Chen Y R, Tan T H
Department of Immunology, Baylor College of Medicine, Houston, TX 77030, USA.
Int J Oncol. 2000 Apr;16(4):651-62. doi: 10.3892/ijo.16.4.651.
The c-Jun N-terminal kinase (JNK) group of mitogen-activated protein kinases (MAPKs) is activated in mammalian cells by environmental stress, pro-inflammatory cytokines, and mitogenic stimuli. Biochemical and genetic studies demonstrate that JNK regulates the activities of many transcription factors, and that the JNK pathway is required for the regulation of inflammatory responses, cell proliferation, and apoptosis. The involvement of JNK in apoptotic cell death is particularly intriguing, and has been actively studied in recent years. An improved understanding of JNK-mediated apoptotic signaling may provide novel strategies in prevention and treatment of cancers.
丝裂原活化蛋白激酶（MAPK）中的c-Jun氨基末端激酶（JNK）组，在哺乳动物细胞中可被环境应激、促炎细胞因子和促有丝分裂刺激激活。生化和遗传学研究表明，JNK调节许多转录因子的活性，并且JNK信号通路是调节炎症反应、细胞增殖和细胞凋亡所必需的。JNK参与凋亡性细胞死亡这一现象尤其引人关注，近年来一直是研究的热点。对JNK介导的凋亡信号转导有更深入的了解，可能会为癌症的预防和治疗提供新的策略。
