Science signaling podcast for 9 May 2017

Trafficking of BK channel subunits in arterial myocytes

Jonathan Jaggar, Annalisa M. Van Hook

Research output: Contribution to journalReview article

Abstract

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 p1 BK channel subunit to the plasma membrane. Membrane depolarization caused the p1 subunit to translocate to the plasma membrane, where it associated with the pore-forming a 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.

Original languageEnglish (US)
Article numberaan4849
JournalScience Signaling
Volume10
Issue number478
DOIs
StatePublished - May 9 2017

Fingerprint

Webcasts
Large-Conductance Calcium-Activated Potassium Channels
Muscle Cells
Depolarization
Membranes
Cell membranes
Potassium
Cell Membrane
Calcium
Potassium Channels
Calcium Channels
Vasoconstriction
Ion Channels
Vasodilation
Feedback
Research

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Science signaling podcast for 9 May 2017 : Trafficking of BK channel subunits in arterial myocytes. / Jaggar, Jonathan; Van Hook, Annalisa M.

In: Science Signaling, Vol. 10, No. 478, aan4849, 09.05.2017.

Research output: Contribution to journalReview article

@article{cc0a3e33b8e24adcab01a37d14d79b76,
title = "Science signaling podcast for 9 May 2017: Trafficking of BK channel subunits in arterial myocytes",
abstract = "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 p1 BK channel subunit to the plasma membrane. Membrane depolarization caused the p1 subunit to translocate to the plasma membrane, where it associated with the pore-forming a 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.",
author = "Jonathan Jaggar and {Van Hook}, {Annalisa M.}",
year = "2017",
month = "5",
day = "9",
doi = "10.1126/scisignal.aan4849",
language = "English (US)",
volume = "10",
journal = "Science Signaling",
issn = "1937-9145",
publisher = "American Association for the Advancement of Science",
number = "478",

}

TY - JOUR

T1 - Science signaling podcast for 9 May 2017

T2 - Trafficking of BK channel subunits in arterial myocytes

AU - Jaggar, Jonathan

AU - Van Hook, Annalisa M.

PY - 2017/5/9

Y1 - 2017/5/9

N2 - 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 p1 BK channel subunit to the plasma membrane. Membrane depolarization caused the p1 subunit to translocate to the plasma membrane, where it associated with the pore-forming a 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.

AB - 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 p1 BK channel subunit to the plasma membrane. Membrane depolarization caused the p1 subunit to translocate to the plasma membrane, where it associated with the pore-forming a 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.

UR - http://www.scopus.com/inward/record.url?scp=85019222066&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85019222066&partnerID=8YFLogxK

U2 - 10.1126/scisignal.aan4849

DO - 10.1126/scisignal.aan4849

M3 - Review article

VL - 10

JO - Science Signaling

JF - Science Signaling

SN - 1937-9145

IS - 478

M1 - aan4849

ER -