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首页> 外文期刊>Molecular and Cellular Biology >Requirement of JIP1-Mediated c-Jun N-Terminal Kinase Activation for Obesity-Induced Insulin Resistance
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Requirement of JIP1-Mediated c-Jun N-Terminal Kinase Activation for Obesity-Induced Insulin Resistance

机译：JIP1介导的c-Jun N末端激酶激活对肥胖诱导的胰岛素抵抗的要求

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The c-Jun NH2-terminal kinase (JNK) interacting protein 1 (JIP1) has been proposed to act as a scaffold protein that mediates JNK activation. However, recent studies have implicated JIP1 in multiple biochemical processes. Physiological roles of JIP1 that are related to the JNK scaffold function of JIP1 are therefore unclear. To test the role of JIP1 in JNK activation, we created mice with a germ line point mutation in the Jip1 gene (Thr103 replaced with Ala) that selectively blocks JIP1-mediated JNK activation. These mutant mice exhibit a severe defect in JNK activation caused by feeding of a high-fat diet. The loss of JIP1-mediated JNK activation protected the mutant mice against obesity-induced insulin resistance. We conclude that JIP1-mediated JNK activation plays a critical role in metabolic stress regulation of the JNK signaling pathway.
机译：c-Jun NH 2 末端激酶（JNK）相互作用蛋白1（JIP1）已被提议充当介导JNK激活的支架蛋白。但是，最近的研究表明JIP1涉及多个生化过程。因此尚不清楚与JIP1的JNK支架功能相关的JIP1的生理作用。为了测试JIP1在JNK激活中的作用，我们创建了在 Jip1 基因（Thr 103 被Ala取代）中具有种系点突变的小鼠，该小鼠选择性地阻断了JIP1介导的JNK激活。这些突变小鼠的高脂饮食喂养导致JNK激活严重缺陷。 JIP1介导的JNK激活的丧失保护了突变小鼠免受肥胖诱导的胰岛素抵抗。我们得出的结论是，JIP1介导的JNK激活在JNK信号通路的代谢应激调节中起关键作用。

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