mediates brain damage when it is over-activated by oxidative/nitrosative stress.
Nonetheless, it remains unclear how PARP-1 is activated in neuropathological contexts.
Here we report that PARP-1 interacts with a pool of glyceradehyde-3-phosphate
dehydrogenase (GAPDH) that translocates into the nucleus under oxidative/nitrosative
stress both in vitro and in vivo. A well conserved amino acid at the N terminus of GAPDH …