Parkinson’s disease is increasing with prevalence and mutations in the DJ-1 gene have been linked with the development of a genetically inherited form of the disease. DJ-1’s role in Parkinson’s disease is largely unknown, however, due to its ability to protect from oxidative stress, DJ-1 is an exciting focus for therapeutic interventions. Dietary fructose intake is thought to result in glycosylated DNA damage, which was previously thought to be irreversible, however, it is possible that DJ-1 plays a role in reversing this damage by acting as a deglycase enzyme. DJ-1 has also been identified as a copper binding protein that may play a role in protection from copper toxicity.
Docking experiments involving glycosylated ligands and DJ-1 mutant variant C106A assessed the ability of the protein to act as a deglycase. Copper toxicity assay involving C106A, C53A and wild type DJ-1 assessed the copper protection capabilities of the protein. The results showed DJ-1 has multiple functions in the protection of neuronal cells and that mutations of the protein affect its functionality, however the two active sites investigated appear to have different functions. This study highlights the importance of further research into DJ-1 as a therapeutic avenue.
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