ArticlePflugers Archiv : European journal of physiology2026
PKC isoform-specific targeting of the phosphorylation site Serine
Article in Pflugers Archiv : European journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
G Protein activated inwardly rectifying K+ (GIRK) channels are inhibited during stimulation of Gq Protein-coupled receptors (GqPCRs) by depletion of phosphatidyl-4,5-bisphosphate (PIP2) and/or channel phosphorylation by proteinkinase C (PKC). Receptor-specific effects of Gq signaling pathways on GIRK channel activity comprise the activation of different PKC isoforms that target distinct phosphorylation sites within the GIRK4 subunit. The serine residue S191 in the GIRK4 subunit is an important phosphorylation site for PKC which contributes to GIRK channel inhibition. Until now, the specific PKC isoform that phosphorylates this residue is unknown. Furthermore, the functional impact of S191 for Gq-receptor-specific GIRK channel modulation has not been investigated. To evaluate the contribution of this PKC phosphorylation site to receptor-specific GIRK channel modulation, we monitored the activity of phosphorylation-deficient GIRK4 (S191A) channel mutants during stimulation of adrenergic α1B-receptors (α1B-ARs) or Angiotensin AT1-receptors. GqPCR-dependent modulation of GIRK currents was analyzed in voltage-clamp experiments in rat atrial myocytes and in CHO cells expressing phosphorylation-deficient GIRK channels of various subunit compositions. As a novel finding, we demonstrate that the inhibition of phosphorylation-deficient GIRK4 (S191A) channels is impaired during stimulation of AT1-Rs, indicating that this phosphorylation site is targeted at least by the Angiotensin II-activated PKCε isoform. In contrast, ablation of the S191 phosphorylation site does not attenuate phenylephrine-induced GIRK reduction, suggesting that S191 is not a primary target for the α1B-AR activated PKCα. Our data indicate that the different GqPCR-activated PKC isoforms target distinct phosphorylation sites within the GIRK4 subunit, resulting in receptor-specific regulation of the phosphorylation-deficient GIRK4 (S191A) channel mutant.
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