| First Author | Barhanin J | Year | 1996 |
| Journal | Nature | Volume | 384 |
| Issue | 6604 | Pages | 78-80 |
| PubMed ID | 8900282 | Mgi Jnum | J:36442 |
| Mgi Id | MGI:83868 | Doi | 10.1038/384078a0 |
| Citation | Barhanin J, et al. (1996) K(V)LQT1 and lsK (minK) proteins associate to form the I(Ks) cardiac potassium current [see comments]. Nature 384(6604):78-80 |
| abstractText | In mammalian cardiac cells, a variety of transient or sustained K+ currents contribute to the repolarization of action potentials. There are two main components of the delayed-rectifier sustained K+ current, I(Kr) (rapid) and I(Ks), (slow). I(Kr) is the product of the gene HERG, which is altered in the long-QT syndrome, LQT2. A channel with properties similar to those of the I(Ks) channel is produced when the cardiac protein IsK is expressed in Xenopus oocytes. However, it is a small protein with a very unusual structure for a cation channel. The LQT1 gene is another gene associated with the LQT syndrome, a disorder that causes sudden death from ventricular arrhythmias. Here we report the cloning of the full-length mouse K(V)LQT1 complementary DNA and show that K(V)LQT1 associates with IsK to form the channel underlying the I(Ks) cardiac current, which is a target of class-III anti-arrhythmic drugs and is involved in the LQT1 syndrome. |
