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The translation of tumour necrosis factor alpha (TNFalpha) mRNA is regulated by the stress-activated protein kinase p38, which also controls the stability of several pro-inflammatory mRNAs. The regulation of TNFalpha gene expression in a mouse macrophage cell line RAW264.7 was re-examined using an inhibitor of stress-activated protein kinases. Stimulation of these cells with bacterial lipopolysaccharide resulted in stabilisation of TNFalpha mRNA, which was reversed by specific inhibition of p38. An adenosine/uridine-rich element from the TNFalpha 3' untranslated region conferred p38-sensitive decay in a tetracycline-regulated mRNA stability assay. Therefore the p38 pathway also controls TNFalpha mRNA turnover.

Original publication




Journal article


Febs lett

Publication Date





57 - 61


3' Untranslated Regions, Animals, Cell Line, Dose-Response Relationship, Drug, Enzyme Inhibitors, Gene Expression Regulation, HeLa Cells, Humans, Imidazoles, JNK Mitogen-Activated Protein Kinases, Lipopolysaccharides, Mitogen-Activated Protein Kinases, Pyridines, RNA Stability, RNA, Messenger, Regulatory Sequences, Nucleic Acid, Signal Transduction, Tetracycline, Time Factors, Tumor Necrosis Factor-alpha, p38 Mitogen-Activated Protein Kinases