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XB-ART-7048
Biochem Biophys Res Commun 2002 Jun 07;2942:199-204. doi: 10.1016/S0006-291X(02)00459-X.
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A truncated splice variant of KCNQ1 cloned from rat heart.

Yamada Y , Chen X , Kobayashi T , Kamada Y , Nagashima M , Tsutsuura M , Seki S , Yamakage M , Namiki A , Tohse N .


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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.

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Species referenced: Xenopus
Genes referenced: kcne1 kcnq1 mink1