A plethora of mechanisms in the HERG-related long QT syndrome Genetics meets electrophysiology

D Roden
1999 Cardiovascular Research  
See article by Nakajima et al. [15] ( pages 283 -293) in physiology, and the pathophysiology, of the channel. this issue. Therefore, mutagenesis of HERG is proceeding along two complementary lines: directed by physiology (often target-The ether a-go-go-related gene (eag) was cloned from a ing residues or domains known to be important in other Drosophila mutant displaying a dance-like movement voltage-gated channels) or by clinical genetics, as new disorder on exposure to ether [1]. Homologs of
more » ... ag have mutations are identified and characterized in patients with been cloned in mouse and rat, but not (at least yet) in LQT2. The two approaches together are developing aǹ human. However, a related gene, the human ether a-go-go-increasingly sophisticated view of the role of individual related gene (HERG) was cloned from a human hippocam-residues, or specific domains, in modulating I function Kr
doi:10.1016/s0008-6363(99)00224-2 pmid:10690299 fatcat:srryvehx5vhr3brr56ogte3me4