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. 2015 Sep 17;6(9):e1886. doi: 10.1038/cddis.2015.243

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Copyright © 2015 Macmillan Publishers Limited

Cell Death and Disease 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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The PINK1-Parkin pathway regulates mitochondrial apoptosis by the breakdown of IPAS. In healthy neurons, IPAS Thr12 is phosphorylated by PINK1. This phosphorylation may induce conformational changes in IPAS to make the C-terminal region accessible to Parkin, and Parkin ubiquitinates IPAS for proteasomal degradation (left). IPAS is strongly induced in dopaminergic neurons of SNpc following administration of MPTP, and accumulating IPAS induces apoptosis in the neurons (right). bHLH, basic helix–loop–helix motif; PAS like, PAS-like domain; Ub, ubiquitin; MPP⁺, 1-methyl-4-phenylpyridinium