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

被引:76
作者
Matalon, S
Hardiman, KM
Jain, L
Eaton, DC
Kotlikoff, M
Eu, JP
Sun, JH
Meissner, G
Stamler, JS
机构
[1] Univ Alabama, Dept Physiol & Biophys, Birmingham, AL 35233 USA
[2] Univ Alabama, Med Sci Training Program, Birmingham, AL 35233 USA
[3] Univ Alabama, Dept Anesthesiol, Birmingham, AL 35233 USA
[4] Emory Univ, Sch Med, Dept Pediat, Atlanta, GA 30322 USA
[5] Emory Univ, Sch Med, Dept Physiol, Atlanta, GA 30322 USA
[6] Emory Univ, Sch Med, Ctr Cell & Mol Signaling, Atlanta, GA 30322 USA
[7] Cornell Univ, Coll Vet Med, Dept Biomed Sci, Ithaca, NY 14853 USA
[8] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA
[9] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA
[10] Duke Univ, Med Ctr, Howard Hughes Med Inst, Durham, NC 27710 USA
[11] Univ N Carolina, Dept Biochem & Biophys, Chapel Hill, NC 27599 USA
关键词
calcium channels; potassium channels; sodium channels; chloride channels; nitric oxide; cystic fibrosis transmembrane conductance regulator;
D O I
10.1152/ajplung.00281.2003
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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.
引用
收藏
页码:L1184 / L1189
页数:6
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