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Journal of Neuroscience, Vol 16, 930-938, Copyright © 1996 by Society for Neuroscience
A G-protein-activated inwardly rectifying K+ channel (GIRK4) from human hippocampus associates with other GIRK channels
A Spauschus, KU Lentes, E Wischmeyer, E Dissmann, C Karschin and A Karschin
Molecular Neurobiology of Signal Transduction, Max Planck Institute for Biophysical Chemistry, Gottingen, Germany.
Transcripts of a gene, GIRK4, that encodes for a 419-amino-acid protein and
shows high structural similarity to other subfamily members of G-
protein-activated inwardly rectifying K+ channels (GIRK) have been
identified in the human hippocampus. When expressed in Xenopus oocytes,
GIRK4 yielded functional GIRK channels with activity that was enhanced by
the stimulation of coexpressed serotonin 1A receptors. GIRK4 potentiated
basal and agonist-induced currents mediated by other GIRK channels,
possibly because of channel heteromerization. Despite the structural
similarity to a putative rat KATP channel, no ATP sensitivity or
KATP-typical pharmacology was observed for GIRK4 alone or GIRK4 transfected
in conjunction with other GIRK channels in COS-7 cells. In rat brain, GIRK4
is expressed together with three other subfamily members, GIRK1-3, most
likely in identical hippocampal neurons. Thus, heteromerization or an
unknown molecular interaction may cause the physiological diversity
observed within this class of K+ channels.
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