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Allele Publication :

Type  Indexed Publication . Mgi Jnum  J:269422
Publication . Citation  Hilton JB, et al. (2018) 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. Exp Neurol 307:118-128

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