Bennett Brydon L, Satoh Yoshitaka, Lewis Alan J
Celgene Corporation, 4550 Towne Centre Court, San Diego, CA 92121, USA.
Curr Opin Pharmacol. 2003 Aug;3(4):420-5. doi: 10.1016/s1471-4892(03)00068-7.
Jun N-terminal kinase (JNK) regulates the transcription factor AP-1, which is implicated in the controlled expression of many genes involved in the immune response. For this reason, drug discovery efforts have focused on the development of JNK inhibitors for chronic inflammatory diseases. However, recent genetic evidence and emerging pharmacological data indicate that activated JNK could be critical in causing diabetes, insulin resistance and obesity. Indeed, if JNK is considered as a stress-activated protein kinase, there appear to be multiple mechanisms through which it might promote diabetes.
Jun氨基末端激酶（JNK）调节转录因子AP-1，AP-1与许多参与免疫反应的基因的可控表达有关。因此，药物研发工作集中在开发用于慢性炎症性疾病的JNK抑制剂上。然而，最近的遗传学证据和新出现的药理学数据表明，活化的JNK可能在引发糖尿病、胰岛素抵抗和肥胖方面起关键作用。事实上，如果将JNK视为一种应激激活蛋白激酶，那么似乎有多种机制可能导致糖尿病。
