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内质网应激、朊蛋白运输与神经退行性变

Endoplasmic reticulum stress, PrP trafficking, and neurodegeneration.

作者信息

Soto Claudio

机构信息

George and Cynthia Mitchell Center for Neurodegenerative Diseases, Departments of Neurology, Neuroscience, and Cell Biology and Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.

出版信息

Dev Cell. 2008 Sep;15(3):339-341. doi: 10.1016/j.devcel.2008.09.001.

Abstract

In this issue of Developmental Cell, Rane et al. report a cellular pathway to link PrP(Sc), via ER stress and the activation of a preemptive quality control process, to neurodegeneration in a PrP-dependent manner. This pathway puts together several pieces in the puzzle of the relationship between PrP(Sc) and brain damage and may in part explain the mechanism of prion neurodegeneration.

摘要

在本期《发育细胞》杂志中,拉内等人报告了一条细胞通路,该通路通过内质网应激和激活一种先发制人的质量控制过程,以依赖朊蛋白(PrP)的方式将朊病毒蛋白(PrP(Sc))与神经退行性变联系起来。这条通路将PrP(Sc)与脑损伤之间关系谜题中的几个部分拼凑在一起,可能部分解释了朊病毒神经退行性变的机制。

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本文引用的文献

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Reduced translocation of nascent prion protein during ER stress contributes to neurodegeneration.
Dev Cell. 2008 Sep;15(3):359-370. doi: 10.1016/j.devcel.2008.06.015.
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