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
Hilton, James B., Kysenius, Kai, White, Anthony R., Crouch, Peter J.Language:
english
Journal:
Experimental Neurology
DOI:
10.1016/j.expneurol.2018.06.006
Date:
June, 2018
File:
PDF, 1.95 MB
english, 2018