Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse
  1. Datensatz ansehen / 
  2. Datensatz Übersicht

Datensatz

DATENSATZ AKTIONENEXPORT
Zur Ablage hinzufügen
  Lokale TagsFreigabegeschichteDetailsÜbersicht

Freigegeben
Zeitschriftenartikel

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

MPG-Autoren
/persons/resource/persons95043

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

/persons/resource/persons93829

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;

Externe Ressourcen

https://www.nature.com/articles/352711a0.pdf
(beliebiger Volltext)

https://doi.org/10.1038/352711a0
(beliebiger Volltext)

Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte in PuRe verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

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.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0019-ACA9-5
Zusammenfassung
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.