The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
GLUCOCORTICOID AND MINERALOCORTICOID RECEPTORS: Biology and Clinical Relevance
Abstract
Mineralocorticoid and glucocorticoid receptors act as homodimers via canonical pentadecamer hormone response elements to regulate transcription. Glucocorticoid, but as yet not mineralocorticoid, receptors have been shown also to modulate AP-1- and NF kappa B-induced transcription by direct protein-protein interactions. The role of 11 beta-hydroxysteroid dehydrogenase in conferring aldosterone specificity on epithelial mineralocorticoid receptors has been proven by the demonstration of sequence mutations in all cases of apparent mineralocorticoid excess examined to date. The autosomal form of aldosterone resistance (pseudohypoaldosteronism) has been shown to reflect loss-of-function mutations in epithelial sodium channel subunit sequence. (Patho)physiological roles for aldosterone and glucocorticoid membrane receptors, and for the recently described nuclear receptors for 11-ketosteroids in 11 beta-hydroxysteroid dehydro-genase-protected epithelia, remain to be established.
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“Once bound to their hormone ligand, MRs and GRs act as transcription factors by migrating to the nucleus and binding to hormone response elements often found in gene promoters (Funder, 1997).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Funder, 1997
In the citing paper
“These corticosteroids are commonly known as “stress hormones,” and are capable of binding to two intracellular receptors: mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Funder, 1997
Citations
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Cited by
Sorted by citations
Brain corticosteroid receptor balance in health and disease
de Kloet, E. R., Vreugdenhil, E., Oitzl, M. S., & Joëls, M. (1998) · Endocrine Reviews · doi:10.1210/edrv.19.3.0331 · Cited by 2,614
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“Type 2 11 -HSD (11 -HSD2) inactivates glucocorticoids in vivo, thus protecting the otherwise non-selective MR from occupation by glucocorticoids (Funder, 1997; Seckl, 2000).”
Molecular and cellular endocrinology
Gianaroli, L., Ferraretti, A., Canale, D., Foresta, C., & Magli, M. (2000) · Molecular and Cellular Endocrinology · doi:10.1016/s0303-7207(00)00232-x · Cited by 1,741
“* p < 0.05 and ** p < 0.01, when compared with the non-insulinic group. and cardiovascular diseases (Shimomura et al., 1999).”
InfluentialThe stressed synapse: the impact of stress and glucocorticoids on glutamate transmission
Popoli, M., Yan, Z., McEwen, B. S., & Sanacora, G. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3138 · Cited by 1,393
Cyclic Decidualization of the Human Endometrium in Reproductive Health and Failure
Gellersen, B., & Brosens, J. J. (2014) · Endocrine Reviews · doi:10.1210/er.2014-1045 · Cited by 1,176
Metadata
- Authors
- Funder, M.
- Affiliations
- Baker Medical Research Institute, Prahran, 3181 Australia
- Venue
- Annual Review of Medicine
- Publisher
- Annual Reviews
- Published
- 1997-02
- Volume
- 48
- Issue
- 1
- Pages
- 231-240
- ISSN
- 0066-4219 (ISSN-L)
- 1545-326X
- OpenAlex
- W2128569914
- Cited by
- 320
- References
- 0
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 10 · 2023: 3 · 2022: 2 · 2021: 13 · 2020: 6 · 2019: 10 · 2018: 8 · 2017: 13 · 2016: 17 · 2015: 13 · 2014: 21 · 2013: 16 · 2012: 18
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- glucocorticoid receptor, mineralocorticoid receptor, nuclear receptors, hormone response elements, transcriptional regulation, AP-1, NF-κB, protein-protein interaction, 11β-hydroxysteroid dehydrogenase, aldosterone, apparent mineralocorticoid excess, pseudohypoaldosteronism, epithelial sodium channel, cell surface receptors
- MeSH terms
- Aldosterone, Animals, DNA Mutational Analysis, Humans, Receptors, Glucocorticoid, Gene Expression, NF-kappa B, Receptors, Mineralocorticoid, Transcription Factor AP-1, Mice
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