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_21
Snippet: Having placed a portion of parkin loss from L-DOPA in the same pathway as L-DOPAinduced formation of phospho-Ub, we next asked whether, and to what extent, parkin interaction with phospho-Ub plays a role in its loss from other stressors. Given that hydrogen peroxide causes parkin loss (Fig. 2D ) and induces phospho-poly-Ub formation (Fig. 4D) , we first queried whether parkin loss from this oxidative stressor is also mediated by its interaction w.....
Document: Having placed a portion of parkin loss from L-DOPA in the same pathway as L-DOPAinduced formation of phospho-Ub, we next asked whether, and to what extent, parkin interaction with phospho-Ub plays a role in its loss from other stressors. Given that hydrogen peroxide causes parkin loss (Fig. 2D ) and induces phospho-poly-Ub formation (Fig. 4D) , we first queried whether parkin loss from this oxidative stressor is also mediated by its interaction with phospho-Ub. To achieve this, we utilized neuronal PC12 cells moderately over-expressing either wildtype or various mutant forms of parkin. Indeed, while wild-type parkin levels decreased by half upon peroxide treatment (50.9 ± 4.3% parkin remaining; p = 0.001, N = 5), the H302A and K151E parkin mutants were nearly completely rescued from loss induced by this agent (K151E + peroxide: 96.2 ± 8.0% parkin remaining, N = 5, p = 0.97 vs. no treatment; H302A + peroxide:
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