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_6
Snippet: Neuronally differentiated PC12 cells also possess levels of parkin that are easily detected by WB, making them a fitting model in which to evaluate the effect of stress on endogenous parkin. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder.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 Next, we asked whether decreased production and/or increased degradation is responsible for parkin loss after .....
Document: Neuronally differentiated PC12 cells also possess levels of parkin that are easily detected by WB, making them a fitting model in which to evaluate the effect of stress on endogenous parkin. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder.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 Next, we asked whether decreased production and/or increased degradation is responsible for parkin loss after L-DOPA treatment. We did not observe a significant decrease in parkin mRNA levels after L-DOPA treatment (relative mRNA level after 27 or with L-DOPA treatment, respectively. In contrast, there was no effect of L-DOPA on the halflife of ERK1 protein (Fig. S3B) . These findings suggest that the loss of parkin that occurs with L-DOPA is due at least in part to its enhanced degradation.
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