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  • Title: A truncated splice variant of KCNQ1 cloned from rat heart.
    Author: Yamada Y, Chen X, Kobayashi T, Kamada Y, Nagashima M, Tsutsuura M, Seki S, Yamakage M, Namiki A, Tohse N.
    Journal: Biochem Biophys Res Commun; 2002 Jun 07; 294(2):199-204. PubMed ID: 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.
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