鉴定α-突触核蛋白介导的帕金森病细胞毒性机制:基于生物信息学的新见解

IF 0.6 Q4 CLINICAL NEUROLOGY
S. Chakrabarti, V. S. Sunder, Upinder Kaur, Sapna Bala, Priyanka Sharma, Manjari Kiran, R. Rawal, S. Chakrabarti
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引用次数: 3

摘要

目的:大量证据表明α-突触核蛋白在帕金森病(PD)中具有细胞毒性。我们计划使用基于生物信息学的方法来进一步了解这一过程。材料和方法:使用STRING版本10,我们鉴定了α-突触核蛋白的相互作用蛋白。使用α-突触核蛋白和其中一种参与细胞凋亡的相互作用蛋白作为查询蛋白,我们鉴定了其他连接蛋白。我们使用ClusPro通过蛋白质-蛋白质对接进一步分析了其中一些蛋白质之间的相互作用。结果:BAX为α-突触核蛋白的相互作用蛋白。测定了α-突触核蛋白与BAX、BAX与BCL2L1的相互作用。结论:α-突触核蛋白与BAX的相互作用可能在PD的细胞死亡过程中起着至关重要的作用,细胞凋亡和线粒体通透性转换驱动的坏死可能共存。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Identifying the mechanisms of α-synuclein-mediated cytotoxicity in Parkinson’s disease: new insights from a bioinformatics-based approach
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.
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来源期刊
Future Neurology
Future Neurology CLINICAL NEUROLOGY-
CiteScore
2.10
自引率
0.00%
发文量
10
期刊介绍: The neurological landscape is changing rapidly. From the technological perspective, advanced molecular approaches and imaging modalities have greatly increased our understanding of neurological disease, with enhanced prospects for effective treatments in common but very serious disorders such as stroke, epilepsy, multiple sclerosis and Parkinson’s disease. Nevertheless, at the same time, the healthcare community is increasingly challenged by the rise in neurodegenerative diseases consequent upon demographic changes in developed countries.
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