Published in
Elsevier, Experimental Neurology, (307), p. 118-128
DOI: 10.1016/j.expneurol.2018.06.006
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The accumulation of enzymatically inactive cuproenzymes is a CNS-specific phenomenon of the SOD1G37R mouse model of ALS and can be restored by overexpressing the human copper transporter hCTR1
Journal article published in 2018 by
James B. Hilton 
,
Kai Kysenius,
Anthony R. White,
Peter J. Crouch
,
Kai Kysenius,
Anthony R. White,
Peter J. Crouch
This paper is made freely available by the publisher.
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