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. 2021 Apr 6;9(4):388. doi: 10.3390/biomedicines9040388

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Proposed mechanism of action of Nut-3a and WIP1i combined treatment in AML cells. MDM2 inhibition enhances p53-dependent response to DNA damages induced by chemotherapy agents or replicative stress. Once Nut-3a binds to MDM2, p53 is released and activated through phosphorylation. Active p53 promotes the induction of apoptosis. (A) WIP1 is involved in the regulation of response to Nut-3a and dephosphorylates p53. WIP1 and p53 are co-regulated by a feedback-loop. (B) When WIP1i is simultaneously added to Nut-3a, p53 activation is enforced, resulting in enhanced apoptosis of AML cells. The arrows represent a stimulatory signal, truncated arrows represent a inhibition signal.