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. 2013 Jul 4;5(3):838–856. doi: 10.3390/cancers5030838

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© 2013 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 license (http://creativecommons.org/licenses/by/3.0/).

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Treatments with UV radiation, flavopiridol, DRB, roscovitine, actinomycin D, and doxorubicin, etoposide, and nutlin-3 increase the HEXIM1-p53 interaction and lead to induction of p53. UV, flavopiridol, DRB, roscovitine, and actinomycin D treatments can release more “free” HEXIM1 from the large P-TEFb complexes and may further enhance the association between p53 and HEXIM1. HEXIM1 not only competes with HDM2 in binding to p53, but also interacts with HDM2, resulting in activation of p53. The HDM2-ubiquitinated HEXIM1, which is not degraded through the proteasome-mediated pathway, exerts stronger inhibition on P-TEFb activity.