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

被引：195

作者：

Brook, M ^{[1
]}

Sully, G ^{[1
]}

Clark, AR ^{[1
]}

Saklatvala, J ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Sch Med, Kennedy Inst Rheumatol Div, London W6 8LH, England

来源：

FEBS LETTERS | 2000年 / 483卷 / 01期

关键词：

tumor necrosis factor alpha; mitogen-activated protein kinase p38; mRNA stability; translation; macrophage; lipopolysaccharide;

D O I：

10.1016/S0014-5793(00)02084-6

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The translation of tumour necrosis factor alpha (TNF alpha) mRNA is regulated by the stress-activated protein kinase p38, which also controls the stability of several pro-inflammatory mRNAs. The regulation of TNF alpha 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 TNF alpha mRNA, which was reversed by specific inhibition of p38, An adenosine/uridine-rich element from the TNF alpha 3' untranslated region conferred p38-sensitive decay in a tetracycline-regulated mRNA stability assay. Therefore the p38 pathway also controls TNF alpha mRNA turnover. (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：57 / 61

页数：5

共 28 条

[1] Feedback inhibition of macrophage tumor necrosis factor-α production by tristetraprolin [J].