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Regulation of ion channel structure and function by reactive oxygen-nitrogen species

Departments of ¹Physiology and Biophysics and ²Anesthesiology and the ³Medical Scientists Training Program, University of Alabama at Birmingham, Birmingham Alabama 35233; Departments of ⁴Pediatrics and ⁵Physiology and the Center for Cell and Molecular Signaling, Emory University School of Medicine, Atlanta, Georgia 30322; ⁶Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853-6401; Departments of ⁷Medicine and ⁹Biochemistry and Howard Hughes Medical Institute, Duke University Medical Center, Durham 27710; and ⁸Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599-7260

Ion channels subserve diverse cellular functions. Reactive oxygen and nitrogen species modulate ion channel function by a number of mechanisms including 1) transcriptional regulation of gene expression, 2) posttranslational modifications of channel proteins, i.e. nitrosylation, nitration, and oxidation of key amino acid residues, 3) by altering the gain in other signaling pathways that may in turn lead to changes in channel activity or channel gene expression, and 4) by modulating trafficking or turnover of channel proteins, as typified by oxygen radical activation of NF-kB, with subsequent changes in proteasomal degradation of channel degradation. Regardless of the mechanism, as was discussed in a symposium at the 2003 Experimental Biology Meeting in San Diego, CA, changes in the cellular level of reactive oxygen and nitrogen species can have profound effects on the activity of ion channels and cellular function.

calcium channels; potassium channels; sodium channels; chloride channels; nitric oxide; cystic fibrosis transmembrane conductance regulator

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