IndraLab

Statements

PRKN activates UCHL1. 3 / 3
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"Taken together, these results suggest that loss of parkin mediated UCH-L1 regulation may be a pathogenic mechanism contributing to neurodegeneration in human ARJP patients with parkin mutations."
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"The parkin induced UCH-L1 degradation was blocked by the lysosome inhibitor chloroquine (CQ) or the autophagy inhibitor 3MA but not by the proteasome inhibitor MG132 (XREF_FIG)."
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"Consistent with the accelerated UCH-L1 turnover rate induced by parkin overexpression, the steady-state level of endogenous UCH-L1 protein was significantly lower in parkin WT overexpressing SH-SY5Y cells than that in the vector transfected control cells (XREF_FIG)."
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