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. 2001 Feb 1;117(2):103–118. doi: 10.1085/jgp.117.2.103

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© 2001 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Schematic interpretation of the experiments. Irradiation leads to decaging of Tyr242 of Kir 2.1. Pathway A shows direct phosphorylation of the newly revealed tyrosine, which may be reversible/transient. Failure to observe phosphotyrosine directly makes this pathway unlikely. Pathways B and C involve the μ subunit of AP-1, AP-2, or AP-3 or a similar molecule. In pathway B the adaptor protein (AP) is phosphorylated, which enables it to bind to the now available tyrosine-based interaction motif of Kir 2.1 and inhibit the channel. Endocytosis follows. Pathway C includes phosphorylation of an unspecified protein, which, in combination with the adaptor protein, binds to and inhibits Kir 2.1 and leads to endocytosis.