Evidence map›Paper›PMID 30659202›Full record

ArticleNature communications2019

E47 modulates hepatic glucocorticoid action.

M Charlotte Hemmer, Michael Wierer, Kristina Schachtrup, Michael Downes, Norbert Hübner, Ronald M Evans, N Henriette Uhlenhaut

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 56 citations in OpenAlex.

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  16. Nuclear Receptors in Energy Metabolism.Advances in experimental medicine and biology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 2 countries.

M Charlotte HemmerMolecular Endocrinology, Helmholtz Diabetes Center (HMGU) and German Center for Diabetes Research (DZD), IDO, Ingolstädter Landstr. 1, 85764, Neuherberg, Munich, Germany.
Michael WiererDepartment of Proteomics and Signal Transduction, Max Planck Institute for Biochemistry, Am Klopferspitz 18, 82152, Martinsried, Germany.
Kristina SchachtrupCenter for Chronic Immunodeficiency, University Medical Center and Faculty of Biology, University of Freiburg, 79106, Freiburg, Germany.
Michael DownesThe Salk Institute for Biological Studies & HHMI, 10010 N Torrey Pines Rd, La Jolla, CA, 92037, USA.
Norbert HübnerCardiovascular and Metabolic Sciences & DZHK (German Center for Cardiovascular Research), Charité-Universitätsmedizin & Berlin Institute of Health (BIH), Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle Strasse 10, 13125, Berlin, Germany.
Ronald M EvansThe Salk Institute for Biological Studies & HHMI, 10010 N Torrey Pines Rd, La Jolla, CA, 92037, USA.
N Henriette UhlenhautMolecular Endocrinology, Helmholtz Diabetes Center (HMGU) and German Center for Diabetes Research (DZD), IDO, Ingolstädter Landstr. 1, 85764, Neuherberg, Munich, Germany. henriette.uhlenhaut@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0002-4220-4779
Salk Institute for Biological Studies · USDeutsches Diabetes-Zentrum e.V. · DEMax Delbrück Center · DEMax Planck Institute of Biochemistry · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsChromatin ImmunoprecipitationFatty LiverGene Expression ProfilingGlucocorticoidsGlucoseLipid MetabolismLiverMaleMice, KnockoutReceptors, GlucocorticoidTranscription Factor 3GlucocorticoidsGlucoseReceptors, GlucocorticoidTranscription Factor 3

Identifiers

PMID30659202
PMCPMC6338785
OpenAlexW2910163863

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.