Familial Periodic Paralysis
Author:
Publisher
Springer US
Link
http://link.springer.com/content/pdf/10.1007/978-1-4613-1143-0_31.pdf
Reference97 articles.
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3. Rojas, C. V., Wang, J., Schwartz, L. S., Hoffman, E. P., Powell, B. R., and Brown, R. H. (1991). A met-to-val mutation in the skeletal muscle Na+ channel α-subunit in hyperkalaemic periodic paralysis. Nature 354:387–389.
4. McClatchey, A., Van den Bergh, P., Pericak-Vance, M., Raskind, W., Verellen, C., McKenna-Yasek, D., Rao, K., Haines, J. L., Bird, T., Brown, R. H., Jr., and Gusella, J. F. (1992). Temperature-sensitive mutations in the III-IV cytoplasmic loop region of the skeletal muscle sodium channel gene in paramyotonia congenita. Cell 68: 769–774.
5. Ptáček, L. J., George, A. L., Barchi, R. L., Griggs, R. C., Riggs, J. E., Robertson, M., and Leppert, M. F. (1992). Mutations in an S4 segment of the adult skeletal muscle sodium channel gene cause paramyotonia congenita. Neuron 8:891–897.
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1. Impairment of slow inactivation as a common mechanism for periodic paralysis in DIIS4-S5;Neurology;2002-04-23
2. Characterization of a new sodium channel mutation at arginine 1448 associated with moderate paramyotonia congenita in humans;The Journal of Physiology;1999-07
3. Exercise Intolerance and Muscle Pain in Myotonic Disorders;Exercise Intolerance and Muscle Contracture;1999
4. A defect in skeletal muscle sodium channel deactivation exacerbates hyperexcitability in human paramyotonia congenita;The Journal of Physiology;1998-02
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