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. 2022 Apr 13;32(2):10521. doi: 10.4081/ejtm.2022.10521

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Fig 1. — The p97 and Nploc4 complex participates in the degradation of muscle proteins during atrophy upon cancer and ALS. Ways to block this complex preserve muscles from wasting in both diseases. The electroporation of a plasmid that silences Nploc4 obviates muscle atrophy in situ in models of cancer cachexia and ALS. The oral administration of Disulfiram (DSF) blocks muscle atrophy in mice with cancer cachexia. The ET compound derived from DSF binds free copper (Cu) and Cu-ET sequesters Nploc4 from p97.