...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neuron >Akt1 Regulates a JNK Scaffold during Excitotoxic Apoptosis.
【24h】

Akt1 Regulates a JNK Scaffold during Excitotoxic Apoptosis.

机译：Akt1调节兴奋性细胞凋亡期间的JNK支架。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Cell survival is determined by a balance among signaling cascades, including those that recruit the Akt and JNK pathways. Here we describe a novel interaction between Akt1 and JNK interacting protein 1 (JIP1), a JNK pathway scaffold. Direct association between Akt1 and JIP1 was observed in primary neurons. Neuronal exposure to an excitotoxic stimulus decreased the Akt1-JIP1 interaction and concomitantly increased association between JIP1 and JNK. Akt1 interaction with JIP1 inhibited JIP1-mediated potentiation of JNK activity by decreasing JIP1 binding to specific JNK pathway kinases. Consistent with this view, neurons from Akt1-deficient mice exhibited higher susceptibility to kainate than wild-type littermates. Overexpression of Akt1 mutants that bind JIP1 reduced excitotoxic apoptosis. These results suggest that Akt1 binding to JIP1 acts as a regulatory gate preventing JNK activation, which is released under conditions of excitotoxic injury.
机译：细胞存活取决于信号级联之间的平衡，包括募集Akt和JNK途径的级联。在这里，我们描述了Akt1和JNK相互作用蛋白1（JIP1），JNK途径支架之间的新型相互作用。在原代神经元中观察到Akt1和JIP1之间的直接关联。神经元暴露于兴奋性毒性刺激会降低Akt1-JIP1的相互作用，并随之增加JIP1和JNK之间的关联。 Akt1与JIP1的相互作用通过降低JIP1与特定JNK途径激酶的结合来抑制JIP1介导的JNK活性增强。与这种观点一致的是，来自Akt1缺陷小鼠的神经元与野生型同窝仔相比对红藻氨酸的敏感性更高。结合JIP1的Akt1突变体的过表达减少了兴奋性细胞凋亡。这些结果表明，与JIP1结合的Akt1充当了抑制JNK激活的调节门，JNK激活在兴奋性毒性损伤的条件下释放。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号