The c-jun kinase/stress-activated pathway: Regulation, function and role in human disease

被引：401
作者：
Johnson, Gary L.
Nakamura, Kazuhiro
机构：
[1] Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA
来源：
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2007年 / 1773卷 / 08期
关键词：
c-Jun; N-terminal kinase (JNK); stress-activated protein kinase (SAPK); ischemia; apoptosis; metabolic regulation; obesity; neurodegeneration; chronic inflammation;
D O I：
10.1016/j.bbamcr.2006.12.009
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：
c-Jun N-terminal kinases (JNKs), also referred to as stress-activated kinases (SAPKs), were initially characterized by their activation in response to cell stress such as UV irradiation. JNK/SAPKs have since been characterized to be involved in proliferation, apoptosis, motility, metabolism and DNA repair. Dysregulated JNK signaling is now believed to contribute to many diseases involving neurodegeneration, chronic inflammation, birth defects, cancer and ischemia/reperfusion injury. In this review, we present our current understanding of JNK regulation and their involvement in homeostasis and dysregulation in human disease. (C) 2007 Elsevier B.V. All rights reserved.
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收藏
页码：1341 / 1348
页数：8
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