Parkin suppresses wild-type alpha-synuclein-induced toxicity in SHSY-5Y cells.

Current hypotheses concerning the mechanism of neuronal cell death in Parkinson's disease (PD) and related synucleopathies propose a functional interaction between parkin and alpha-synuclein (alphaS). Recently parkin was shown to suppress mutant alphaS-induced toxicity in primary neurons, providing a basis for an association between these proteins and neuronal loss [Neuron ...
36 (2000) 1007-1019]. We have asked if a similar association could be made between wild-type (wt) alphaS and parkin. We examined inducible over-expression of alphaS in SHSY-5Y cells through adenoviral infection under conditions which produce cellular toxicity through a reduction in ATP levels. We demonstrate that parkin suppresses toxicity induced by mutant (A53T) and wt alphaS. Parkin over-expression was also associated with the appearance of higher molecular weight alphaS-immunoreactive bands by Western blot analysis. These data, consistent with a protective role for parkin, extend previous findings to include a functional association between parkin and the wt form of alphaS.
Mesh Terms:
Adenosine Triphosphate, Adenoviridae, Cell Line, Cell Survival, Cytoprotection, Gene Expression, Genetic Vectors, Ligases, Mutation, Nerve Tissue Proteins, Neurons, Synucleins, Transfection, Ubiquitin-Protein Ligases, alpha-Synuclein
Biochem. Biophys. Res. Commun.
Date: Sep. 26, 2003
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