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Journal Article

Regulation of fast inactivation of cloned mammalian IK(A) channels by cysteine oxidation

MPS-Authors
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Ruppersberg,  J. Peter
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Koenen,  Michael
Molecular anatomy of the neuromuscular junction, Max Planck Institute for Medical Research, Max Planck Society;
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society;
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Ruppersberg, J. P., Stocker, M., Pongs, O., Heinemann, S. H., Frank, R., & Koenen, M. (1991). Regulation of fast inactivation of cloned mammalian IK(A) channels by cysteine oxidation. Nature, 352(6337), 711-714. doi:10.1038/352711a0.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-ACA9-5
Abstract
Modulation of neuronal excitability by regulation of K+ channels potentially plays a part in short-term memory but has not yet been studied at the molecular level. Regulation of K+ channels by protein phosphorylation and oxygen has been described for various tissues and cell types; regulation of fast-inactivating K+ channels mediating IK(A) currents has not yet been described. Functional expression of cloned mammalian K+ channels has provided a tool for studying their regulation at the molecular level. We report here that fast-inactivating K+ currents mediated by cloned K+ channel subunits derived from mammalian brain expressed in Xenopus oocytes are regulated by the reducing agent glutathione. This type of regulation may have a role in vivo to link metabolism to excitability and to regulate excitability in specific membrane areas of mammalian neurons.