Abstract / Description of output
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 language | English |
|---|---|
| Pages (from-to) | 57-61 |
| Number of pages | 5 |
| Journal | FEBS Letters |
| Volume | 483 |
| Issue number | 1 |
| Publication status | Published - 13 Oct 2000 |
Keywords / Materials (for Non-textual outputs)
- 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