GAPDH as a sensor of NO stress: S-nitrosylation of GAPDH

TOXI 12

Akira Sawa, asawa1@jhmi.edu, Psychiatry, Johns Hopkins University, 600 N. Wolfe Street, CMSC 8-117, Baltimore, MD 21287
Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a classic glycolytic enzyme, but its role as a mediator for cell death has recently been highlighted. Many groups reported that a pool of GAPDH translocates to the nucleus under a variety of stressors, most of which are associated with oxidative stress. Here I report its sequential molecular mechanism as follows: first, a catalytic cysteine in GAPDH (C150 in rat GAPDH) is S-nitrosylated by nitric oxide (NO) that is generated from inducible nitric oxide synthase (iNOS) and/or neuronal NOS (nNOS); second, the modified GAPDH becomes capable of binding with Siah1, an E3 ubiquitin ligase, and stabilizes it; third, the GAPDH-Siah protein complex translocates to the nucleus, dependent on Siah1's nuclear localization signal, and degrades Siah1's substrates in the nucleus, which results in cytotoxicity. I will further discuss a possible role of GAPDH in neurodegenerative disorders.