Phosphatase-mediated crosstalk between MAPK signalling pathways in the regulation of cell survival

被引:667
作者
Junttila, Melissa R. [1 ,2 ]
Li, Song-Ping [3 ,4 ]
Westermarck, Jukka [1 ,2 ,5 ]
机构
[1] Univ Turku, Turku Ctr Biotechnol, Turku, Finland
[2] Abo Akad Univ, Turku, Finland
[3] Univ Helsinki, Inst Biomed, Helsinki, Finland
[4] Natl Publ Hlth Inst KTL, Helsinki, Finland
[5] Univ Tampere, Inst Med Technol, Tampere 33250, Finland
关键词
protein phosphatase; MKK; p38; ERK; transformation; cancer;
D O I
10.1096/fj.06-7859rev
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
Mitogen-activated protein kinase (MAPK) pathways constitute a large modular network that regulates a variety of physiological processes, such as cell growth, differentiation, and apoptotic cell death. The function of the ERK pathway has been depicted as survival-promoting, in essence by opposing the proapoptotic activity of the stress-activated c-Jun NH2 terminal kinase (JNK)/p38 MAPK pathways. However, recently published work suggests that extracellular regulated kinase (ERK) pathway activity is suppressed by JNK/p38 kinases during apoptosis induction. In this review, we will summarize the current knowledge about JNK/p38-mediated mechanisms that negatively regulate the ERK pathway. In particular, we will focus on phosphatases (PP2A, MKPs) as inhibitors of ERK pathway activity in regulating apoptosis. A model proposed in this review places the negative regulation of the ERK pathway in a central position for the cellular decision-making process that determines whether cells will five or die in response to apoptosis-promoting signals. In addition, we will discuss the potential functional relevance of negative regulation of ERK pathway activity, for physiological and pathological conditions (e.g:, cellular transformation).
引用
收藏
页码:954 / 965
页数:12
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