Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium: [Inkl. corrigendum]

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Standard

Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium : [Inkl. corrigendum]. / Pedersen, Philip Juul; Thomsen, Kirsten B.; Flak, Jon B.; Tejada, Maria de los Angeles; Hauser, Frank; Trachsel, Dagmar Senta; Buhl, Rikke; Kalbfleisch, Theodore; DePriest, Michael Scott; MacLeod, James N.; Callø, Kirstine; Klærke, Dan Arne.

I: Research in Veterinary Science, Bind 113, 08.2017, s. 79-86.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Pedersen, PJ, Thomsen, KB, Flak, JB, Tejada, MDLA, Hauser, F, Trachsel, DS, Buhl, R, Kalbfleisch, T, DePriest, MS, MacLeod, JN, Callø, K & Klærke, DA 2017, 'Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium: [Inkl. corrigendum]', Research in Veterinary Science, bind 113, s. 79-86. https://doi.org/10.1016/j.rvsc.2017.09.010, https://doi.org/10.1016/j.rvsc.2017.12.014

APA

Pedersen, P. J., Thomsen, K. B., Flak, J. B., Tejada, M. D. L. A., Hauser, F., Trachsel, D. S., Buhl, R., Kalbfleisch, T., DePriest, M. S., MacLeod, J. N., Callø, K., & Klærke, D. A. (2017). Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium: [Inkl. corrigendum]. Research in Veterinary Science, 113, 79-86. https://doi.org/10.1016/j.rvsc.2017.09.010, https://doi.org/10.1016/j.rvsc.2017.12.014

Vancouver

Pedersen PJ, Thomsen KB, Flak JB, Tejada MDLA, Hauser F, Trachsel DS o.a. Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium: [Inkl. corrigendum]. Research in Veterinary Science. 2017 aug.;113:79-86. https://doi.org/10.1016/j.rvsc.2017.09.010, https://doi.org/10.1016/j.rvsc.2017.12.014

Author

Pedersen, Philip Juul ; Thomsen, Kirsten B. ; Flak, Jon B. ; Tejada, Maria de los Angeles ; Hauser, Frank ; Trachsel, Dagmar Senta ; Buhl, Rikke ; Kalbfleisch, Theodore ; DePriest, Michael Scott ; MacLeod, James N. ; Callø, Kirstine ; Klærke, Dan Arne. / Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium : [Inkl. corrigendum]. I: Research in Veterinary Science. 2017 ; Bind 113. s. 79-86.

Bibtex

@article{2a7206cbf38349968cc348c530fafa57,
title = "Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium: [Inkl. corrigendum]",
abstract = "Background The voltage-gated K+-channel KV7.1 and the subunit KCNE1, encoded by the KCNQ1 and KCNE1 genes, respectively, are responsible for termination of the cardiac action potential. In humans, mutations in these genes can predispose patients to arrhythmias and sudden cardiac death (SCD). Aim To characterize equine KV7.1/KCNE1 currents and compare them to human KV7.1/KCNE1 currents to determine whether KV7.1/KCNE1 plays a similar role in equine and human hearts. Methods mRNA encoding KV7.1 and KCNE1 was isolated from equine hearts, sequenced, and cloned into expression vectors. The channel subunits were heterologously expressed in Xenopus laevis oocytes or CHO-K1 cells and characterized using voltage-clamp techniques. Results Equine KV7.1/KCNE1 expressed in CHO-K1 cells exhibited electrophysiological properties that are overall similar to the human orthologs; however, a slower deactivation was found which could result in more open channels at fast rates. Conclusion The results suggest that the equine KV7.1/KCNE1 channel may be important for cardiac repolarization and this could indicate that horses are susceptible to SCD caused by mutations in KCNQ1 and KCNE1.",
keywords = "Cardiac electrophysiology, Equine, Horse, K7.1, KCNE1, KCNQ1",
author = "Pedersen, {Philip Juul} and Thomsen, {Kirsten B.} and Flak, {Jon B.} and Tejada, {Maria de los Angeles} and Frank Hauser and Trachsel, {Dagmar Senta} and Rikke Buhl and Theodore Kalbfleisch and DePriest, {Michael Scott} and MacLeod, {James N.} and Kirstine Call{\o} and Kl{\ae}rke, {Dan Arne}",
note = "Corrigendum: 10.1016/j.rvsc.2017.12.014",
year = "2017",
month = aug,
doi = "10.1016/j.rvsc.2017.09.010",
language = "English",
volume = "113",
pages = "79--86",
journal = "Research in Veterinary Science",
issn = "0034-5288",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium

