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. 2017 Jan 2;216(1):167–179. doi: 10.1083/jcb.201608071

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© 2017 Kadlecova et al.

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Figure 6. — Increased phosphorylation of µ2 at T156 compensates to maintain efficient TfnR internalization in µ2^PIP2− cells. (A) Schematic representation of the potential roles for AAK1 activation and phosphorylation of T156 on µ2. The question mark and arrows point to possible compensatory mechanisms and a positive feed-forward loop that can restore efficient CME in µ2^PIP2− cells. (B) Quantification (mean ± SD, n = 3; two-tailed Student’s t tests were used to assess statistical significance: *, P < 0.05) of total and phosphorylated µ2^pT156 subunit in µ2^WT, µ2^PIP2-, and α^PIP2− cells (see also Fig. S5 B). (C) TfnR uptake measured at 10 min in control, µ2^PIP2−, and α^PIP2− cells with or without treatment with the 10-µM AAK1 inhibitor (inhib), Compound 2. Data shown are mean ± SD, n = 3; normalized to total surface bound; *, P < 0.05; ***, P < 0.0005. n.s., not significant.