RAFTK/Pyk2-mediated cellular signalling

被引:406
作者
Avraham, H [1 ]
Park, SY [1 ]
Schinkmann, K [1 ]
Avraham, S [1 ]
机构
[1] Beth Israel Deaconess Med Ctr, Harvard Inst Med, Div Expt Med & Hematol Oncol, Boston, MA 02115 USA
关键词
tyrosine kinases; RAFTK/Pyk2; FAK; signalling;
D O I
10.1016/S0898-6568(99)00076-5
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Intracellular signal transduction following extracellular ligation by a wide variety of surface molecules involves the activation and tyrosine phosphorylation of protein tyrosine kinases (PTKs). Tyrosine phosphorylation, controlled by the coordinated actions of protein tyrosine phosphatases (PTPs) and tyrosine kinases, is a critical regulatory mechanism for various physiological processes, including cell growth, differentiation, metabolism, cell cycle regulation and cytoskeleton function. The focal adhesion PTK family consists of the focal adhesion kinase (FAK) and the RAFTK/Pyk2 kinase (also known as CAK-beta and CADTK). RAFTK/Pyk2 can be activated by a variety of extracellular signals that elevate intracellular calcium concentration, and by stress signals. RAFTK/Pyk2 is expressed mainly in the central nervous system and in cells derived from hematopoietic lineages, while FAK is widely expressed in various tissues and links transmembrane integrin receptors to intracellular pathways. This review describes the role of RAFTK/Pyk2 in Various signalling cascades and details the differential signalling by FAK and RAFTK/Pyk2. (C) 2000 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:123 / 133
页数:11
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