The accumulation of enzymatically inactive cuproenzymes is a CNS-specific phenomenon of the SOD1 G37R mouse model of ALS and can be restored by overexpressing the human copper transporter hCTR1
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doi: 10.1016/j.bbrc.2014.08.042 100 XuXLaiYHuaZC
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Thanks to this process, all the cells in our body can function healthily