ERK signalling as a regulator of cell motility

被引：138

作者：

Tanimura, Susumu ^{[1
]}

Takeda, Kohsuke ^{[1
]}

机构：

[1] Nagasaki Univ, Grad Sch Biomed Sci, Dept Cell Regulat, 1-14 Bunkyo Machi, Nagasaki 8528521, Japan

来源：

JOURNAL OF BIOCHEMISTRY | 2017年 / 162卷 / 03期

关键词：

cell motility; ERK; phosphorylation; RSK; tumour; ACTIVATED PROTEIN-KINASE; EPIDERMAL-GROWTH-FACTOR; FOCAL ADHESION KINASE; EPITHELIAL-MESENCHYMAL TRANSITION; MEDIATED PHOSPHORYLATION; ADAPTER PROTEIN; MAP KINASES; MYOSIN; 1E; CYTOSKELETAL ORGANIZATION; RHO-GTPASES;

D O I：

10.1093/jb/mvx048

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：

Cell motility is regulated by multiple processes, including cell protrusion, cell retraction, cell-matrix adhesion, polarized exocytosis and polarized vesicle trafficking, each of which is spatiotemporally controlled by various intracellular signalling pathways. Dysregulation of cell motility leads to pathological conditions, such as tumour invasion and metastasis. Accumulating evidence has revealed that extracellular signal-regulated kinase (ERK) signalling is one of the critical regulators of cell motility, although it is classically known as an important regulator of cell proliferation, differentiation and survival through regulation of gene expression. ERK and its downstream kinase, p90 ribosomal S6 kinase (RSK), dynamically regulate cell motility mainly through direct phosphorylation of various molecules that are not necessarily involved in the regulation of gene transcription and translation. In this review, we summarize how ERK signalling regulates cell motility by focusing on the components of the cell motility machinery that are directly regulated by ERK or RSK.

引用

页码：145 / 154

页数：10

共 97 条

[51] GROWTH-FACTORS INDUCE NUCLEAR TRANSLOCATION OF MAP KINASES (P42(MAPK) AND P44(MAPK)) BUT NOT OF THEIR ACTIVATOR MAP KINASE KINASE (P45(MAPKK)) IN FIBROBLASTS [J].