ArticleMolecular and cellular biology1995
A STAT factor mediates the sexually dimorphic regulation of hepatic cytochrome P450 3A10/lithocholic acid 6 beta-hydroxylase gene expression by growth hormone.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 66 citations in OpenAlex.
- Classical and novel GH receptor signaling pathways.Molecular and cellular endocrinology · 2020Review
- Hypothesis: Neuroendocrine Mechanisms (Hypothalamus-Growth Hormone-STAT5 Axis) Contribute to Sex Bias in Pulmonary Hypertension.Molecular medicine (Cambridge, Mass.) · 2015Article
- Review
- Growth hormone-dependent changes in the rat lung proteome during alveorization.Molecular and cellular biochemistry · 2009Article
- Sex-specific early growth hormone response genes in rat liver.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Transgenic mice showing inflammation-inducible overexpression of granulocyte macrophage colony-stimulating factor.Clinical and diagnostic laboratory immunology · 2004Article
- Suppression of sterol 12alpha-hydroxylase transcription by the short heterodimer partner: insights into the repression mechanism.Nucleic acids research · 2001Article
- Role of FXR and FTF in bile acid-mediated suppression of cholesterol 7alpha-hydroxylase transcription.Nucleic acids research · 2000Article
- The role of STAT proteins in growth hormone signaling.Oncogene · 2000Review
- Hepatocyte nuclear factor 6: organization and chromosomal assignment of the rat gene and characterization of its promoter.The Biochemical journal · 1998Article
- Male-specific transcription initiation of the C4-Slp gene in mouse liver follows activation of STAT5.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- STAT 5 and NF-Y are involved in expression and growth hormone-mediated sexually dimorphic regulation of cytochrome P450 3A10/lithocholic acid 6beta-hydroxylase.Nucleic acids research · 1998Article
- Requirement of STAT5b for sexual dimorphism of body growth rates and liver gene expression.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Organization and chromosomal localization of the gene encoding the mouse acid labile subunit of the insulin-like growth factor binding complex.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Growth hormone (GH) action in the brain: neural expression of a GH-response gene.Journal of molecular neuroscience : MNArticle
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Adult male rodents have a pulsatile profile of growth hormone (GH) release, whereas female rodents have a relatively steady-state pattern with uniform, albeit lower levels of GH. The expression of a number of sexually differentiated hepatic proteins is primarily determined by these plasma GH profiles and only secondarily regulated by gonadal hormones. An important subset of these sexually dimorphic proteins is cytochrome P450s. CYP3A10/6 beta-hydroxylase is a cytochrome P450 that catalyzes the 6 beta-hydroxylation of lithocholic acid. CYP3A10/6 beta-hydroxylase is expressed only in male hamsters; however, mimicking the male GH secretion pattern in females induces expression of the gene to male levels. Using chimeric CYP3A10/6 beta-hydroxylase promoter/luciferase reporter genes transfected into hamster primary hepatocytes, we have shown a GH-mediated induction of promoter activity. A combination of 5'-deletion constructs, heterologous promoter constructs, and specific mutagenesis was used to localize the DNA element involved in the GH-mediated regulation of CYP3A10/6 beta-hydroxylase promoter activity, which resembles a STAT binding site. Footprint and gel shift analyses confirmed that the expression of the protein binding to this site is regulated by GH and that the DNA-protein complex can be partially supershifted by anti-STAT-5 antibodies. This protein is 50% more abundant in male than in female hamster livers, is absent in hypophysectomized female livers, and is restored when hypophysectomized females are injected with GH in a manner that masculinizes female hamsters in terms of CYP3A10/6 beta-hydroxylase expression. The system characterized and described here is ideally suited for dissecting the molecular details governing the sexually dimorphic expression of liver-specific genes.
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