通过神经元特异性表达ATG5对Atg5基因敲除小鼠进行新生儿致死性的转基因拯救：成年Atg5基因缺陷小鼠的系统分析。
Transgenic rescue of Atg5-null mice from neonatal lethality with neuron-specific expression of ATG5: Systemic analysis of adult Atg5-deficient mice.
作者信息
Yoshii Saori R, Kuma Akiko, Mizushima Noboru
机构信息
a Department of Biochemistry and Molecular Biology , Graduate School and Faculty of Medicine, The University of Tokyo , Tokyo , Japan.
b Japan Science and Technology Agency , PRESTO , Saitama , Japan.
出版信息
Autophagy. 2017 Apr 3;13(4):763-764. doi: 10.1080/15548627.2017.1280221. Epub 2017 Feb 22.
Abstract
Atg5-null mice are neonatal lethal. We have revealed in our recent paper that these mice die due to neuronal dysfunction resulting in suckling failure. Our new mouse model, atg5;Eno2/Nse-Atg5 mice, where Atg5 is deficient in the whole body except for neurons, enables us to analyze the consequences of macroautophagy/autophagy-deficiency in the whole body of adult mice.
摘要
Atg5基因敲除小鼠在出生时即死亡。我们在最近的论文中揭示，这些小鼠因神经元功能障碍导致哺乳失败而死亡。我们的新小鼠模型，即atg5;Eno2/Nse-Atg5小鼠，其中Atg5在除神经元外的全身均有缺陷，这使我们能够分析成年小鼠全身自噬/自噬缺陷的后果。
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