ArticleProceedings of the National Academy of Sciences of the United States of America2000
Glucocorticoids repress NF-kappaB-driven genes by disturbing the interaction of p65 with the basal transcription machinery, irrespective of coactivator levels in the cell.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
104 citing papers in PubMed, 1 synthesis or guideline pooled it, 330 citations in OpenAlex.
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- The regulation of COX-2, ABCA1, and ABCG1 by the lncRNA PACERR links the inflammatory response and cholesterol homeostasis.Cell reports · 2026Article
- Diagnostic and management guidelines for biliary atresia in 2025.Hepatobiliary surgery and nutrition · 2026Review
- Agent-specific training directs distinctive immune response againstFrontiers in immunology · 2026Article
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- Glucocorticoid receptor epigenetic activity in the heart.Epigenetics · 2025Review
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Linkage of circadian rhythm disruptions with Alzheimer's disease and therapeutic interventions.Acta pharmaceutica Sinica. B · 2025Review
- The Bidirectional Interaction Between NF-Journal of immunology research · 2025Review
- The FcRn from gene to protein and function: comparison between species.Frontiers in immunology · 2025Review
- Omega-3 fatty acid synergy with glucocorticoid in mouse lupus macrophage model: targeting pathogenic pathways to reduce steroid dependence.Frontiers in immunology · 2025Article
- COVID-19-Associated Sepsis: Potential Role of Phytochemicals as Functional Foods and Nutraceuticals.International journal of molecular sciences · 2024Review
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- Emerging technology has a brilliant future: the CRISPR-Cas system for senescence, inflammation, and cartilage repair in osteoarthritis.Cellular & molecular biology letters · 2024Review
- The glucocorticoid receptor acts locally to protect dystrophic muscle and heart during disease.Disease models & mechanisms · 2024Article
- Hangeshashinto InhibitsEvidence-based complementary and alternative medicine : eCAM · 2024Article
- Orbital inflammatory pseudotumor: new advances in diagnosis, pathogenesis, and treatment.European journal of medical research · 2023Review
- RELA governs a network of islet-specific metabolic genes necessary for beta cell function.Diabetologia · 2023Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GCs) are used to combat inflammatory diseases. Their beneficial effect relies mainly on the inhibition of NF-kappaB- and/or AP-1-driven proinflammatory gene expression. Previously, we have shown that GCs repress tumor necrosis factor-induced IL-6 gene expression by an NF-kappaB-dependent nuclear mechanism without changing the DNA-binding capacity of NF-kappaB or the expression levels of the cytoplasmic inhibitor of NF-kappaB (IkappaB-alpha). In the present work, we investigate the effect of GC repression on different natural and/or recombinant NF-kappaB-driven reporter gene constructs in the presence of increasing amounts of various coactivator molecules, such as CREB-binding protein (CBP), p300, and SRC-1. We found that GCs maintain their repressive capacities, irrespective of the amount of cofactor present in the cell. Similar results were obtained for the reciprocal transrepression of a GC receptor (GR) element-driven reporter gene by p65. We demonstrate that neither the expression levels of p65 and CBP nor their physical association are affected by activated GR. Using Gal4 chimeras, we show that repression by GCs is specific for p65-mediated transactivation, ruling out competition for limiting nuclear factors as the major underlying mechanism of gene repression. In addition, the transactivation potential of a point-mutated Gal4-p65 variant with a decreased CBP interaction capability is still repressed by GR. Finally, we present evidence that the specificity of GC repression on p65-driven gene expression is codetermined by the TATA box context.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.