Table 1.

Neural roles of nitrosylation

Protein targets	Alteration in function	Physiological/pathophysiological relevance	Refs
COX2	Increase in activity, binds nNOS	Decrease in NMDA-mediated neurotoxicity	[34,35]
Dexras	Increase in activity	Enhanced iron uptake and NMDA-mediated neurotoxicity	[23]
Drp1	Increase in GTPase activity and mitochondrial fission	Increase in cell death in Alzheimer’s disease	[33]
GAPDH	Decrease in activity, nuclear translocation	Increase in cell death in MPTP parkinsonism	[25,27]
GOSPEL	Increase in binding to GAPDH, prevent nuclear translocation of GAPDH	Decrease in cell death in NMDA-mediated neurotoxicity	[26]
NMDAR	Decrease in activity	Decrease in NO production	[10]
NSF	Increase in activity and decrease in platelet granules	Increase in AMPAR surface expression	[17]
Parkin	Decrease in activity	Increase in cell death in Parkinson’s disease and Alzheimer’s disease	[28]
Stargazin	Increase in interaction with AMPAR	Increase in surface expression of AMPAR	[19]
Serine racemase	Decrease in activity	Increase in stroke	[20]

COX2, cyclo-oxygenase-2; Drp1, dynamin related protein-1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GOSPEL, GAPDH’s competitor of Siah protein enhances life; NMDAR, N-methyl-D-aspartate receptor; NSF, N-ethylmaleimide sensitive factor; AMPAR, α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.