Markovian model for cardiac sodium channel (Clancy, Rudy 2002)

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Accession:62661
Complex physiological interactions determine the functional consequences of gene abnormalities and make mechanistic interpretation of phenotypes extremely difficult. A recent example is a single mutation in the C terminus of the cardiac Na(+) channel, 1795insD. The mutation causes two distinct clinical syndromes, long QT (LQT) and Brugada, leading to life-threatening cardiac arrhythmias. Coexistence of these syndromes is seemingly paradoxical; LQT is associated with enhanced Na(+) channel function, and Brugada with reduced function. Using a computational approach, we demonstrate that the 1795insD mutation exerts variable effects depending on the myocardial substrate. We develop Markov models of the wild-type and 1795insD cardiac Na(+) channels. See reference for more and details. The model files were submitted by: Dr. Jiun-Shian Wu, Dr. Sheng-Nan Wu, Dr. Ruey J. Sung, Han-Dong Chang.
Reference:
1 . Clancy CE, Rudy Y (2002) Na(+) channel mutation that causes both Brugada and long-QT syndrome phenotypes: a simulation study of mechanism. Circulation 105:1208-13 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type: Channel/Receptor;
Brain Region(s)/Organism:
Cell Type(s):
Channel(s): I Sodium;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: XPP;
Model Concept(s): Ion Channel Kinetics; Pathophysiology; Heart disease; Brugada; Long-QT;
Implementer(s): Wu, Sheng-Nan [snwu at mail.ncku.edu.tw]; Chang, Han-Dong; Wu, Jiun-Shian [coolneon at gmail.com]; Sung, Ruey J ;
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Ina_Markov