Cited by 831NF-κB Signaling PathwaysEstrogen and related hormone effectsGenomics and Chromatin Dynamics

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Characterization of Mechanisms Involved in Transrepression of NF-κB by Activated Glucocorticoid Receptors

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Scheinman, Robert I., Gualberto, Antonio, Jewell, Christine M., Cidlowski, John A., Baldwin, Albert S.·1995·Molecular and Cellular Biology

DOI 10.1128/mcb.15.2.943PMC PMC231982

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Abstract

Glucocorticoids are potent immunosuppressants which work in part by inhibiting cytokine gene transcription. We show here that NF-kappa B, an important regulator of numerous cytokine genes, is functionally inhibited by the synthetic glucocorticoid dexamethasone (DEX). In transfection experiments, DEX treatment in the presence of cotransfected glucocorticoid receptor (GR) inhibits NF-kappa B p65-mediated gene expression and p65 inhibits GR activation of a glucocorticoid response element. Evidence is presented for a direct interaction between GR and the NF-kappa B subunits p65 and p50. In addition, we demonstrate that the ability of p65, p50, and c-rel subunits to bind DNA is inhibited by DEX and GR. In HeLa cells, DEX activation of endogenous GR is sufficient to block tumor necrosis factor alpha or interleukin 1 activation of NF-kappa B at the levels of both DNA binding and transcriptional activation. DEX treatment of HeLa cells also results in a significant loss of nuclear p65 and a slight increase in cytoplasmic p65. These data reveal a second mechanism by which NF-kappa B activity may be regulated by DEX. We also report that RU486 treatment of wild-type GR and DEX treatment of a transactivation mutant of GR each can significantly inhibit p65 activity. In addition, we found that the zinc finger domain of GR is necessary for the inhibition of p65. This domain is also required for GR repression of AP-1. Surprisingly, while both AP-1 and NF-kappa B can be inhibited by activated GR, synergistic NF-kappa B/AP-1 activity is largely unaffected. These data suggest that NF-kappa B, AP-1, and GR interact in a complex regulatory network to modulate gene expression and that cross-coupling of NF-kappa B and GR plays an important role in glucocorticoid-mediated repression of cytokine transcription.

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10.1128/mcb.13.6.3782-3791.1993 · DOI
10.1128/mcb.10.5.2327-2334.1990 · DOI
10.1128/mcb.10.3.1281-1286.1990 · DOI
10.1128/mcb.10.2.561-568.1990 · DOI · Paper page

Sorted by citations

THE NF-κB AND IκB PROTEINS: New Discoveries and Insights
Baldwin, A. S. (1996) · Annual Review of Immunology · doi:10.1146/annurev.immunol.14.1.649 · Cited by 5,882
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Nuclear Factor-κB — A Pivotal Transcription Factor in Chronic Inflammatory Diseases
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Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress
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TNF- and Cancer Therapy-Induced Apoptosis: Potentiation by Inhibition of NF-κB
Wang, C.-Y., Mayo, M. W., & Baldwin, A. S. (1996) · Science · doi:10.1126/science.274.5288.784 · Cited by 2,586
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Immunosuppression by Glucocorticoids: Inhibition of NF-κB Activity Through Induction of IκB Synthesis
Auphan, N., DiDonato, J. A., Rosette, C., Helmberg, A., & Karin, M. (1995) · Science · doi:10.1126/science.270.5234.286 · Cited by 2,390

See all 831

Authors: Scheinman, R. I., Gualberto, A., Jewell, C. M., Cidlowski, J. A., & Baldwin, A. S.
Affiliations: University of North Carolina at Chapel Hill (US)
ORCID: Scheinman, Robert I.
Gualberto, Antonio
Jewell, Christine M.
Cidlowski, John A.
Baldwin, Albert S.
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 1995-02
Volume: 15
Issue: 2
Pages: 943-953
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.15.2.943
PMC: PMC231982
OpenAlex: W2158110584
Cited by: 819
References: 82
Citations by year: 2026: 12 · 2025: 9 · 2024: 2 · 2023: 6 · 2022: 6 · 2021: 10 · 2020: 11 · 2019: 8 · 2018: 17 · 2017: 12 · 2016: 16 · 2015: 16 · 2014: 17 · 2013: 25 · 2012: 19
FWCI: 23.58
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Molecular and Cellular Biology (publishedVersion)
PubMed Central (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 › Genomics and Chromatin Dynamics
Keywords: NF-κB, glucocorticoid receptor, dexamethasone, transrepression, NF-κB p65, P50, c-Rel, AP-1, cytokine gene transcription, zinc finger, transcriptional repression, TNF-α, interleukin-1, glucocorticoid response element, protein-protein interaction, immunosuppression
MeSH terms: Animals, Cell Line, Chlorocebus aethiops, Dexamethasone, Drug Synergism, Glutathione Transferase, HeLa Cells, Humans, Interleukin-1, Kinetics, Receptors, Glucocorticoid, Recombinant Fusion Proteins, Recombinant Proteins, Transfection, Tumor Necrosis Factor-alpha, Chloramphenicol O-Acetyltransferase, Mifepristone, Gene Expression, NF-kappa B, Transcription Factor AP-1, Macromolecular Substances, Transcription Factor RelA, NF-kappa B p50 Subunit

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Characterization of Mechanisms Involved in Transrepression of NF-κB by Activated Glucocorticoid Receptors

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