Regulation of tumour necrosis factor α mRNA stability by the mitogen-activated protein kinase p38 signalling cascade

Research output: Contribution to journalArticle

Authors

  • Matthew Brook
  • Gareth Sully
  • Andy Clark
  • Jeremy Saklatvala

Colleges, School and Institutes

External organisations

  • St Mark's NHS Trust

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.

Details

Original languageEnglish
Pages (from-to)57-61
Number of pages5
JournalFEBS Letters
Volume483
Issue number1
Publication statusPublished - 13 Oct 2000

Keywords

  • Lipopolysaccharide, Macrophage, Mitogen-activated protein kinase p38, mRNA stability, Translation, Tumor necrosis factor α