The c-Jun N-terminal protein kinase family of mitogen-activated protein kinases (JNK MAPKs)

被引:252
作者
Barr, RK [1 ]
Bogoyevitch, MA [1 ]
机构
[1] Univ Western Australia, Dept Biochem, Cell Signallling Lab, Crawley, WA 6009, Australia
基金
英国医学研究理事会;
关键词
protein kinases; scaffolds; signalling pathways; stress-activated MAPKs; JNK MAPKs;
D O I
10.1016/S1357-2725(01)00093-0
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 c-Jun N-terminal protein kinase mitogen-activated protein kinases (JNK MAPKs) are an evolutionarily-conserved family of serine/threonine protein kinases. First identified in 1990 when intraperitoneal injection of the protein synthesis inhibitor cycloheximide activated a 54 kDa protein kinase, the JNK MAPKs have now taken on a prominent role in signal transduction. This research has revealed a number of levels of complexity. Alternative gene splicing is now recognised to result in ten different JNK MAPK isoforms of 46-55 kDa, and these isoforms differ in their substrate affinities. Furthermore, although originally classified as stress-activated protein kinases (SAPKs), or SAPKs, the JNK MAPKs are also critical mediators of signal transduction in response to stimulation by cytokines and some growth factors, JNK MAPKs have been shown to be critical mediators in dorsal closure in developing Drosophila embryos, and targeted knockout of murine JNK MAPKs has suggested a critical involvement of these kinases in mammalian embryonic development. Recent work has also highlighted their importance in programmed cell death. Thus, the JNK MAPKs may provide a critical target for regulation in both normal and diseased states. (C) 2001 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:1047 / 1063
页数:17
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