Genetic variation in the two-pore domain potassium channel, TASK-1, may contribute to an atrial substrate for arrhythmogenesis

Bo Liang; Magdalena Soka; Alex Horby Christensen; Morten S Olesen; Anders P Larsen; Filip K Knop; Fan Wang; Jonas B Nielsen; Martin Andersen; David Humphreys; Stefan A Mann; Inken G Huttner; Jamie I Vandenberg; Jesper H Svendsen; Stig Haunsø; Thomas Preiss; Guiscard Seebohm; Søren Peter Olesen; Nicole Schmitt; Diane Fatkin

doi:10.1016/j.yjmcc.2013.12.014

Genetic variation in the two-pore domain potassium channel, TASK-1, may contribute to an atrial substrate for arrhythmogenesis

Bo Liang, Magdalena Soka, Alex Horby Christensen, Morten S Olesen, Anders P Larsen, Filip K Knop, Fan Wang, Jonas B Nielsen, Martin Andersen, David Humphreys, Stefan A Mann, Inken G Huttner, Jamie I Vandenberg, Jesper H Svendsen, Stig Haunsø, Thomas Preiss, Guiscard Seebohm, Søren Peter Olesen, Nicole Schmitt, Diane Fatkin

68 Citationer (Scopus)

Abstract

The two-pore domain potassium channel, K2P3.1 (TASK-1) modulates background conductance in isolated human atrial cardiomyocytes and has been proposed as a potential drug target for atrial fibrillation (AF). TASK-1 knockout mice have a predominantly ventricular phenotype however, and effects of TASK-1 inactivation on atrial structure and function have yet to be demonstrated in vivo. The extent to which genetic variation in KCNK3, that encodes TASK-1, might be a determinant of susceptibility to AF is also unknown. To address these questions, we first evaluated the effects of transient knockdown of the zebrafish kcnk3a and kcnk3b genes and cardiac phenotypes were evaluated using videomicroscopy. Combined kcnk3a and kcnk3b knockdown in 72 hour post fertilization embryos resulted in lower heart rate (p

Originalsprog	Engelsk
Tidsskrift	Journal of Molecular and Cellular Cardiology
Vol/bind	67
Sider (fra-til)	69-76
ISSN	0022-2828
DOI	https://doi.org/10.1016/j.yjmcc.2013.12.014
Status	Udgivet - 2014

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10.1016/j.yjmcc.2013.12.014

Citationsformater

Liang, B., Soka, M., Christensen, A. H., Olesen, M. S., Larsen, A. P., Knop, F. K., Wang, F., Nielsen, J. B., Andersen, M., Humphreys, D., Mann, S. A., Huttner, I. G., Vandenberg, J. I., Svendsen, J. H., Haunsø, S., Preiss, T., Seebohm, G., Olesen, S. P., Schmitt, N., & Fatkin, D. (2014). Genetic variation in the two-pore domain potassium channel, TASK-1, may contribute to an atrial substrate for arrhythmogenesis. Journal of Molecular and Cellular Cardiology, 67, 69-76. https://doi.org/10.1016/j.yjmcc.2013.12.014

Liang, B, Soka, M, Christensen, AH, Olesen, MS, Larsen, AP, Knop, FK, Wang, F, Nielsen, JB, Andersen, M, Humphreys, D, Mann, SA, Huttner, IG, Vandenberg, JI, Svendsen, JH , Haunsø, S, Preiss, T, Seebohm, G, Olesen, SP, Schmitt, N & Fatkin, D 2014, 'Genetic variation in the two-pore domain potassium channel, TASK-1, may contribute to an atrial substrate for arrhythmogenesis', Journal of Molecular and Cellular Cardiology, bind 67, s. 69-76. https://doi.org/10.1016/j.yjmcc.2013.12.014

