scholarly journals Correction for Yao et al., Nitrosative stress linked to sporadic Parkinson's disease: S-nitrosylation of parkin regulates its E3 ubiquitin ligase activity, PNAS 2004 101:10810-10814

2004 ◽  
Vol 101 (38) ◽  
pp. 13969-13969 ◽  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ubiquitin Ligase ◽  
Nitrosative Stress ◽  
E3 Ubiquitin Ligase ◽  
Ubiquitin Ligase Activity ◽  
Sporadic Parkinson’S Disease

scholarly journals CHIP Is Associated with Parkin, a Gene Responsible for Familial Parkinson's Disease, and Enhances Its Ubiquitin Ligase Activity

2002 ◽  
Vol 10 (1) ◽  
pp. 55-67 ◽  
Author(s):  
Yuzuru Imai ◽  
Mariko Soda ◽  
Shigetsugu Hatakeyama ◽  
Takumi Akagi ◽  
Tsutomu Hashikawa ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ubiquitin Ligase ◽  
Ubiquitin Ligase Activity ◽  
Familial Parkinson’S Disease

scholarly journals The Landscape of Parkin Variants Reveals Pathogenic Mechanisms and Therapeutic Targets in Parkinson’s Disease

2018 ◽  
Author(s):  
Wei Yi ◽  
Emma J. MacDougall ◽  
Matthew Y. Tang ◽  
Andrea I. Krahn ◽  
Ziv Gan-Or ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Specific Drug ◽  
Common Cause ◽  
Naturally Occurring ◽  
Population Databases ◽  
Early Onset Parkinson’S Disease

AbstractMutations in Parkin (PARK2), which encodes an E3 ubiquitin ligase implicated in mitophagy, are the most common cause of early onset Parkinson’s Disease (PD). Hundreds of naturally occurring Parkin variants have been reported, both in PD patient and population databases. However, the effects of the majority of these variants on the function of Parkin and in PD pathogenesis remains unknown. Here we develop a framework for classification of the pathogenicity of Parkin variants based on the integration of clinical and functional evidence – including measures of mitophagy and protein stability, and predictive structural modeling – and assess 51 naturally occurring Parkin variants accordingly. Surprisingly, only a minority of Parkin variants, even among those previously associated with PD, disrupted Parkin function. Moreover, a few of these naturally occurring Parkin variants actually enhanced mitophagy. Interestingly, impaired mitophagy in several of the most common pathogenic Parkin variants could be rescued both by naturally-occurring (p.V224A) and structure-guided designer (p.W403A; p.F146A) hyperactive Parkin variants. Together, the findings provide a coherent framework to classify Parkin variants based on pathogenicity and suggest that several pathogenic Parkin variants represent promising targets to stratify patients for genotype-specific drug design.

The FBXO7 homologue nutcracker and binding partner PI31 in Drosophila melanogaster models of Parkinson’s disease

Genome ◽  
2017 ◽  
Vol 60 (1) ◽  
pp. 46-54 ◽  
Author(s):  
Eric M. Merzetti ◽  
Lindsay A. Dolomount ◽  
Brian E. Staveley
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Drosophila Melanogaster ◽  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Severe Form ◽  
Altered Expression ◽  
Binding Partner ◽  
Locomotor Control ◽  
Dependent Model

Parkinsonian-pyramidal syndrome (PPS) is an early onset form of Parkinson’s disease (PD) that shows degeneration of the extrapyramidal region of the brain to result in a severe form of PD. The toxic protein build-up has been implicated in the onset of PPS. Protein removal is mediated by an intracellular proteasome complex: an E3 ubiquitin ligase, the targeting component, is essential for function. FBXO7 encodes the F-box component of the SCF E3 ubiquitin ligase linked to familial forms of PPS. The Drosophila melanogaster homologue nutcracker (ntc) and a binding partner, PI31, have been shown to be active in proteasome function. We show that altered expression of either ntc or PI31 in dopaminergic neurons leads to a decrease in longevity and locomotor ability, phenotypes both associated with models of PD. Furthermore, expression of ntc-RNAi in an established α-synuclein-dependent model of PD rescues the phenotypes of diminished longevity and locomotor control.

scholarly journals TRIM9, a novel brain-specific E3 ubiquitin ligase, is repressed in the brain of Parkinson's disease and dementia with Lewy bodies

2010 ◽  
Vol 38 (2) ◽  
pp. 210-218 ◽  
Author(s):  
Kunikazu Tanji ◽  
Tetsu Kamitani ◽  
Fumiaki Mori ◽  
Akiyoshi Kakita ◽  
Hitoshi Takahashi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ubiquitin Ligase ◽  
Dementia With Lewy Bodies ◽  
E3 Ubiquitin Ligase ◽  
Lewy Bodies ◽  
The Brain
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