Identification of cysteine involved in oxidation-induced inhibition of channel function

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Nitric-oxide-induced calcium release (NICR) in cerebellar Purkinje cells was revealed to be inhibited by oxidative signal and aging. Correspondingly, S-nitrosylation of calcium-release channels, essential for NICR, was also impaired by oxidative signal and aging. Biochemical analysis further confirmed that oxidation was induced in the channels by oxidative signal and aging. These observations indicate that oxidative signal inhibit S-nitrosylation as well as NICR through formation of disulfide bond in which cysteine residue of S-nitrosylation site is involved. Because the cysteine residue is incorporated into the disulfide bond, the residue is no longer susceptible to NO and S-nitrosylation.