Focal adhesion kinase regulation by oxidative stress in different cell types

被引:70
作者
Ben Mahdi, MH
Andrieu, V
Pasquier, C
机构
[1] Ctr Hosp Xavier Bichat, INSERM, U479, F-75870 Paris 18, France
[2] Ctr Hosp Xavier Bichat, Hematol Lab, F-75870 Paris 18, France
关键词
apoptosis; cancer; cell survival; focal adhesion kinase; reactive oxygen species; superoxide anion; tyrosine kinase;
D O I
10.1080/15216540051081038
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
Focal adhesion kinase (FAK) is a tyrosine kinase ubiquitously expressed in cells. It was initially shown to be the initiator of focal adhesion formation in adherent cells, after its binding to integrins which induce its autophosphorylation. However, it can be also activated by a great variety of other stimuli able to act on different intracellular signaling. Reactive oxygen species (ROS), which have been shown to act as external or internal cell stimuli, induce tyrosine phosphorylation of FAK, Its autophosphorylation is followed by a submembranous localization which is crucial for many of the biological roles of FAK, including cell spreading, cell migration, cell proliferation, and prevention of apoptosis, It plays an important role in development of tumor cells, its regulation could be thus a way of impairing cell proliferation in cancer, We describe in this review the structure, activity, and functions of FAK in different cells and how ROS are able, like other stimuli, to induce its phosphorylation and modification of cell morphology and structure. The link between ROS and FAK activation could explain the role of ROS in mediating cell proliferation, cell migration, or apoptosis.
引用
收藏
页码:291 / 299
页数:9
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