Inactivation of Parkin by Oxidative Stress and C-terminal Truncations

Loss of parkin function is linked to autosomal recessive juvenile parkinsonism. Here we show that proteotoxic stress and short C-terminal truncations induce misfolding of parkin. As a consequence, wild-type parkin was depleted from a high molecular weight complex and inactivated by aggregation. Simi...

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Veröffentlicht in:	The Journal of biological chemistry 2003-11, Vol.278 (47), p.47199-47208
Hauptverfasser:	Winklhofer, Konstanze F., Henn, Iris H., Kay-Jackson, Penelope C., Heller, Ulrich, Tatzelt, Jörg
Format:	Artikel
Sprache:	eng
Online-Zugang:	Volltext
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