The ubiquitin E3 ligase parkin regulates the proapoptotic function of Bax

Autosomal recessive loss-of-function mutations within the PARK2 gene functionally inactivate the E3 ubiquitin ligase parkin, resulting in neurodegeneration of catecholaminergic neurons and a familial form of Parkinson disease. Current evidence suggests both a mitochondrial function for parkin and a...

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 2012-04, Vol.109 (16), p.6283-6288
Hauptverfasser:	Johnson, Bethann N., Berger, Alison K., Cortese, Giuseppe P., LaVoie, Matthew J.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis Bax protein bcl-2-Associated X Protein - genetics bcl-2-Associated X Protein - metabolism Binding Sites - genetics Biological Sciences Blotting, Western Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology Cell culture Cell death Cell lines Cells, Cultured CHO Cells Cricetinae Cricetulus Cytochrome c Cytochromes Cytosol Data processing Genetic mutation Green Fluorescent Proteins - genetics Green Fluorescent Proteins - metabolism Lysine - genetics Lysine - metabolism Mice Mice, Knockout Microscopy, Fluorescence Mitochondria Mitochondria - metabolism Movement disorders Mutation Neurodegeneration Neurodegenerative diseases Neurons Neurons - cytology Neurons - metabolism Neuroprotection Parkin protein Parkinson disease Parkinson's disease Protein Binding Protein Transport - drug effects Proton Ionophores - pharmacology Transfection Translocation Ubiquitin-protein ligase Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism ubiquitination Ubiquitination - drug effects Ubiquitins
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