Referenced in: none

Automatically associated channels: Kv7.1

Title: A truncated splice variant of KCNQ1 cloned from rat heart.

Authors: Yoichi Yamada, Xiangdong Chen, Takeshi Kobayashi, Yasuhiro Kamada, Masato Nagashima, Masaaki Tsutsuura, Sumihiko Seki, Michiaki Yamakage, Akiyoshi Namiki, Noritsugu Tohse

Journal, date & volume: Biochem. Biophys. Res. Commun., 2002 Jun 7 , 294, 199-204

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/12051693

Abstract
KCNQ1 encodes a pore-forming subunit of potassium channels. Mutations in this gene cause inherited diseases, i.e., Romano-Ward syndrome and Jervell and Lange-Nielsen syndrome. A truncated isoform of KCNQ1 was reported to be expressed physiologically and to suppress a delayed rectifier potassium current dominant-negatively in human heart. However, it is not known whether this way of modulation occurs in other species. We cloned another truncated splice variant of KCNQ1 (tr-rKCNQ1) from rat heart. Judging from the deleted sequence of the tr-rKCNQ1, the genomic structure of rat in this portion might be different from those of human and mouse. Otherwise, an unknown exon might exist. RT-PCR analysis demonstrated that the tr-rKCNQ1 was expressed in fetal and neonatal hearts. When this gene was expressed along with a full-length KCNQ1, it suppressed potassium currents, whether a regulatory subunit minK was co-expressed or not.