| First Author | Steinmeyer K | Year | 1991 |
| Journal | Nature | Volume | 354 |
| Issue | 6351 | Pages | 301-4 |
| PubMed ID | 1659664 | Mgi Jnum | J:49033 |
| Mgi Id | MGI:1276456 | Doi | 10.1038/354301a0 |
| Citation | Steinmeyer K, et al. (1991) Primary structure and functional expression of a developmentally regulated skeletal muscle chloride channel. Nature 354(6351):301-4 |
| abstractText | Skeletal muscle is unusual in that 70-85% of resting membrane conductance is carried by chloride ions. This conductance is essential for membrane-potential stability, as its block by 9-anthracene-carboxylic acid and other drugs causes myotonia. Fish electric organs are developmentally derived from skeletal muscle, suggesting that mammalian muscle may express a homologue of the Torpedo mamorata electroplax chloride channel. We have now cloned the complementary DNA encoding a rat skeletal muscle chloride channel by homology screening to the Cl- channel from Torpedo. 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- conductance. 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 myotonia suggests that we have cloned the major skeletal muscle chloride channel. |
