The DOI matches its Crossref record; 172 of the 174 references it cites were found in a registry or an index.
How glucocorticoid receptors modulate the activity of other transcription factors: A scope beyond tethering
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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“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].”
From G-protein-coupled receptor participates in 20-hydroxyecdysone signaling on the plasma membrane (2014) · cites this paper as [1]
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1 retracted
RETRACTED: Maturation of MicroRNA Is Hormonally Regulated by a Nuclear Receptor
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RetractedComprehensive Mapping of Long-Range Interactions Reveals Folding Principles of the Human Genome
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The peroxisome proliferator-activated receptor-γ is a negative regulator of macrophage activation
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Mechanisms involved in the side effects of glucocorticoids
SCHACKE, H. (2002) · Pharmacology & Therapeutics · doi:10.1016/s0163-7258(02)00297-8 · Cited by 1,847
Molecular and Cellular Endocrinology
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HDAC6 Regulates Hsp90 Acetylation and Chaperone-Dependent Activation of Glucocorticoid Receptor
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Activation of human aortic smooth-muscle cells is inhibited by PPARα but not by PPARγ activators
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DNA binding of the glucocorticoid receptor is not essential for survival
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Metadata
- 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 › Endocrinology › 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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