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Reference cited by multiple papers
Wang DW, Yazawa K, George AL, Bennett PB (1996) Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome.
Proc Natl Acad Sci U S A
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Clancy CE, Rudy Y (1999)
Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia.
Ventricular cell model (Guinea-pig-type) (Luo, Rudy 1991, +11 other papers!) (C++) [Model]
Clancy CE, Rudy Y (2002)
Na(+) channel mutation that causes both Brugada and long-QT syndrome phenotypes: a simulation study of mechanism.
Markovian model for cardiac sodium channel (Clancy, Rudy 2002) [Model]
Kahlig KM, Misra SN, George AL (2006)
Impaired inactivation gate stabilization predicts increased persistent current for an epilepsy-associated SCN1A mutation.
Song W, Xiao Y, Chen H, Ashpole NM, Piekarz AD, Ma P, Hudmon A, Cummins TR, Shou W (2012)
The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity.