
Identifying the mechanisms of α-synuclein-mediated cytotoxicity in Parkinson’s disease: new insights from a bioinformatics-based approach
Author(s) -
Sankha Shubhra Chakrabarti,
Venkatadri S Sunder,
Upinder Kaur,
Sapna Bala,
Priyanka Sharma,
Manjari Kiran,
Ravindra K. Rawal,
Sasanka Chakrabarti
Publication year - 2020
Publication title -
future neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.419
H-Index - 32
eISSN - 1748-6971
pISSN - 1479-6708
DOI - 10.2217/fnl-2020-0007
Subject(s) - mitochondrial permeability transition pore , parkinson's disease , cytotoxicity , apoptosis , programmed cell death , docking (animal) , protein–protein interaction , bax protein , microbiology and biotechnology , bioinformatics , biology , computational biology , disease , chemistry , biochemistry , medicine , protein expression , in vitro , pathology , gene , nursing
Aim: A large body of evidence has implicated the cytotoxicity of α-synuclein in Parkinson’s disease (PD). We planned to use a bioinformatics-based approach to gain further insight into this process. Materials & methods: Using STRING version 10, we identified interacting proteins of α-synuclein. Using α-synuclein and one of these interactors involved in apoptosis as query proteins, we identified other linked proteins. We further analyzed the interactions between some of these proteins by Protein–Protein Docking using ClusPro. Results: We identified BAX as an interacting protein of α-synuclein. Interactions of α-synuclein and BAX as well as BAX and BCL2L1 were determined. Conclusion: The interaction of α-synuclein and BAX could play a crucial role in the cell death process of PD where apoptosis and mitochondrial permeability transition-driven necrosis may coexist.