IndraLab

Statements


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"Here, the complete loss of Scn2a led to an increase in Na 1.6 axon initial segment staining and persistent sodium current, similar to previous work showing Na 1.2 compensation for loss of Na 1.6."

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"Lower levels of SCN1A, SCN2A, SCN3A, SCN4A and SCN8A expression have also been reported in heart and shown to contribute approximately 23% of the total functional sodium channels in mouse ventricular myocytes and 27% in human atrial myocytes, based on TTX sensitivity."