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. 2016 Jul 22;54(6):4716–4722. doi: 10.1007/s12035-016-0008-y

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© The Author(s) 2016

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 3 — Illustration for DAPK1-p53. The interaction of DAPK1–p53 activates both necrotic and apoptotic signaling through transcription- and mitochondria-dependent pathways. DAPK1 binds to p53DM and phosphorylates p53 at serine 23 (pS23), which on one hand translocates into the nucleus and activates the proapoptotic gene expression and apoptosis. On the other hand, the pS23 also enters into the mitochondrial matrix and interacts with CypD and induces necrosis. A peptide Tat-p53DM blocks the interaction of DAPK1 and p53 effectively (modified from Pei et al., The Journal of Neuroscience, 2014. 34(19): p. 6546–56 )