Figure 3

Schematic diagram showing proposed neuroprotective properties of UCP4 against oxidative stress in the pro-survival NF-κB pathway. External stimuli (e.g. TNF-α) activate NF-κB subunits (e.g. c-Rel, p50) via phosphorylation of IκB-α. Nuclear translocation of c-Rel and p50 promote transcription of UCP4 gene. Increased expression of UCP4 in mitochondria suppresses oxidative stress by stabilizing mitochondrial membrane potential and preserving cellular ATP level.