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Smcr8 deficiency disrupts axonal transport-dependent lysosomal function and promotes axonal swellings and gain of toxicity in C9ALS/FTD mouse models.
Human Molecular Genetics ( IF 3.5 ) Pub Date : 2020-04-15 , DOI: 10.1093/hmg/ddaa012
Chen Liang 1, 2 , Qiang Shao 1 , Wei Zhang 1 , Mei Yang 1 , Qing Chang 1 , Rong Chen 3 , Jian-Fu Chen 1
Affiliation  

Since article was originally published online, some minor corrections which had been missed at the proof stage (due to OUP error) have since been updated: 1) In Fig, 5F, WT, and Smcr8-/- have been added into the labels, and also *, n.s. in the notes; 2) In Fig. 9C, GR has been amended to GP following a re-calculation, because the authors found that previous GR antibody recognizes non-specific autofluorescent proteins. The modifications did not change the conclusions and interpretation of the results.

中文翻译:

在C9ALS / FTD小鼠模型中,Smcr8缺乏症破坏了依赖轴突运输的溶酶体功能,并促进了轴突肿胀和毒性增加。

自从文章最初在线发布以来,由于在更新阶段由于OUP错误而错过了一些小更正:1)在图5F,WT和Smcr8-/-中已添加到标签中,以及注释中的*,ns;2)在图9C中,由于作者发现先前的GR抗体识别非特异性自体荧光蛋白,因此在重新计算后将GR修改为GP。修改并没有改变结论和结果解释。
更新日期:2020-04-17
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