Why the study?
Does Scn1b deletion alter sodium current, calcium homeostasis, and arrhythmia susceptibility in murine hearts?
Does Scn1b deletion alter sodium current, calcium homeostasis, and arrhythmia susceptibility in murine hearts?
Life-threatening arrhythmias associated with Scn1b mutations may be partly driven by disrupted intracellular calcium homeostasis resulting from increased tetrodotoxin-sensitive sodium current.
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Scn1b effects in mice remain hypothesis-generating; leaves open whether TTX-sensitive INa drives human arrhythmia risk or offers a therapeutic target.
Lin et al. (2014) studied this question.
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