1Saviane C, Conti F, Pusch M. The muscle chloride channel ClC-1has a double-barreled appearance that is differentially affected in dominant and recessive myotonia. J Gen Physiol, 1999, 113: 457-468.
2Dutzler R, Campbell EB, Cadene M, et al. X-ray structure of a C1C chloride channel at 3.0 A reveals the molecular basis of anion selectivity. Nature, 2002, 415: 287-294.
3Bhalerao DP, Rajpurohit Y, Vite CH, et al. Detection of a genetic mutation for myotonia congenita among Miniature Schnauzers and identification of a common cartier ancestor. Am J Vet Res, 2002,63: 1443-1447.
4Pusch M. Myotonia caused by mutations in the muscle chloride channel gene CLCN1. Hum Mutat, 2002, 19: 423-434.
5Shirakawa T, Sakai K, Kitagawa Y, et al. A novel murine myotonia congenita without molecular defects in the C1C-1 and the SCN4A.Neurology, 2002, 59: 1091-1094.
6Rogers CS, Vanoye CG, Sullenger BA, et al. Functional repair of a mutant chloride channel using a trans-splicing ribozyme. J Clin Invest, 2002, 110: 1783-1789.
8Charlet-BN, Savkur RS, Singh G, et al. Loss of the muscle-specific chloride channel in type 1 myotonic dystrophy due to misregulated alternative splicing. Mol Cell, 2002, 10: 45-53.
9Kaasik A, Kalda A, Jaako K, et al. Dehydroepiandrosterone sulphate prevents oxygen-glucose deprivation-induced injury in cerebellar granule cell culture. Neuroscience, 2001, 102: 427-432.
10De Luca A, Pierno S, Liantonio A, et al. Pre-clinical trials in Duchenne dystrophy: what animal models can tell us about potentialdrugeffectiveness. Neuromuscul Disord, 2002, 12 Suppl 1: S142-S146.
