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Supporting the idea that lack of copper metalation of Sod1 contributes to the ALS phenotype in these mutant animals is the finding that overexpression of human CTR1 in the SOD1 G37R mouse spinal cord elicited a modest improvement in Sod1 activity (Hilton et al., 2018)

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doi: 10.1016/j.metabol.2009.12.019 411 KitamiTFukudaSKatoTYamagutiKNakatomiYYamanoEet al