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Approximately 10% of sudden infant death syndrome (SIDS) may stem from cardiac channelopathies. The KCNJ8-encoded Kir6.1 (K(ATP)) channel critically regulates vascular tone and cardiac adaptive response to systemic metabolic stressors, including sepsis. KCNJ8-deficient mice are prone to premature sudden death, particularly with infection. We determined the spectrum, prevalence, and function of KCNJ8 mutations in a large SIDS cohort.

Loss-of-Function Mutations in the KCNJ8 -Encoded Kir6.1 K ATP Channel and Sudden Infant Death Syndrome

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