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. 2008 May 5;181(3):537–549. doi: 10.1083/jcb.200707022

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© 2008 Kakinuma 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 3. — The interaction between 14-3-3 and Kank occurs downstream of PI3K–Akt signaling and is enhanced by growth factors. (A) The association between 14-3-3 and Kank occurs downstream of the PI3K–Akt signaling. After IMCD cells were treated with vehicle (DMSO, lanes 1 and 2), 50 μM LY294002 (lane 3), 100 nM wortmannin (lane 4), or 0.2 nM rapamycin (lane 5) for 24 h, the cells were collected, lysed, and subjected to immunoprecipitation using anti–mouse Kank antibody. The results of Western blotting are shown on the left and the intensities of the bands quantified using an ImageQuant image analyzer are shown on the right. *, P < 0.01 compared with the vehicle; **, P < 0.05 compared with the vehicle. (B) The interaction between 14-3-3 and Kank is enhanced by insulin and EGF. IMCD cells either pretreated (lanes 4 and 6) or not pretreated (lanes 3 and 5) with 50 μM LY294002 (LY) were treated with 10 μg/ml insulin (lanes 3 and 4) or 10 ng/ml EGF (lanes 5 and 6). The experiments were performed as described in A. *, P < 0.01 compared with the control; **, P < 0.05 compared with the control. The results shown are the mean ± SD of at least triplicate experiments.