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New uses for old drugs: neonatal diabetes and sulphonylureas.
Cell Metab. 2010 Mar 3;11(3):179-81. doi: 10.1016/j.cmet.2010.02.004.
2
Adjacent mutations in the gating loop of Kir6.2 produce neonatal diabetes and hyperinsulinism.
EMBO Mol Med. 2009 Jun;1(3):166-77. doi: 10.1002/emmm.200900018.
3
Molecular mechanisms underlying nutrient-stimulated incretin secretion.
Expert Rev Mol Med. 2010 Jan 5;12:e1. doi: 10.1017/S146239940900132X.
4
Coexpression of the type 2 diabetes susceptibility gene variants KCNJ11 E23K and ABCC8 S1369A alter the ATP and sulfonylurea sensitivities of the ATP-sensitive K(+) channel.
Diabetes. 2009 Oct;58(10):2419-24. doi: 10.2337/db09-0143. Epub 2009 Jul 8.
5
Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance.
Diabetes. 2009 Aug;58(8):1869-78. doi: 10.2337/db09-0025. Epub 2009 Jun 2.
6
Sar1-GTPase-dependent ER exit of KATP channels revealed by a mutation causing congenital hyperinsulinism.
Hum Mol Genet. 2009 Jul 1;18(13):2400-13. doi: 10.1093/hmg/ddp179. Epub 2009 Apr 8.
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Regulation of insulin secretion: a matter of phase control and amplitude modulation.
Diabetologia. 2009 May;52(5):739-51. doi: 10.1007/s00125-009-1314-y. Epub 2009 Mar 14.
8
Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus.
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9
Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic beta cells recapitulates neonatal diabetes.
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10
Update of mutations in the genes encoding the pancreatic beta-cell K(ATP) channel subunits Kir6.2 (KCNJ11) and sulfonylurea receptor 1 (ABCC8) in diabetes mellitus and hyperinsulinism.
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