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
James B Hilton, Kai Kysenius, Anthony R White, Peter J Crouch
Experimental Neurology | ACADEMIC PRESS INC ELSEVIER SCIENCE | Published : 2018
Awarded by Australian National Health and Medical Research Council (NHMRC)
The research in this study was supported through funds from the Australian National Health and Medical Research Council (NHMRC; grant number 1061550), the Motor Neurone Disease Research Institute of Australia (the Betty Laidlaw MND Research Grant), the Sigrid Juselius Foundation and the University of Melbourne.