Abstract
We have cloned by homology screening from a rat brain cDNA library a GIRK3-type (Kir 3.3) inwardly rectifying K+ channel subunit with high structural similarity to other subfamily members whose activity is thought to be controlled by receptor-stimulated G proteins. When heterologously expressed both in Xenopus oocytes and in mammalian COS-7 cells, rbGIRK3 subunits individually fail to form functional channels. In contrast, when coexpressed with other GIRK subunits, rbGIRK3 gives rise to prominent currents which are enhanced by the stimulation of coexpressed 5-HT1A receptors. In situ hybridizations show that of all GIRK subunits rbGIRK3 is most widely distributed and strongly expressed throughout the rat brain and thus may play an important role in central signal processing.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Base Sequence
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Brain / metabolism*
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Cell Line
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Chlorocebus aethiops
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DNA, Complementary
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Female
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G Protein-Coupled Inwardly-Rectifying Potassium Channels
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GTP-Binding Proteins / metabolism*
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Gene Library
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In Situ Hybridization
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Molecular Sequence Data
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Oocytes / physiology
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Open Reading Frames
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Potassium Channels / biosynthesis*
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Potassium Channels / physiology
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Potassium Channels, Inwardly Rectifying*
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RNA, Messenger / analysis
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RNA, Messenger / biosynthesis*
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Rats
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Rats, Wistar
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Recombinant Proteins / metabolism
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Sequence Homology, Amino Acid
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Transfection
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Xenopus
Substances
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DNA, Complementary
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G Protein-Coupled Inwardly-Rectifying Potassium Channels
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Kcnj9 protein, rat
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Potassium Channels
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Potassium Channels, Inwardly Rectifying
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RNA, Messenger
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Recombinant Proteins
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GTP-Binding Proteins