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_38
Snippet: We first assessed Mfn2 ubiquitination following CCCP treatment, which revealed rapid poly-ubiquitination and ultimate loss of the former (32.4 ± 4.5% loss after 25 hours relative to time zero, p = 0.004 vs. no treatment, N = 3) (Fig. 9A,B) . By contrast, we did not observe any ubiquitination or loss of Mfn2 after up to 48 hours of L-DOPA treatment despite robust (~50%) parkin loss (115.9 ± 4.5% Mfn2 remaining after 48 hours relative to time zer.....
Document: We first assessed Mfn2 ubiquitination following CCCP treatment, which revealed rapid poly-ubiquitination and ultimate loss of the former (32.4 ± 4.5% loss after 25 hours relative to time zero, p = 0.004 vs. no treatment, N = 3) (Fig. 9A,B) . By contrast, we did not observe any ubiquitination or loss of Mfn2 after up to 48 hours of L-DOPA treatment despite robust (~50%) parkin loss (115.9 ± 4.5% Mfn2 remaining after 48 hours relative to time zero, p = 0.77 vs. no The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. It . https://doi.org/10.1101/484857 doi: bioRxiv preprint treatment, N = 3) (Fig. 9C,D; Fig. 10A ). This result is in line with our findings using overexpressed parkin and indicates that phospho-Ub-dependent degradation of endogenous parkin does not require parkin's canonical mitochondrial poly-ubiquitination activity.
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