David S. Park

This study shows that mitochondrial proteostasis stress causes a biphasic cortisol response, with mild stress increasing and severe stress decreasing cortisol production, linking mitochondrial function to steroidogenesis in Parkinson's disease models.

This study identifies VDAC1 as a regulator of DJ-1's mitochondrial matrix localization, showing its role in maintaining mitochondrial homeostasis and neuronal survival under stress.

The paper develops a computational model of mitochondrial bioenergetics and integrates it with experimental data from Parkinson's Disease models to predict molecular defects and provide a resource for interpreting bioenergetic experiments.

This study identifies PFTK1's role in axogenesis by regulating RhoA phosphorylation and activity during CNS development in Drosophila and mice.

This study investigates how parkin's redox state and insolubility in human midbrain relate to oxidative stress and dopamine metabolism, showing that parkin's cysteine modifications affect H2O2 levels and neuroprotection.

This study shows that parkin reduces oxidative stress in mammalian brains by mediating H2O2 reduction and glutathione regeneration, but its absence leads to increased oxidative stress despite compensatory mechanisms.