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Primary structure and functional expression of a developmentally regulated skeletal muscle chloride channel

Nature volume 354, pages 301304 (28 November 1991) | Download Citation

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Abstract

SKELETAL muscle is unusual in that 70–85% of resting membrane conductance is carried by chloride ions1. This conductance is essential for membrane-potential stability, as its block by 9-anthracene-carboxylic acid and other drugs causes myotonia2,3. Fish electric organs are developmentally derived from skeletal muscle, suggesting that mammalian muscle may express a homologue of the Torpedo mamorataelectroplax chloride channel4,5. We have now cloned the complementary DNA encoding a rat skeletal muscle chloride channel by homology screening to the Cl channel from Torpedo4 (Fig. la). It encodes a 994-amino-acid protein which is about 54% identical to the Torpedo channel and is predominantly expressed in skeletal muscle. Messenger RNA amounts in that tissue increase steeply in the first 3–4 weeks after birth, in parallel with the increase in muscle Cl conductance6. Expression from cRNA in Xenopus oocytes leads to 9-anthracene-carboxylic acid-sensitive currents with time and voltage dependence typical for macroscopic muscle Cl conductance. This and the functional destruction of this channel in mouse myotonia7 suggests that we have cloned the major skeletal muscle chloride channel.

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  1. Centre for Molecular Neurobiology (ZMNH), Hamburg University, Martinistrasse 52, D-2000 Hamburg 20,Germany

    • Klaus Steinmeyer
    • , Christoph Ortland
    •  & Thomas J. Jentsch

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https://doi.org/10.1038/354301a0

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