ArticleProceedings of the National Academy of Sciences of the United States of America2004
Molecular basis for the inhibition of G protein-coupled inward rectifier K(+) channels by protein kinase C.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 91 citations in OpenAlex.
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- Consequences of somatic mutations of GIRK1 detected in primary malign tumors on expression and function of G-protein activated, inwardly rectifying, KFrontiers in oncology · 2022Article
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- Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH.American journal of physiology. Cell physiology · 2021Article
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- The Signaling Pathways Involved in the Anticonvulsive Effects of the Adenosine AInternational journal of molecular sciences · 2020Review
- The antitussive cloperastine improves breathing abnormalities in a Rett Syndrome mouse model by blocking presynaptic GIRK channels and enhancing GABA release.Neuropharmacology · 2020Article
- Oxytocin receptors excite lateral nucleus of central amygdala by phospholipase Cβ- and protein kinase C-dependent depression of inwardly rectifying KThe Journal of physiology · 2020Article
- Selective binding of a toxin and phosphatidylinositides to a mammalian potassium channel.Nature communications · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
G protein-coupled inward rectifier K(+) (GIRK) channels regulate cellular excitability and neurotransmission. The GIRK channels are activated by a number of inhibitory neurotransmitters through the G protein betagamma subunit (G(betagamma)) after activation of G protein-coupled receptors and inhibited by several excitatory neurotransmitters through activation of phospholipase C. If the inhibition is produced by PKC, there should be PKC phosphorylation sites in GIRK channel proteins. To identify the PKC phosphorylation sites, we performed systematic mutagenesis analysis on GIRK4 and GIRK1 subunits expressed in Xenopus oocytes. Our data showed that the heteromeric GIRK1/GIRK4 channels were inhibited by a PKC activator phorbol 12-myristate 13-acetate (PMA) through reduction of single channel open-state probability. Direct application of the catalytic subunit of PKC to excised patches had a similar inhibitory effect. This inhibition was greatly eliminated by mutation of Ser-185 in GIRK1 and Ser-191 in GIRK4 that remained G protein sensitive. The PKC-dependent phosphorylation seems to mediate the channel inhibition by the excitatory neurotransmitter substance P (SP) as specific PKC inhibitors and mutation of these PKC phosphorylation sites abolished the SP-induced inhibition of GIRK1/GIRK4 channels. Thus, these results indicate that the PKC-dependent phosphorylation underscores the inhibition of GIRK channels by SP, and Ser-185 in GIRK1 and Ser-191 in GIRK4 are the PKC phosphorylation sites.
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