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确认死亡受体 5 和半胱天冬酶-8 在内质网应激诱导细胞凋亡中的关键作用。

Confirming a critical role for death receptor 5 and caspase-8 in apoptosis induction by endoplasmic reticulum stress.

机构信息

Howard Hughes Medical Institute, Department of Biochemistry and Biophysics, University of California at San Francisco, San Francisco, CA, 94158, USA.

Cancer Immunology, Genentech, Inc., South San Francisco, CA, 94080, USA.

出版信息

Cell Death Differ. 2018 Aug;25(8):1530-1531. doi: 10.1038/s41418-018-0155-y. Epub 2018 Jul 10.

DOI:10.1038/s41418-018-0155-y
PMID:29991746
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6113221/
Abstract

Several studies implicate specific death receptors (DRs) and caspase-8 in mediating apoptosis in response to endoplasmic reticulum (ER) stress; however, a recent paper challenges this conclusion. Here we validate the importance of DR5 and caspase-8 as critical signal conduits for apoptosis activation upon ER stress.

摘要

几项研究表明,特定的死亡受体(DRs)和半胱天冬酶-8 在介导内质网(ER)应激反应中的细胞凋亡中起作用;然而,最近的一篇论文对这一结论提出了挑战。在这里,我们验证了 DR5 和半胱天冬酶-8 作为 ER 应激时细胞凋亡激活的关键信号传导物的重要性。

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本文引用的文献

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A role for caspase-8 and TRAIL-R2/DR5 in ER-stress-induced apoptosis.半胱天冬酶-8和肿瘤坏死因子相关凋亡诱导配体受体2/死亡受体5在内质网应激诱导的细胞凋亡中的作用。
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DR5 and caspase-8 are dispensable in ER stress-induced apoptosis.DR5和半胱天冬酶-8在内质网应激诱导的细胞凋亡中并非必需。
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