is essential for development of hepatocellular carcinomas and is negatively regulated by the p19ARF tumor suppressor.Genes & development · 2004Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The winged helix transcription factor, hepatocyte nuclear factor-3beta (HNF-3beta), mediates the hepatocyte-specific transcription of numerous genes important for liver function. However, the in vivo role of HNF-3beta in regulating these genes remains unknown because homozygous null HNF3beta mouse embryos die in utero prior to liver formation. In order to examine the regulatory function of HNF-3beta, we created transgenic mice in which the -3-kb transthyretin promoter functions to increase hepatocyte expression of the rat HNF-3beta protein. Postnatal transgenic mice exhibit growth retardation, depletion of hepatocyte glycogen storage, and elevated levels of bile acids in serum. The retarded growth phenotype is likely due to a 20-fold increase in hepatic expression of insulin-like growth factor binding protein 1 (IGFBP-1), which results in elevated levels in serum of IGFBP-1 and limits the biological availability of IGFs required for postnatal growth. The defects in glycogen storage and serum bile acids coincide with diminished postnatal expression of hepatocyte genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase and glycogen synthase) and sinusoidal bile acid uptake (Ntcp), respectively. These changes in gene transcription may result from the disruptive effect of HNF-3beta on the hepatic expression of the endogenous mouse HNF-3alpha,-3beta, -3gamma, and -6 transcription factors. Furthermore, adult transgenic livers lack expression of the canalicular phospholipid transporter, mdr2, which is consistent with ultrastructure evidence of damage to transgenic hepatocytes and bile canaliculi. These transgenic studies represent the first in vivo demonstration that the HNF-3beta transcriptional network regulates expression of hepatocyte-specific genes required for bile acid and glucose homeostasis, as well as postnatal growth.
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