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Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels

Department of Cell Biology, Division of Cellular and Molecular Neurobiology, University of Salzburg, Salzburg 5020, Austria
Department of Physiology of Man and Animals, Kazan Federal University, Kazan 420008, Russia
Author to whom correspondence should be addressed.
Academic Editors: Michael Breitenbach and Peter Eckl
Biomolecules 2015, 5(3), 1870-1911;
Received: 8 May 2015 / Revised: 17 July 2015 / Accepted: 20 July 2015 / Published: 17 August 2015
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals)
All cells contain ion channels in their outer (plasma) and inner (organelle) membranes. Ion channels, similar to other proteins, are targets of oxidative impact, which modulates ion fluxes across membranes. Subsequently, these ion currents affect electrical excitability, such as action potential discharge (in neurons, muscle, and receptor cells), alteration of the membrane resting potential, synaptic transmission, hormone secretion, muscle contraction or coordination of the cell cycle. In this chapter we summarize effects of oxidative stress and redox mechanisms on some ion channels, in particular on maxi calcium-activated potassium (BK) channels which play an outstanding role in a plethora of physiological and pathophysiological functions in almost all cells and tissues. We first elaborate on some general features of ion channel structure and function and then summarize effects of oxidative alterations of ion channels and their functional consequences. View Full-Text
Keywords: Maxi calcium-activated potassium ion channels; BK channels; KCNMA1; redox mechanisms; oxidation; hypoxia; ischemia Maxi calcium-activated potassium ion channels; BK channels; KCNMA1; redox mechanisms; oxidation; hypoxia; ischemia
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Hermann, A.; Sitdikova, G.F.; Weiger, T.M. Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels. Biomolecules 2015, 5, 1870-1911.

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