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27. Mutations of the same conserved glutamate residue in NBD2 of the sulfonylurea receptor 1 subunit of the KATP channel can result in either hyperinsulinism or neonatal diabetes. Männikkö R; Flanagan SE; Sim X; Segal D; Hussain K; Ellard S; Hattersley AT; Ashcroft FM Diabetes; 2011 Jun; 60(6):1813-22. PubMed ID: 21617188 [TBL] [Abstract][Full Text] [Related]
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29. The structure and function of the ATP-sensitive K+ channel in insulin-secreting pancreatic beta-cells. Miki T; Nagashima K; Seino S J Mol Endocrinol; 1999 Apr; 22(2):113-23. PubMed ID: 10194514 [TBL] [Abstract][Full Text] [Related]
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33. Genotype-phenotype correlations in children with congenital hyperinsulinism due to recessive mutations of the adenosine triphosphate-sensitive potassium channel genes. Henwood MJ; Kelly A; Macmullen C; Bhatia P; Ganguly A; Thornton PS; Stanley CA J Clin Endocrinol Metab; 2005 Feb; 90(2):789-94. PubMed ID: 15562009 [TBL] [Abstract][Full Text] [Related]
34. Cloning of rabbit Kir6.1, SUR2A, and SUR2B: possible candidates for a renal K(ATP) channel. Brochiero E; Wallendorf B; Gagnon D; Laprade R; Lapointe JY Am J Physiol Renal Physiol; 2002 Feb; 282(2):F289-300. PubMed ID: 11788443 [TBL] [Abstract][Full Text] [Related]
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37. An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetes. Masia R; Koster JC; Tumini S; Chiarelli F; Colombo C; Nichols CG; Barbetti F Diabetes; 2007 Feb; 56(2):328-36. PubMed ID: 17259376 [TBL] [Abstract][Full Text] [Related]
38. Sar1-GTPase-dependent ER exit of KATP channels revealed by a mutation causing congenital hyperinsulinism. Taneja TK; Mankouri J; Karnik R; Kannan S; Smith AJ; Munsey T; Christesen HB; Beech DJ; Sivaprasadarao A Hum Mol Genet; 2009 Jul; 18(13):2400-13. PubMed ID: 19357197 [TBL] [Abstract][Full Text] [Related]
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