Abstract
The transcription factor nuclear factor-kappa B (NF-kappa B) is critical for the inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules. The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B, which further explains the mechanism of action of these drugs. This inhibition prevented the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B was retained in the cytosol. Sodium salicylate and aspirin also inhibited NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Aspirin / pharmacology*
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Cell Line
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Enhancer Elements, Genetic
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Gene Expression / drug effects
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Genes, Reporter
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HIV Long Terminal Repeat
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HIV-1 / genetics
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Humans
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Immunoglobulin kappa-Chains / genetics
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Lipopolysaccharides / pharmacology
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Mice
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NF-kappa B / antagonists & inhibitors*
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NF-kappa B / metabolism
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Phosphorylation
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Promoter Regions, Genetic
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Protein Biosynthesis / drug effects
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Proto-Oncogene Proteins / metabolism
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Sodium Salicylate / pharmacology*
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T-Lymphocytes / metabolism
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Transcription Factor RelB
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Transcription Factors*
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Transfection
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Tumor Cells, Cultured
Substances
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Immunoglobulin kappa-Chains
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Lipopolysaccharides
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NF-kappa B
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Proto-Oncogene Proteins
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RELB protein, human
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Relb protein, mouse
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Transcription Factors
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Transcription Factor RelB
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Aspirin
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Sodium Salicylate