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Antimycin A (AntA) is a potent Electron Transport System (ETS) inhibitor exerting its effect through inhibiting the transfer of the electrons by binding to the quinone reduction site of the cytochrome bc1 complex (Complex III), which is known to be impaired in Huntington’s Disease (HD). The current studies were undertaken to investigate the effect of complex III inhibition in the SH-SY5Y cell line to delineate the molecular and cellular processes, which may play a role in the pathogenesis of HD.

We treated SH-SY5Y neuroblastoma cells with AntA in order to establish an in vitro mitochondrial dysfunction model for HD. Differential proteome analysis was performed by the nLCMS/ MS system. Protein expression was assessed by western blot analysis.

Thirty five differentially expressed proteins as compared to the vehicle-treated controls were detected. Functional pathway analysis …