首页> 美国卫生研究院文献>PLoS Clinical Trials >Endoplasmic Reticulum Stress-Induced JNK Activation Is a Critical Event Leading to Mitochondria-Mediated Cell Death Caused by β-Lapachone Treatment
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Endoplasmic Reticulum Stress-Induced JNK Activation Is a Critical Event Leading to Mitochondria-Mediated Cell Death Caused by β-Lapachone Treatment

机译:内质网应激诱导的JNK激活是导致线粒体介导的β-拉帕酮治疗引起的细胞死亡的关键事件。

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摘要

Backgroundβ-lapachone (β-lap) is a bioreductive agent that is activated by the two-electron reductase NAD(P)H quinone oxidoreductase 1 (NQO1). Although β-lap has been reported to induce apoptosis in various cancer types in an NQO1-dependent manner, the signaling pathways by which β-lap causes apoptosis are poorly understood.
机译:背景β-lapachone(β-lap)是一种生物还原剂,可被双电子还原酶NAD(P)H醌氧化还原酶1(NQO1)激活。尽管据报道β-lap以NQO1依赖性的方式诱导各种癌症类型的凋亡,但对β-lap引起凋亡的信号传导途径知之甚少。

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