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  E47 modulates hepatic glucocorticoid action

Hemmer, M. C., Wierer, M., Schachtrup, K., Downes, M., Huebner, N., Evans, R. M., et al. (2019). E47 modulates hepatic glucocorticoid action. Nature Communications, 10: 306. doi:10.1038/s41467-018-08196-5.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0003-4025-B Version Permalink: http://hdl.handle.net/21.11116/0000-0003-4026-A
Genre: Journal Article

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 Creators:
Hemmer, M. Charlotte1, Author
Wierer, Michael2, Author              
Schachtrup, Kristina1, Author
Downes, Michael1, Author
Huebner, Norbert1, Author
Evans, Ronald M.1, Author
Uhlenhaut, N. Henriette1, Author
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1external, ou_persistent22              
2Mann, Matthias / Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565159              

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Free keywords: TRANSCRIPTION FACTORS; METABOLIC SYNDROME; READ ALIGNMENT; RECEPTOR; MEDIATOR; LIVER; GENE; E2A; FOXO1; INFLAMMATIONScience & Technology - Other Topics;
 Abstract: Glucocorticoids (GCs) are effective drugs, but their clinical use is compromised by severe side effects including hyperglycemia, hyperlipidemia and obesity. They bind to the Glucocorticoid Receptor (GR), which acts as a transcription factor. The activation of metabolic genes by GR is thought to underlie these adverse effects. We identify the bHLH factor E47 as a modulator of GR target genes. Using mouse genetics, we find that E47 is required for the regulation of hepatic glucose and lipid metabolism by GR, and that loss of E47 prevents the development of hyperglycemia and hepatic steatosis in response to GCs. Here we show that E47 and GR co-occupy metabolic promoters and enhancers. E47 is needed for the efficient recruitment of GR and coregulators such as Mediator to chromatin. Altogether, our results illustrate how GR and E47 regulate hepatic metabolism, and might provide an entry point for novel therapies with reduced side effects.

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Language(s): eng - English
 Dates: 2019
 Publication Status: Published online
 Pages: 13
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 Table of Contents: -
 Rev. Method: -
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Title: Nature Communications
  Abbreviation : Nat. Commun.
Source Genre: Journal
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Publ. Info: London : Nature Publishing Group
Pages: - Volume / Issue: 10 Sequence Number: 306 Start / End Page: - Identifier: ISSN: 2041-1723
CoNE: https://pure.mpg.de/cone/journals/resource/2041-1723