...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Biological chemistry >Regulation of mitochondrial plasticity by the i-AAA protease YME1L
【24h】

Regulation of mitochondrial plasticity by the i-AAA protease YME1L

机译：I-AAA蛋白酶YME1L对线粒体塑性的调节

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

Mitochondria are multifaceted metabolic organelles and adapt dynamically to various developmental transitions and environmental challenges. The metabolic flexibility of mitochondria is provided by alterations in the mitochondrial proteome and is tightly coupled to changes in the shape of mitochondria. Mitochondrial proteases are emerging as important posttranslational regulators of mitochondrial plasticity. The i-AAA protease YME1L, an ATP-dependent proteolytic complex in the mitochondrial inner membrane, coordinates mitochondrial biogenesis and dynamics with the metabolic output of mitochondria. mTORC1-dependent lipid signaling drives proteolytic rewiring of mitochondria by YME1L. While the tissue-specific loss of YME1L in mice is associated with heart failure, disturbed eye development, and axonal degeneration in the spinal cord, YME1L activity supports growth of pancreatic ductal adenocarcinoma cells. YME1L thus represents a key regulatory protease determining mitochondrial plasticity and metabolic reprogramming and is emerging as a promising therapeutic target.
机译：线粒体是多方面的代谢细胞器，并动态适应各种发育过渡和环境挑战。线粒体的代谢柔韧性通过线粒体蛋白质组的改变提供，并且紧密地联接到线粒体形状的变化。线粒体蛋白酶作为线粒体塑性的重要癌症调节因子。 I-AAA蛋白酶YME1L，在线粒体内膜中的ATP依赖性蛋白水解复合物，与线粒体代谢产量协调线粒体生物发生和动力学。 MTORC1依赖性脂质信号传导通过YME1L驱动线粒体的蛋白水解重新烫。虽然小鼠的YME1L的组织特异性损失与心力衰竭，干扰的眼睛发育和脊髓中的轴突变性相关，但是YME1L活性支持胰腺导管腺癌细胞的生长。因此，YME1L表示关键调节蛋白酶，确定线粒体塑性和代谢重编程，并作为有前途的治疗靶标。

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