Author: Lyudmila Kovalchuke; Eugene V. Mosharov; Oren A. Levy; Lloyd A. Greene
Title: Stress-induced phospho-ubiquitin formation causes parkin degradation Document date: 2018_12_5
ID: ceepyyxj_57
Snippet: We also observed that treatments with L-DOPA or CCCP that promoted parkin loss did not cause a loss of mitochondrial proteins consistent with robust induction of mitophagy. These results therefore indicate that mitophagy is not required for phospho-Ub-dependent parkin degradation. This finding is inconsistent with suggestions that parkin degradation downstream of mitochondrial depolarization is linked to mitochondrial elimination [36] [37] [38] [.....
Document: We also observed that treatments with L-DOPA or CCCP that promoted parkin loss did not cause a loss of mitochondrial proteins consistent with robust induction of mitophagy. These results therefore indicate that mitophagy is not required for phospho-Ub-dependent parkin degradation. This finding is inconsistent with suggestions that parkin degradation downstream of mitochondrial depolarization is linked to mitochondrial elimination [36] [37] [38] [39] . Instead, our results indicate that parkin's association with phospho-Ub is the key determinant of its depolarization-and oxidative-stress-induced loss and that this loss can occur independently of mitophagy, in line with a previous study [40] .
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