JNK: a new therapeutic target for diabetes

被引：148

作者：

Bennett, BL ^{[1
]}

Satoh, Y ^{[1
]}

Lewis, AJ ^{[1
]}

机构：

[1] Celgene Corp, San Diego, CA 92121 USA

来源：

CURRENT OPINION IN PHARMACOLOGY | 2003年 / 3卷 / 04期

关键词：

D O I：

10.1016/S1471-4892(03)00068-7

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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.

引用

收藏

页码：420 / 425

页数：6

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