Abstract
Glucocorticoids are the most widely used anti-inflammatory and immunomodulatory agents, whose mechanism of action is based mainly on interference with the activity of transcription factors, such as nuclear factor kappaB (NF-kappaB) and activator protein-1 (AP-1). The precise molecular mechanisms of gene repression by glucocorticoids are a controversial matter, due to the existence of many conflicting hypotheses. We discuss the three main paradigms reported in the literature, namely the inhibitor kappaB-alpha (IkappaB-alpha) upregulatory model, the protein-protein interaction model and the competition model.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology*
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Cyclic AMP Response Element-Binding Protein / physiology
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DNA-Binding Proteins / physiology
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Glucocorticoids / pharmacology*
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Humans
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I-kappa B Proteins*
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Immunosuppressive Agents / pharmacology*
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NF-KappaB Inhibitor alpha
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NF-kappa B / physiology
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Receptors, Glucocorticoid / physiology*
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Transcription Factors / physiology*
Substances
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Anti-Inflammatory Agents
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Cyclic AMP Response Element-Binding Protein
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DNA-Binding Proteins
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Glucocorticoids
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I-kappa B Proteins
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Immunosuppressive Agents
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NF-kappa B
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NFKBIA protein, human
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Receptors, Glucocorticoid
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Transcription Factors
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NF-KappaB Inhibitor alpha