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. 2019 Aug;12(3):167–183. doi: 10.2174/1874467212666190304121131

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© 2019 Bentham Science Publishers

This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

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Fig. (1) — Integration of canonical and non-canonical Wnt signaling via differential CBP and p300 usage. Non-canonical Wnt signaling (represented by WNT5a) ƒ?oantagonizesƒ?? canonical Wnt signaling (represented by WNT3a) by inducing a change in Iý-catenin coactivator usage and a corresponding switch in gene expression from a proliferative towards a differentiative program. We have demonstrated that WNT5a induces PKC phosphorylation of Ser89 of p300, thereby increasing the affinity of p300 for Iý-catenin, and we propose this as a mechanism to explain the switch in coactivator usage from CBP/Iý-catenin to p300/Iý-catenin. Small molecule ICG-001 specifically blocks the CBP/Iý-catenin interaction, thus biasing towards p300 usage by Iý-catenin. In contrast, small molecules IQ-1 (indirect antagonist) and YH249/250 (direct antagonist) block the p300/Iý-catenin interaction, thus biasing towards CBP usage by Iý-catenin.