Negative feedback regulation of the ERK1/2 MAPK pathway

被引:408
作者
Lake, David [1 ]
Correa, Sonia A. L. [2 ,3 ]
Muller, Jurgen [1 ,4 ]
机构
[1] Univ Warwick, Warwick Med Sch, Coventry, W Midlands, England
[2] Univ Warwick, Sch Life Sci, Coventry, W Midlands, England
[3] Univ Bradford, Fac Life Sci, Bradford, W Yorkshire, England
[4] Aston Univ, Aston Med Res Inst, Aston Med Sch, Birmingham B4 7ET, W Midlands, England
基金
英国医学研究理事会;
关键词
Cell signalling; Negative feedback; Signalling dynamics; Spatiotemporal regulation; Pathway modelling; Cancer; EPIDERMAL-GROWTH-FACTOR; RAS/MAPK SIGNALING PATHWAY; KSR-1 GENE ENCODES; PROTEIN-KINASE; PHOSPHORYLATION SITES; B-RAF; FACTOR RECEPTOR; MEK INHIBITION; THREONINE PHOSPHORYLATION; SYNAPTIC PLASTICITY;
D O I
10.1007/s00018-016-2297-8
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 extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) signalling pathway regulates many cellular functions, including proliferation, differentiation, and transformation. To reliably convert external stimuli into specific cellular responses and to adapt to environmental circumstances, the pathway must be integrated into the overall signalling activity of the cell. Multiple mechanisms have evolved to perform this role. In this review, we will focus on negative feedback mechanisms and examine how they shape ERK1/2 MAPK signalling. We will first discuss the extensive number of negative feedback loops targeting the different components of the ERK1/2 MAPK cascade, specifically the direct posttranslational modification of pathway components by downstream protein kinases and the induction of de novo gene synthesis of specific pathway inhibitors. We will then evaluate how negative feedback modulates the spatiotemporal signalling dynamics of the ERK1/2 pathway regarding signalling amplitude and duration as well as subcellular localisation. Aberrant ERK1/2 activation results in deregulated proliferation and malignant transformation in model systems and is commonly observed in human tumours. Inhibition of the ERK1/2 pathway thus represents an attractive target for the treatment of malignant tumours with increased ERK1/2 activity. We will, therefore, discuss the effect of ERK1/2 MAPK feedback regulation on cancer treatment and how it contributes to reduced clinical efficacy of therapeutic agents and the development of drug resistance.
引用
收藏
页码:4397 / 4413
页数:17
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