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. 2016 Feb 15;5(2):e196. doi: 10.1038/oncsis.2016.8

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Copyright © 2016 Macmillan Publishers Limited

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Structural effects of R282W mutation. In response to DNA damage, the wild-type p53 binds to DNA in the nucleus and transactivates downstream effector genes, and it interacts with BCL-XL in the mitochondria and induces mitochondrial apoptosis. The R282W mutation causes destabilization of the protein structure, impairing its binding to DNA and BCL-XL. Moreover, the mutation induces exposure of the aggregation-prone region that is normally buried in the hydrophobic core of p53 protein. This induces coaggregation of the wild-type p53 and its homologues p63 and p73.