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Regulation of tumour necrosis factor α mRNA stability by the mitogen‐activated protein kinase p38 signalling cascade
Author(s) -
Brook Matthew,
Sully Gareth,
Clark Andrew R,
Saklatvala Jeremy
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)02084-6
Subject(s) - p38 mitogen activated protein kinases , messenger rna , microbiology and biotechnology , protein kinase a , kinase , tumor necrosis factor alpha , au rich element , biology , chemistry , untranslated region , biochemistry , gene , immunology
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.