New Uses for Old Drugs: Neonatal Diabetes and Sulphonylureas

[1] ASHCROFT FM, 2007, AM J PHYSIOL-ENDOC M, V88, pE889

[2] Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic β cells recapitulates neonatal diabetes [J]. JOURNAL OF CLINICAL INVESTIGATION, 2009, 119 (01) : 80 - 90

[3] Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2004, 350 (18) : 1838 - 1849

[4] Sulphonylurea action revisited - the post-cloning era [J]. DIABETOLOGIA, 2003, 46 (07) : 875 - 891

[5] Activating mutations in Kir6.2 and neonatal diabetes - New clinical syndromes, new scientific insights, and new therapy [J]. DIABETES, 2005, 54 (09) : 2503 - 2513

[6] Targeted overactivity of β cell KATP channels induces profound neonatal diabetes [J]. CELL, 2000, 100 (06) : 645 - 654

[7] Tolerance for ATP-insensitive KATP channels in transgenic mice [J]. CIRCULATION RESEARCH, 2001, 89 (11) : 1022 - 1029

[8] The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2008, 93 (03) : 1054 - 1061

[9] Kir6.2 mutations causing neonatal diabetes prevent endocytosis of ATP-sensitive potassium channels [J]. EMBO JOURNAL, 2006, 25 (17) : 4142 - 4151

[10] Sulfonylurea improves CNS function in a case of intermediate DEND syndrome caused by a mutation in KCNJ11 [J]. NATURE CLINICAL PRACTICE NEUROLOGY, 2007, 3 (11): : 640 - 645

[1] ASHCROFT FM, 2007, AM J PHYSIOL-ENDOC M, V88, pE889

[2] Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic β cells recapitulates neonatal diabetes [J]. JOURNAL OF CLINICAL INVESTIGATION, 2009, 119 (01) : 80 - 90

[3] Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2004, 350 (18) : 1838 - 1849

[4] Sulphonylurea action revisited - the post-cloning era [J]. DIABETOLOGIA, 2003, 46 (07) : 875 - 891

[5] Activating mutations in Kir6.2 and neonatal diabetes - New clinical syndromes, new scientific insights, and new therapy [J]. DIABETES, 2005, 54 (09) : 2503 - 2513

[6] Targeted overactivity of β cell KATP channels induces profound neonatal diabetes [J]. CELL, 2000, 100 (06) : 645 - 654

[7] Tolerance for ATP-insensitive KATP channels in transgenic mice [J]. CIRCULATION RESEARCH, 2001, 89 (11) : 1022 - 1029

[8] The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2008, 93 (03) : 1054 - 1061

[9] Kir6.2 mutations causing neonatal diabetes prevent endocytosis of ATP-sensitive potassium channels [J]. EMBO JOURNAL, 2006, 25 (17) : 4142 - 4151

[10] Sulfonylurea improves CNS function in a case of intermediate DEND syndrome caused by a mutation in KCNJ11 [J]. NATURE CLINICAL PRACTICE NEUROLOGY, 2007, 3 (11): : 640 - 645