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as soon as is submitted to ZB.
E47 modulates hepatic glucocorticoid action.
Nat. Commun. 10:306 (2019)
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.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
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11.878
2.805
14
23
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Transcription Factors; Metabolic Syndrome; Read Alignment; Receptor; Mediator; Liver; Gene; E2a; Foxo1; Inflammation
Language
english
Publication Year
2019
HGF-reported in Year
2019
ISSN (print) / ISBN
2041-1723
e-ISSN
2041-1723
Journal
Nature Communications
Quellenangaben
Volume: 10,
Issue: 1,
Article Number: 306
Publisher
Nature Publishing Group
Publishing Place
London
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Cancer (IDC)
POF-Topic(s)
90000 - German Center for Diabetes Research
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-501900-227
WOS ID
WOS:000456010800003
Scopus ID
85060162087
PubMed ID
30659202
Erfassungsdatum
2019-02-27