Loss-of-Function Mutations in the <i>KCNJ8</i> -Encoded Kir6.1 K _ATP Channel and Sudden Infant Death Syndrome

Abstract

Molecular and functional evidence implicated loss-of-function KCNJ8 mutations as a novel pathogenic mechanism in SIDS, possibly by predisposition of a maladaptive cardiac response to systemic metabolic stressors akin to the mouse models of KCNJ8 deficiency.