T2 - [Inkl. corrigendum]

AU - Pedersen, Philip Juul

AU - Thomsen, Kirsten B.

AU - Flak, Jon B.

AU - Tejada, Maria de los Angeles

AU - Hauser, Frank

AU - Trachsel, Dagmar Senta

AU - Buhl, Rikke

AU - Kalbfleisch, Theodore

AU - DePriest, Michael Scott

AU - MacLeod, James N.

AU - Callø, Kirstine

AU - Klærke, Dan Arne

N1 - Corrigendum: 10.1016/j.rvsc.2017.12.014

PY - 2017/8

Y1 - 2017/8

N2 - Background The voltage-gated K+-channel KV7.1 and the subunit KCNE1, encoded by the KCNQ1 and KCNE1 genes, respectively, are responsible for termination of the cardiac action potential. In humans, mutations in these genes can predispose patients to arrhythmias and sudden cardiac death (SCD). Aim To characterize equine KV7.1/KCNE1 currents and compare them to human KV7.1/KCNE1 currents to determine whether KV7.1/KCNE1 plays a similar role in equine and human hearts. Methods mRNA encoding KV7.1 and KCNE1 was isolated from equine hearts, sequenced, and cloned into expression vectors. The channel subunits were heterologously expressed in Xenopus laevis oocytes or CHO-K1 cells and characterized using voltage-clamp techniques. Results Equine KV7.1/KCNE1 expressed in CHO-K1 cells exhibited electrophysiological properties that are overall similar to the human orthologs; however, a slower deactivation was found which could result in more open channels at fast rates. Conclusion The results suggest that the equine KV7.1/KCNE1 channel may be important for cardiac repolarization and this could indicate that horses are susceptible to SCD caused by mutations in KCNQ1 and KCNE1.

AB - Background The voltage-gated K+-channel KV7.1 and the subunit KCNE1, encoded by the KCNQ1 and KCNE1 genes, respectively, are responsible for termination of the cardiac action potential. In humans, mutations in these genes can predispose patients to arrhythmias and sudden cardiac death (SCD). Aim To characterize equine KV7.1/KCNE1 currents and compare them to human KV7.1/KCNE1 currents to determine whether KV7.1/KCNE1 plays a similar role in equine and human hearts. Methods mRNA encoding KV7.1 and KCNE1 was isolated from equine hearts, sequenced, and cloned into expression vectors. The channel subunits were heterologously expressed in Xenopus laevis oocytes or CHO-K1 cells and characterized using voltage-clamp techniques. Results Equine KV7.1/KCNE1 expressed in CHO-K1 cells exhibited electrophysiological properties that are overall similar to the human orthologs; however, a slower deactivation was found which could result in more open channels at fast rates. Conclusion The results suggest that the equine KV7.1/KCNE1 channel may be important for cardiac repolarization and this could indicate that horses are susceptible to SCD caused by mutations in KCNQ1 and KCNE1.

KW - Cardiac electrophysiology

KW - Equine

KW - Horse

KW - K7.1

KW - KCNE1

KW - KCNQ1

UR - https://www.sciencedirect.com/science/article/pii/S0034528817312845?via%3Dihub

U2 - 10.1016/j.rvsc.2017.09.010

DO - 10.1016/j.rvsc.2017.09.010

M3 - Journal article

C2 - 28917093

AN - SCOPUS:85029361238

VL - 113

SP - 79

EP - 86

JO - Research in Veterinary Science

JF - Research in Veterinary Science

SN - 0034-5288

ER -

ID: 184071548