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Items: 1 to 20 of 245

1.

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.

Hamming KS, Soliman D, Matemisz LC, Niazi O, Lang Y, Gloyn AL, Light PE.

Diabetes. 2009 Oct;58(10):2419-24. doi: 10.2337/db09-0143. Epub 2009 Jul 8.

2.

Pharmacogenomic analysis of ATP-sensitive potassium channels coexpressing the common type 2 diabetes risk variants E23K and S1369A.

Lang VY, Fatehi M, Light PE.

Pharmacogenet Genomics. 2012 Mar;22(3):206-14. doi: 10.1097/FPC.0b013e32835001e7.

PMID:
22209866
3.

The ATP-sensitive K(+) channel ABCC8 S1369A type 2 diabetes risk variant increases MgATPase activity.

Fatehi M, Raja M, Carter C, Soliman D, Holt A, Light PE.

Diabetes. 2012 Jan;61(1):241-9. doi: 10.2337/db11-0371.

4.

A rare mutation in ABCC8/SUR1 leading to altered ATP-sensitive K+ channel activity and beta-cell glucose sensing is associated with type 2 diabetes in adults.

Tarasov AI, Nicolson TJ, Riveline JP, Taneja TK, Baldwin SA, Baldwin JM, Charpentier G, Gautier JF, Froguel P, Vaxillaire M, Rutter GA.

Diabetes. 2008 Jun;57(6):1595-604. doi: 10.2337/db07-1547. Epub 2008 Mar 17.

5.

Large-scale association studies of variants in genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) confirm that the KCNJ11 E23K variant is associated with type 2 diabetes.

Gloyn AL, Weedon MN, Owen KR, Turner MJ, Knight BA, Hitman G, Walker M, Levy JC, Sampson M, Halford S, McCarthy MI, Hattersley AT, Frayling TM.

Diabetes. 2003 Feb;52(2):568-72.

6.

Analysis of two KCNJ11 neonatal diabetes mutations, V59G and V59A, and the analogous KCNJ8 I60G substitution: differences between the channel subtypes formed with SUR1.

Winkler M, Lutz R, Russ U, Quast U, Bryan J.

J Biol Chem. 2009 Mar 13;284(11):6752-62. doi: 10.1074/jbc.M805435200. Epub 2009 Jan 12.

7.

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. doi: 10.2337/db10-1583.

8.

Genetic variations in the pancreatic ATP-sensitive potassium channel, beta-cell dysfunction, and susceptibility to type 2 diabetes.

Chistiakov DA, Potapov VA, Khodirev DC, Shamkhalova MS, Shestakova MV, Nosikov VV.

Acta Diabetol. 2009 Mar;46(1):43-9. doi: 10.1007/s00592-008-0056-5. Epub 2008 Aug 29.

PMID:
18758683
9.

Effects of single nucleotide polymorphisms in K(ATP) channel genes on type 2 diabetes in a Turkish population.

Gonen MS, Arikoglu H, Erkoc Kaya D, Ozdemir H, Ipekci SH, Arslan A, Kayis SA, Gogebakan B.

Arch Med Res. 2012 May;43(4):317-23. doi: 10.1016/j.arcmed.2012.06.001. Epub 2012 Jun 13.

PMID:
22704848
10.

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.

Villareal DT, Koster JC, Robertson H, Akrouh A, Miyake K, Bell GI, Patterson BW, Nichols CG, Polonsky KS.

Diabetes. 2009 Aug;58(8):1869-78. doi: 10.2337/db09-0025. Epub 2009 Jun 2.

11.

Neonatal diabetes caused by a homozygous KCNJ11 mutation demonstrates that tiny changes in ATP sensitivity markedly affect diabetes risk.

Vedovato N, Cliff E, Proks P, Poovazhagi V, Flanagan SE, Ellard S, Hattersley AT, Ashcroft FM.

Diabetologia. 2016 Jul;59(7):1430-1436. doi: 10.1007/s00125-016-3964-x. Epub 2016 Apr 27.

12.

Haplotype structure and genotype-phenotype correlations of the sulfonylurea receptor and the islet ATP-sensitive potassium channel gene region.

Florez JC, Burtt N, de Bakker PI, Almgren P, Tuomi T, Holmkvist J, Gaudet D, Hudson TJ, Schaffner SF, Daly MJ, Hirschhorn JN, Groop L, Altshuler D.

Diabetes. 2004 May;53(5):1360-8.

13.

Compound heterozygous mutations in the SUR1 (ABCC 8) subunit of pancreatic K(ATP) channels cause neonatal diabetes by perturbing the coupling between Kir6.2 and SUR1 subunits.

Lin YW, Akrouh A, Hsu Y, Hughes N, Nichols CG, De León DD.

Channels (Austin). 2012 Mar-Apr;6(2):133-8. doi: 10.4161/chan.19980. Epub 2012 Mar 1.

14.

Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11.

Edghill EL, Flanagan SE, Ellard S.

Rev Endocr Metab Disord. 2010 Sep;11(3):193-8. doi: 10.1007/s11154-010-9149-x. Review.

PMID:
20922570
15.
16.

SNPs in the KCNJ11-ABCC8 gene locus are associated with type 2 diabetes and blood pressure levels in the Japanese population.

Sakamoto Y, Inoue H, Keshavarz P, Miyawaki K, Yamaguchi Y, Moritani M, Kunika K, Nakamura N, Yoshikawa T, Yasui N, Shiota H, Tanahashi T, Itakura M.

J Hum Genet. 2007;52(10):781-93. Epub 2007 Sep 6.

PMID:
17823772
17.

A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes.

Proks P, Arnold AL, Bruining J, Girard C, Flanagan SE, Larkin B, Colclough K, Hattersley AT, Ashcroft FM, Ellard S.

Hum Mol Genet. 2006 Jun 1;15(11):1793-800. Epub 2006 Apr 13.

PMID:
16613899
18.

The molecular genetics of sulfonylurea receptors in the pathogenesis and treatment of insulin secretory disorders and type 2 diabetes.

Lang V, Youssef N, Light PE.

Curr Diab Rep. 2011 Dec;11(6):543-51. doi: 10.1007/s11892-011-0233-8. Review.

PMID:
21968738
19.

Neonatal diabetes caused by mutations in sulfonylurea receptor 1: interplay between expression and Mg-nucleotide gating defects of ATP-sensitive potassium channels.

Zhou Q, Garin I, Castaño L, Argente J, Muñoz-Calvo MT, Perez de Nanclares G, Shyng SL.

J Clin Endocrinol Metab. 2010 Dec;95(12):E473-8. doi: 10.1210/jc.2010-1231. Epub 2010 Sep 1.

20.

Increased ATPase activity produced by mutations at arginine-1380 in nucleotide-binding domain 2 of ABCC8 causes neonatal diabetes.

de Wet H, Rees MG, Shimomura K, Aittoniemi J, Patch AM, Flanagan SE, Ellard S, Hattersley AT, Sansom MS, Ashcroft FM.

Proc Natl Acad Sci U S A. 2007 Nov 27;104(48):18988-92. Epub 2007 Nov 19.

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