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Likewise, depletion of folliculin (FLCN), a component of the FNIP/FLCN GAP complex that promotes GDP-loading of RAGC (Lawrence et al, 2019), resulted in TFE3-L stabilization (Fig

Simonian, 2021

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Honzik T, Adamovicova M, Smolka V, et al

The molecular mechanisms proposed to explain how ROS could specifically mediate brain damage are the following: (1) The lower levels of antioxidants can promote increased activity of lipoxygenase in CNS stimulating leukotriene production, thereby increasing the immunoinflammatory processes in the cerebral cortex