IndraLab

Statements

KCND3 inhibits sodium atom. 3 / 3
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"Multiple mutations of genes, SCN5A, SCN1B, SCN3B, GPD1L, CACNA1C, CACNB2, KCNE3 and KCND3, have been shown to decrease cardiac Na + and Ca 2+ channel activity or increase fast transient outward K + channel activity, and they are linked to BrS."
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"Moreover, BrS and SCA19/22 KCND3 variants associated with a gain of function of I to, significantly reduced I Na, whereas the SCA19/22 KCND3 variants associated with a loss of function (LOF) of I to significantly increased I Na."
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"115 In a subsequent study, co-expression of mutant SCN1B with WT-SCN5A and WT-KCND3 (separately) induced a 55.6% decrease in peak I Na and 70.6% gain of function in I to, moreover, co-immunoprecipitation revealed structural association between Na V beta1B, Na V 1.5 and K V 4.3, suggesting that the elevated level of transient outward potassium current is predominantly responsible for pathogenesis in these cases of BrS."
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