Abstract
The translation of tumour necrosis factor α (TNFα) mRNA is regulated by the stress-activated protein kinase p38, which also controls the stability of several pro-inflammatory mRNAs. The regulation of TNFα 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 TNFα mRNA, which was reversed by specific inhibition of p38. An adenosine/uridine-rich element from the TNFα 3' untranslated region conferred p38-sensitive decay in a tetracycline-regulated mRNA stability assay. Therefore the p38 pathway also controls TNFα mRNA turnover. Copyright (C) 2000 Federation of European Biochemical Societies.
Original language | English |
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Pages (from-to) | 57-61 |
Number of pages | 5 |
Journal | FEBS Letters |
Volume | 483 |
Issue number | 1 |
DOIs | |
Publication status | Published - 13 Oct 2000 |
Keywords
- Lipopolysaccharide
- Macrophage
- Mitogen-activated protein kinase p38
- mRNA stability
- Translation
- Tumor necrosis factor α
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology