Abstract
Several loci and genes are associated with Parkinson's disease (IPD) with some interacting at a cellular level. For example PINK1 activates Parkin through phosphorylation of ubiquitin and enhances Parkin-mediated elimination of damaged mitochondria (mitophagy). Mutations in both may result in deregulation of mitochondrial homeostasis leading to neurodegeneration (Olszewska et al., 2014). Intimate knowledge of the interplay between gene products will be crucial for targeted-therapeutic development and pathway-based treatment initiatives (e.g., Parkin activators to enhance its housekeeping abilities in PD; Kazlauskaite et al., 2014).
Highlights
Specialty section: This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
It is important to understand the role of VPS35 and EIF4G1 first to fully appreciate complex interactions between them
VPS35 is a subunit of the retromer complex first described in yeast in 1998 (Small and Petsko, 2015)
Summary
Specialty section: This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience. A commentary on Parkinson’s Disease Genes VPS35 and EIF4G1 Interact Genetically and Converge on αSynuclein by Dhungel, N., Eleuteri, S., Li, L. Reviewed by: Diego Ezequiel Berman, Columbia University, USA Lynch T (2016) Commentary: Parkinson’s Disease Genes VPS35 and EIF4G1 Interact Genetically and Converge on α-Synuclein.
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