Perturbation to the function of the human cardiac sodium channel (NaV1.5) can result in arrhythmias and in some cases stroke or death. Inactivation of the channel utilizes specific elements of the NaV1.5 C-terminus and calmodulin to translate changes in intracellular calcium. Combining structural biology and electrophysiology this research will elucidate important molecular details of this process and provide insight into the molecular basis of specific cardiac life threatening arrhythmias.
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