Science Signaling Podcast for 9 May 2017: Trafficking of BK channel subunits in arterial myocytes

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Science Signaling  09 May 2017:
Vol. 10, Issue 478, eaan4849
DOI: 10.1126/scisignal.aan4849

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This Podcast features a conversation with Jonathan Jaggar, senior author of a Research Article that appears in the 9 May 2017 issue of Science Signaling, about trafficking of big potassium (BK) channel subunits in arterial myocytes. Depolarization of the arterial myocyte membrane causes a rise in intracellular calcium that stimulates the cell to contract, which leads to vasoconstriction. Membrane depolarization also activates BK channels, which allow potassium to flow out of the cell, thus repolarizing the membrane and promoting vasodilation. Leo et al. found that a critical aspect of this negative feedback mechanism was the trafficking of the regulatory β1 BK channel subunit to the plasma membrane. Membrane depolarization caused the β1 subunit to translocate to the plasma membrane, where it associated with the pore-forming α subunit to increase the calcium sensitivity of the channel. These findings identify trafficking of regulatory subunits as a mode of regulation for multisubunit ion channels.

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