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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

DOI

10.1016/s0014-5793(00)02084-6

Type

Journal article

Journal

FEBS letters

Publication Date

10/2000

Volume

483

Pages

57 - 61

Addresses

Kennedy Institute of Rheumatology Division, Imperial College School of Medicine, 1 Aspenlea Road, Hammersmith, W6 8LH, London, UK.

Keywords

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