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Brugada Syndrome (BrS) is a familial disease associated with sudden cardiac death. A 20%–25% of BrS patients carry genetic defects that cause loss‐of‐function of the voltage‐gated cardiac sodium channel. Thus, 70%–75% of patients remain without a genetic diagnosis. In this work, we identified a novel missense mutation (p.Asp211Gly) in the sodium β2 subunit encoded by SCN2B, in a woman diagnosed with BrS. We studied the sodium current (I_Na) from cells coexpressing Na_v1.5 and wild‐type (β2WT) or mutant (β2D211G) β2 subunits. Our electrophysiological analysis showed a 39.4% reduction in I_Na density when Na_v1.5 was coexpressed with the β2D211G. Single channel analysis showed that the mutation did not affect the Na_v1.5 unitary channel conductance. Instead, protein membrane detection experiments suggested that β2D211G decreases Na_v1.5 cell surface expression. The effect of the mutant …