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. 2008 Dec 15;183(6):1101–1114. doi: 10.1083/jcb.200805169

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© 2008 Bréchet et al.

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.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 1. — Abrogation of E1111 of the Na_v1.2 ankyrin-binding motif did not impair ion channel segregation at the AIS of hippocampal neurons. Cell surface distribution of K_v2.1 (A), K_v2.1-ΔCter (B), K_v2.1-Na_v1.2 (C), and K_v2.1-Na_v1.2 E1111A mutant (D–F) in cultured hippocampal neurons. The addition of the Na_v1.2 ankyrin-binding motif to the C terminus of K_v2.1-ΔCter segregated K_v2.1 at the AIS (C, arrow). K_v2.1-Na_v1.2 compartmentalization at the AIS was not impaired by the Na_v1.2 E1111A mutation (D and F, arrow). The indicated constructs were immunodetected with an antibody to myc (green) before cell permeabilization; the somatodendritic domain was subsequently identified by MAP2 staining. Bars, 10 μm.