Regulation of fast inactivation of cloned mammalian IK(A) channels by cysteine oxidation.
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.
Ruppersberg
J P
JP
Max-Planck-Institut für medizinische Forschung, Abteilung Zellphysiologie, Heidelberg, Germany.
Stocker
M
M
Pongs
O
O
Heinemann
S H
SH
Frank
R
R
Koenen
M
M
D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D003001:Cloning, Molecular; D003545:Cysteine; D004331:Drosophila melanogaster; D005978:Glutathione / Q000502:physiology; D066298:In Vitro Techniques; D015640:Ion Channel Gating; D007700:Kinetics; D008969:Molecular Sequence Data; D009841:Oligonucleotides / Q000737:chemistry; D009865:Oocytes; D010084:Oxidation-Reduction; D015221:Potassium Channels / Q000737:chemistry*; D011994:Recombinant Proteins; D014982:Xenopus laevis
D009841:Oligonucleotides; D015221:Potassium Channels; D011994:Recombinant Proteins; D005978:Glutathione; D003545:Cysteine