Voltage-gated ion channels are key regulators of cell excitability. There is significant
evidence that these channels are subject to modulation by redox status of the cells. Here we review
the post-translational modifications of ion channels that occur in colonic inflammation. The redox
mechanisms involve tyrosine nitration, covalent modification of cysteine residues and sulfhydration
by hydrogen sulfide in experimental colitis. In the setting of colonic inflammation, modifications of
cysteine and tyrosine are likely to occur at several sites within the same channel complex. In this review
we describe alterations in channel function due to specific modifications of tyrosine and cysteine
residues by reactive nitrogen, oxygen and hydrogen-sulfide resulting in altered motility.
Keywords: Calcium channel, hydrogen sulfide, oxidative stress, tyrosine nitration.
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