Cited by 242NF-κB Signaling PathwaysEstrogen and related hormone effectsSignaling Pathways in Disease

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Negative regulation of nuclear factor-kappaB activation and function by glucocorticoids

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Almawi, WY, Melemedjian, OK·2002·Journal of Molecular Endocrinology

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Abstract

Glucocorticoids (GCs) exert their anti-inflammatory and antiproliferative effects principally by inhibiting the expression of cytokines and adhesion molecules. Mechanistically, GCs diffuse through the cell membrane, and bind to their inactive cytosolic receptors (GRs), which then undergo conformational modifications that allow for their nuclear translocation. In the nucleus, activated GRs modulate transcriptional events by directly associating with DNA elements, compatible with the GCs response elements (GRE) motif, and located in variable copy numbers and at variable distances from the TATA box, in the promoter region of GC-responsive genes. In addition, activated GRs also acted by antagonizing the activity of transcription factors, in particular nuclear factor-kappaB (NF-kappaB), by direct and indirect mechanisms. GCs induced gene transcription and protein synthesis of the NF-kappaB inhibitor, IkappaB. Activated GR also antagonized NF-kappaB activity through protein-protein interaction involving direct complexing with, and inhibition of, NF-kappaB binding to DNA (Simple Model), or association with NF-kappaB bound to the kappaB DNA site (Composite Model). In addition, and according to the Transmodulation Model, GRE-bound GR may interact with and inhibit the activity of kappaB-bound NF-kappaB via a mechanism involving cross-talk between the two transcription factors. Lastly, GR may compete with NF-kappaB for nuclear coactivators, including CREB binding protein and p300, thereby reducing and inhibiting transcriptional activation by NF-kappaB. It should be noted that, in exerting its effect, activated GR did not affect the correct assembly of the pre-initiation (DAB) complex, but acted rather more proximally in inhibiting the correct assembly of transcription factors in the promoter region, and thus transcriptional initiation.

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Authors: Almawi, W., & Melemedjian, O.
Affiliations: Arabian Gulf University (BH)
Venue: Journal of Molecular Endocrinology
Publisher: Bioscientifica
Published: 2002-04-01
Volume: 28
Issue: 2
Pages: 69-78
ISSN: 0952-5041 (ISSN-L)
1479-6813
DOI: 10.1677/jme.0.0280069
OpenAlex: W2157744411
Cited by: 242
References: 74
Citations by year: 2026: 4 · 2025: 5 · 2024: 3 · 2023: 3 · 2022: 5 · 2021: 11 · 2020: 6 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 8 · 2015: 5 · 2014: 8 · 2013: 10 · 2012: 9
FWCI: 1.75
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Molecular Endocrinology (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords: glucocorticoids, glucocorticoid receptor, NF-κB, negative transcriptional regulation, IκB, glucocorticoid response element, protein-protein interaction, CREB-binding protein, P300, transcription initiation, anti-inflammatory activity, cytokine expression
MeSH terms: Animals, Binding, Competitive, Cell Division, Glucocorticoids, Humans, Models, Biological, Protein Binding, T-Lymphocytes, NF-kappa B

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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Negative regulation of nuclear factor-kappaB activation and function by glucocorticoids

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