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. 2016 Apr 6;6:78. doi: 10.3389/fonc.2016.00078

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Copyright © 2016 Arriazu, Pippa and Odero.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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PP2A inactivation by SET in AML. (A) PI3K can phosphorylate SET at serine 9 (S9), located in the nuclear localization signal. This phosphorylation translocates SET to the cytosol and impairs its return to the nucleus, increasing its ability to bind to the catalytic subunit of PP2A (PP2A-C), and inactivating PP2A (92, 93). Treatment with FTY720 disrupts SET–PP2A interaction, allowing PP2A activation (39). (B) SETBP1 binds directly to SET, stabilizing full-length SET and protecting it from protease cleavage. The complex SETBP1–SET binds PP2A through SET, inhibiting PP2A activity (50).