Cited by 415Estrogen and related hormone effectsGenomics and Chromatin DynamicsAdrenal Hormones and Disorders

How glucocorticoid receptors modulate the activity of other transcription factors: A scope beyond tethering

Ratman, Dariusz, Vanden Berghe, Wim, Dejager, Lien, Libert, Claude, Tavernier, Jan, Beck, Ilse M., De Bosscher, Karolien·2013·Molecular and Cellular Endocrinology

Abstract

The activity of the glucocorticoid receptor (GR), a nuclear receptor transcription factor belonging to subclass 3C of the steroid/thyroid hormone receptor superfamily, is typically triggered by glucocorticoid hormones. Apart from driving gene transcription via binding onto glucocorticoid response elements in regulatory regions of particular target genes, GR can also inhibit gene expression via transrepression, a mechanism largely based on protein:protein interactions. Hereby GR can influence the activity of other transcription factors, without contacting DNA itself. GR is known to inhibit the activity of a growing list of immune-regulating transcription factors. Hence, GCs still rule the clinic for treatments of inflammatory disorders, notwithstanding concomitant deleterious side effects. Although patience is a virtue when it comes to deciphering the many mechanisms GR uses to influence various signaling pathways, the current review is testimony of the fact that groundbreaking mechanistic work has been accumulating over the past years and steadily continues to grow.

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Registry

Crossref · 10.1016/j.mce.2012.12.014

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172 of 172 references verified0 citation errors · 0 not checkable

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  • Nuclear receptors act by forming homodimers or heterodimers.

    “Nuclear receptors act by forming homodimers or heterodimers. For example, the glucocorticoid receptor [1] and estrogen receptor [2] form a homodimer, and insect ecdysone receptor (EcR) forms a heterodimer with an ultraspiracle protein (USP), the ortholog of retinoid X receptor in vertebrates [3].”

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Authors
Ratman, D., Vanden Berghe, W., Dejager, L., Libert, C., Tavernier, J., Beck, I. M., & De Bosscher, K.
Affiliations
  • Ghent University (BE)
  • Ghent University Hospital (BE)
Venue
Molecular and Cellular Endocrinology
Publisher
Elsevier BV
Published
2013-11
Volume
380
Issue
1-2
Pages
41-54
ISSN
0303-7207 (ISSN-L)
OpenAlex
W2067181732
Cited by
411
References
174
Citations by year
2026: 17 · 2025: 16 · 2024: 17 · 2023: 25 · 2022: 34 · 2021: 30 · 2020: 30 · 2019: 51 · 2018: 46 · 2017: 45 · 2016: 36 · 2015: 35 · 2014: 22 · 2013: 7
FWCI
2.51
Type
journal article
Language
en
Open access
closed
Locations
  • Molecular and Cellular Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • Ghent University Academic Bibliography (Ghent University) (submittedVersion)
Funders
  • Fonds Wetenschappelijk Onderzoek
  • Universiteit Antwerpen
  • Vlaamse regering
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
glucocorticoid receptor, transrepression, transcription factor regulation, protein-protein interaction, glucocorticoid response element, glucocorticoid signaling, inflammatory diseases, glucocorticoid adverse effects, nuclear receptors
MeSH terms
Animals, Chromatin, Humans, Protein Kinases, Protein Processing, Post-Translational, Receptors, Glucocorticoid, Transcription Factors, Transcriptional Activation, Response Elements, Epigenetic Repression

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