Cui Jie, Zhang Ming, Zhang Yong-Qing, Xu Zhi-Heng
Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
Acta Pharmacol Sin. 2007 May;28(5):601-8. doi: 10.1111/j.1745-7254.2007.00579.x.
c-Jun N-terminal protein kinases (JNK), also known as stress-activated protein kinases, were originally identified by their ability to phosphorylate the N-terminal of the transcription factor c-Jun and by their activation in response to a variety of stresses. JNK are multifunctional kinases involved in many physiological processes. The JNK pathway has been shown to play a major role in apoptosis in many cell death paradigms and its association with a variety of pathological processes is gradually been recognized. This review will concentrate on describing the involvement of the JNK pathway in the context of different diseases and the potential to adopt the JNK pathway components as therapeutic targets.
c-Jun氨基末端蛋白激酶(JNK),也被称为应激激活蛋白激酶,最初是因其能够磷酸化转录因子c-Jun的氨基末端以及在多种应激反应中的激活能力而被发现的。JNK是参与许多生理过程的多功能激酶。JNK通路已被证明在多种细胞死亡模式的凋亡中起主要作用,并且其与各种病理过程的关联也逐渐得到认可。本综述将集中描述JNK通路在不同疾病背景下的参与情况以及将JNK通路成分作为治疗靶点的潜力。