Primary structure and functional expression of a rat G-protein-coupled muscarinic potassium channel

Y Kubo, E Reuveny, PA Slesinger, YN Jan, LY Jan - Nature, 1993 - nature.com
Y Kubo, E Reuveny, PA Slesinger, YN Jan, LY Jan
Nature, 1993nature.com
PARASYMPATHETIC nerve stimulation causes slowing of the heart rate by activation of
muscarinic receptors and the subsequent opening of muscarinic K+ channels in the
sinoatrial node and atrium1–4. This inwardly rectifying K+ channel is coupled directly with G
protein5–10. Based on sequence homology with cloned inwardly rectifying K+ channels,
ROMK1 (ref. 11) and IRK1 (ref. 12), we have isolated a complementary DNA for a G-protein-
coupled inwardly rectifying K+ channel (GIRK1) from rat heart. The GIRK1 channel probably …
Abstract
PARASYMPATHETIC nerve stimulation causes slowing of the heart rate by activation of muscarinic receptors and the subsequent opening of muscarinic K+ channels in the sinoatrial node and atrium1–4. This inwardly rectifying K+ channel is coupled directly with G protein5–10. Based on sequence homology with cloned inwardly rectifying K+ channels, ROMK1 (ref. 11) and IRK1 (ref. 12), we have isolated a complementary DNA for a G-protein-coupled inwardly rectifying K+ channel (GIRK1) from rat heart. The GIRK1 channel probably corresponds to the muscarinic K channel because (1) its functional properties resemble those of the a trial muscarinic K+ channel and (2) its messenger RNA is much more abundant in the atrium than in the ventricle. In addition, GIRK1 mRNA is expressed not only in the heart but also in the brain.
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