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. 2015 Jan 7;24(9):2411–2425. doi: 10.1093/hmg/ddv002

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Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US.

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Figure 5. — The distal motor neuropathy mutation ATP7A^P1386S, an ATP7A C-terminus-truncation (ATP7A^Δ1415-1500) and a di-leucine ATP7A mutation (L¹⁴⁷⁷L¹⁴⁷⁸/AA) diminish physical interaction with AP-2. HEK293T cells were transfected with wild-type ATP7A-Venus, ATP7A^LL/AA-Venus, ATP7A^P1386S-Venus, or ATP7A^Δ1415-1500-Venus. Transfected cells were immunoprecipitated (IP) by an AP-2 alpha subunit antibody and pull-down products detected by anti-GFP (Venus) antibody. (A and B) ATP7A^WT consistently immunoprecipitated AP-2, with interaction markedly impaired by the different mutations. (C) Densitometric summary of AP-2 IP blots (N = 10 for ATP7A^WT, N = 4 for ATP7A^LL/AA, N = 6 for ATP7A^P1386S and N = 3 for ATP7A^Δ1415-1500). Error bars = SD.