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title = "Genetic variation in the two-pore domain potassium channel, TASK-1, may contribute to an atrial substrate for arrhythmogenesis",

abstract = "The two-pore domain potassium channel, K2P3.1 (TASK-1) modulates background conductance in isolated human atrial cardiomyocytes and has been proposed as a potential drug target for atrial fibrillation (AF). TASK-1 knockout mice have a predominantly ventricular phenotype however, and effects of TASK-1 inactivation on atrial structure and function have yet to be demonstrated in vivo. The extent to which genetic variation in KCNK3, that encodes TASK-1, might be a determinant of susceptibility to AF is also unknown. To address these questions, we first evaluated the effects of transient knockdown of the zebrafish kcnk3a and kcnk3b genes and cardiac phenotypes were evaluated using videomicroscopy. Combined kcnk3a and kcnk3b knockdown in 72 hour post fertilization embryos resulted in lower heart rate (p",

author = "Bo Liang and Magdalena Soka and Christensen, {Alex Horby} and Olesen, {Morten S} and Larsen, {Anders P} and Knop, {Filip K} and Fan Wang and Nielsen, {Jonas B} and Martin Andersen and David Humphreys and Mann, {Stefan A} and Huttner, {Inken G} and Vandenberg, {Jamie I} and Svendsen, {Jesper H} and Stig Hauns{\o} and Thomas Preiss and Guiscard Seebohm and Olesen, {S{\o}ren Peter} and Nicole Schmitt and Diane Fatkin",

note = "Copyright {\textcopyright} 2013. Published by Elsevier Ltd.",

year = "2014",

doi = "10.1016/j.yjmcc.2013.12.014",

language = "English",

volume = "67",

pages = "69--76",

journal = "Journal of Molecular and Cellular Cardiology",

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T1 - Genetic variation in the two-pore domain potassium channel, TASK-1, may contribute to an atrial substrate for arrhythmogenesis

AU - Liang, Bo

AU - Soka, Magdalena

AU - Christensen, Alex Horby

AU - Olesen, Morten S

AU - Larsen, Anders P

AU - Knop, Filip K

AU - Wang, Fan

AU - Nielsen, Jonas B

AU - Andersen, Martin

AU - Humphreys, David

AU - Mann, Stefan A

AU - Huttner, Inken G

AU - Vandenberg, Jamie I

AU - Svendsen, Jesper H

AU - Haunsø, Stig

AU - Preiss, Thomas

AU - Seebohm, Guiscard

AU - Olesen, Søren Peter

AU - Schmitt, Nicole

AU - Fatkin, Diane

PY - 2014

Y1 - 2014

N2 - The two-pore domain potassium channel, K2P3.1 (TASK-1) modulates background conductance in isolated human atrial cardiomyocytes and has been proposed as a potential drug target for atrial fibrillation (AF). TASK-1 knockout mice have a predominantly ventricular phenotype however, and effects of TASK-1 inactivation on atrial structure and function have yet to be demonstrated in vivo. The extent to which genetic variation in KCNK3, that encodes TASK-1, might be a determinant of susceptibility to AF is also unknown. To address these questions, we first evaluated the effects of transient knockdown of the zebrafish kcnk3a and kcnk3b genes and cardiac phenotypes were evaluated using videomicroscopy. Combined kcnk3a and kcnk3b knockdown in 72 hour post fertilization embryos resulted in lower heart rate (p

AB - The two-pore domain potassium channel, K2P3.1 (TASK-1) modulates background conductance in isolated human atrial cardiomyocytes and has been proposed as a potential drug target for atrial fibrillation (AF). TASK-1 knockout mice have a predominantly ventricular phenotype however, and effects of TASK-1 inactivation on atrial structure and function have yet to be demonstrated in vivo. The extent to which genetic variation in KCNK3, that encodes TASK-1, might be a determinant of susceptibility to AF is also unknown. To address these questions, we first evaluated the effects of transient knockdown of the zebrafish kcnk3a and kcnk3b genes and cardiac phenotypes were evaluated using videomicroscopy. Combined kcnk3a and kcnk3b knockdown in 72 hour post fertilization embryos resulted in lower heart rate (p

U2 - 10.1016/j.yjmcc.2013.12.014

DO - 10.1016/j.yjmcc.2013.12.014

M3 - Journal article

C2 - 24374141

SN - 0022-2828

VL - 67

SP - 69

EP - 76

JO - Journal of Molecular and Cellular Cardiology

JF - Journal of Molecular and Cellular Cardiology

ER -

Genetic variation in the two-pore domain potassium channel, TASK-1, may contribute to an atrial substrate for arrhythmogenesis

Abstract

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