| First Author | Charpentier F | Year | 1998 |
| Journal | Biochem Biophys Res Commun | Volume | 251 |
| Issue | 3 | Pages | 806-10 |
| PubMed ID | 9790991 | Mgi Jnum | J:50586 |
| Mgi Id | MGI:1306976 | Doi | 10.1006/bbrc.1998.9554 |
| Citation | Charpentier F, et al. (1998) Adult KCNE1-knockout mice exhibit a mild cardiac cellular phenotype. Biochem Biophys Res Commun 251(3):806-10 |
| abstractText | The KCNE1 gene encodes a channel regulator IsK which in association with the KvLQT1 K+ channel protein determines the slow component of the cardiac delayed rectifier current. We have investigated the cellular electrophysiological characteristics of adult KCNE1-knockout mouse hearts by means of the standard microelectrode technique. Action potential parameters from the ventricular endocardium of KCNE1 -/- mice were indistinguishable from those of KCNE1 +/+ animals. In particular, KCNE1 -/- hearts did not exhibit prolonged repolarization. E-4031, a specific blocker of erg K+ channels consistently prolonged repolarization in KCNE1 +/+ but not in KCNE1 -/- hearts. By contrast, the chromanol compound 293B, a specific blocker of KvLQT1 K+ channel produced comparable effects on repolarization in KCNE1 -/- and KCNE1 +/+ mice. We conclude that invalidation of the mouse KCNE1 gene by homologous recombination leads to a mild cardiac phenotype at the cellular level. Copyright 1998 Academic Press. |
