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congenital hyperinsulinism/arginine
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3 results
Characterization and functional restoration of a potassium channel Kir6.2 pore mutation identified in congenital hyperinsulinism.
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The inwardly rectifying potassium channel Kir6.2 assembles with sulfonylurea receptor 1 to form the ATP-sensitive potassium (K(ATP)) channels that regulate insulin secretion in pancreatic beta-cells. Mutations in K(ATP) channels underlie insulin secretion disease. Here, we report the
Destabilization of ATP-sensitive potassium channel activity by novel KCNJ11 mutations identified in congenital hyperinsulinism.
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The inwardly rectifying potassium channel Kir6.2 is the pore-forming subunit of the ATP-sensitive potassium (K(ATP)) channel, which controls insulin secretion by coupling glucose metabolism to membrane potential in beta-cells. Loss of channel function because of mutations in Kir6.2 or its associated
First successful application of preimplantation genetic diagnosis and haplotyping for congenital hyperinsulinism.
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Congenital hyperinsulinism is the most common cause of persistent hypoglycaemia in infancy. Early surgical intervention is usually required to prevent brain damage. The prevention of the transmission to the offspring is important in families carrying the mutated gene. Preimplantation genetic
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