Figure 1.
Figure 1. Phosphorylation of IKs by PKA. Once the G protein–coupled β-adrenergic receptor is activated, GTP binds to the α-subunit of the G protein, which allows for the release of active α-GTP subunits. This complex binds and activates adenylyl cyclase (AC), producing cAMP, which activates cAMP-dependent PKA. Yotiao anchors PKA to the KCNQ1 channel, which allows the activated PKA to phosphorylate the N terminus of the KCNQ1 channel. Protein phosphatase 1 can dephosphorylate cAMP-mediated phosphorylation and is blocked by OA.

Phosphorylation of IKs by PKA. Once the G protein–coupled β-adrenergic receptor is activated, GTP binds to the α-subunit of the G protein, which allows for the release of active α-GTP subunits. This complex binds and activates adenylyl cyclase (AC), producing cAMP, which activates cAMP-dependent PKA. Yotiao anchors PKA to the KCNQ1 channel, which allows the activated PKA to phosphorylate the N terminus of the KCNQ1 channel. Protein phosphatase 1 can dephosphorylate cAMP-mediated phosphorylation and is blocked by OA.

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