期刊
JOURNAL OF NEUROCHEMISTRY
卷 137, 期 5, 页码 673-686出版社
WILEY
DOI: 10.1111/jnc.13599
关键词
DJ-1; Drp1; mitochondria; parkin; Parkinson's; disease; PGC-1 alpha; SUMO; alpha-synuclein
资金
- ISN-CAEN Return Home Grant
- IBRO Return Home Fellowship
- Newton Advanced Fellowship
- PNPD/CAPES post-doctoral fellowship
Parkinson's disease (PD) is the second most common neurodegenerative disorder characterized by cardinal motor signs such as rigidity, bradykinesia or rest tremor that arise from a significant death of dopaminergic neurons. Nondopaminergic degeneration also occurs and it seems to induce the deficits in olfactory, emotional, and memory functions that precede the classical motor symptoms in PD. Despite the majority of PD cases being sporadic, several genes have previously been associated with the hereditary forms of the disease. The proteins encoded by some of these genes, including a-synuclein, DJ-1, and parkin, are modified by small ubiquitin-like modifier (SUMO), a post-translational modification that regulates a variety of cellular processes. Among the several pathogenic mechanisms proposed for PD is mitochondria' dysfunction. Recent studies suggest that SUMOylation can interfere with mitochondrial dynamics, which is essential for neuronal function, and may play a pivotal role in PD pathogenesis. Here, we present an overview of recent studies on mitochondrial disturbance in PD and the potential SUMO-modified proteins and pathways involved in this process.
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