Molecular cloning and functional expression of the K + channel K V 7.1 and the regulatory subunit KCNE1 from equine myocardium
| Autor: | Michael S. DePriest, Dagmar S Trachsel, Kirstine Calloe, Frank Hauser, Theodore S. Kalbfleisch, Maria de los Angeles Tejada, James N. MacLeod, Philip J. Pedersen, Kirsten B. Thomsen, Rikke Buhl, Jon B. Flak, Dan A. Klaerke |
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| Rok vydání: | 2017 |
| Předmět: |
congenital
hereditary and neonatal diseases and abnormalities Messenger RNA medicine.medical_specialty Expression vector General Veterinary biology 040301 veterinary sciences Protein subunit Xenopus Cardiac action potential 04 agricultural and veterinary sciences 030204 cardiovascular system & hematology Molecular cloning biology.organism_classification Molecular biology 0403 veterinary science 03 medical and health sciences 0302 clinical medicine Endocrinology Internal medicine Gene expression cardiovascular system medicine Gene |
| Zdroj: | Research in Veterinary Science |
| ISSN: | 0034-5288 |
| Popis: | Background The voltage-gated K + -channel K V 7.1 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 K V 7.1/KCNE1 currents and compare them to human K V 7.1/KCNE1 currents to determine whether K V 7.1/KCNE1 plays a similar role in equine and human hearts. Methods mRNA encoding K V 7.1 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 K V 7.1/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 K V 7.1/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 . |
| Databáze: | OpenAIRE |
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