The involvement of AU-rich element-binding proteins in p38 mitogen-activated protein kinase pathway-mediated mRNA stabilisation

被引:272
作者
Dean, JLE [1 ]
Sully, G [1 ]
Clark, AR [1 ]
Saklatvala, J [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Kennedy Inst Rheumatol Div, London W6 8LH, England
关键词
p38; MAPK; MAPKAPK-2; AU-rich element; post-transcriptional regulation; mRNA stability;
D O I
10.1016/j.cellsig.2004.04.006
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The p38 mitogen-activated protein kinase (MAPK) pathway plays an important role in the post-transcriptional regulation of inflammatory genes. p38 has been found to regulate both the translation and the stability of inflammatory mRNAs. The mRNAs regulated by p38 share common AU-rich elements (ARE) present in their 3'-untranslated regions. AREs act as mRNA instability determinants but also confer stabilisation of the mRNA by the p38 pathway. In recent years, AREs have shown to be binding sites for numerous proteins including HuR, TTP, AUF1, AUF2, FBP1, FBP2 (KSRP), TIA-1, and TIAR. However, it is unclear which protein is responsible for mRNA stabilisation by p38. This review gives an overview of the major ARE-binding proteins and discusses reasons for and against their involvement in p38-mediated mRNA stabilisation. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:1113 / 1121
页数:9
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