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. 2013 Jun 1;24(11):1735–1748. doi: 10.1091/mbc.E12-08-0625

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© 2013 Holloway et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 9: — Regulators of ATP7A trafficking. Schematic representation of the proposed trafficking routes taken by endogenous ATP7A, either constitutively (left) or induced by copper level changes (right). Routes are marked by arrows, and blocks imposed by RNAi, mutant constructs, or drug treatment are shown (see also Table 1). Putative involvement of AP-2 in the constitutive pathway is shown as (?) (see the text). AP180-C shows a similar phenotype to clathrin knockdown and is not included in the scheme. Rab22a_Q64L expression causes disruption of the TGN, which is not illustrated. Copper-induced forward pathway is shown as a direct trafficking step to the PM, although intermediary vesicles might be involved as in the constitutive route. V, vesicle.