...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Caspase-4 is partially cleaved by calpain via the impairment of Ca2+ homeostasis under the ER stress.
【24h】

Caspase-4 is partially cleaved by calpain via the impairment of Ca2+ homeostasis under the ER stress.

机译：Caspase-4被内切蛋白酶通过内质网应激下Ca2 +稳态的损伤而被部分切割。

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

In the previous reports, we showed that caspase-4, which has high homology to caspase-12, plays an important role in the neural cell death via the endoplasmic reticulum (ER) stress. In addition, we elucidated the involvement of the familial Alzheimer's disease (AD)-linked presenilin-1 (PS1) mutation and beta-amyloid induced-apoptotic signaling in human neural cells in the activation (cleavage) of caspase-4. These results suggest the involvement of caspase-4 in the cell death observed in AD. To elucidate the mechanism of the cleavage of caspase-4 under ER stress, we used EGTA, a Ca(2+) chelator, because the cleavage caspase-12 has reported to be regulated by the calpain. As the results, EGTA inhibited the cleavage of caspase-4 in a concentration-dependent manner. In addition, inhibitors of calpain, which are activated by the Ca(2+), also inhibited the cleavage of caspase-4. Furthermore, EGTA and caplain inhibitors rescued the neural cell death under the ER stress. These results suggest that the disturbance of Ca(2+) homeostasis induced by ER stress should cause the activation of caspase-4 resulting in the neural cell death.
机译：在以前的报告中，我们表明与caspase-12具有高度同源性的caspase-4在通过内质网（ER）应激引起的神经细胞死亡中起重要作用。此外，我们阐明了家族性阿尔茨海默氏病（AD）连锁的早老素1（PS1）突变和β-淀粉样蛋白诱导的细胞凋亡信号传导在caspase-4的激活（裂解）中的作用。这些结果表明caspase-4参与了AD中观察到的细胞死亡。为了阐明在内质网应激下caspase-4裂解的机制，我们使用了EGTA，一种Ca（2+）螯合剂，因为据报道裂解caspase-12受钙蛋白酶调节。结果，EGTA以浓度依赖的方式抑制了caspase-4的切割。此外，钙蛋白酶的抑制剂，由Ca（2+）激活，也抑制了caspase-4的裂解。此外，EGTA和caplain抑制剂在ER应激下挽救了神经细胞的死亡。这些结果表明，由内质网应激引起的Ca（2+）动态平衡的干扰应引起caspase-4激活，导致神经细胞死亡。

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