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227 related items for PubMed ID: 27118464

  • 1. 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. PubMed ID: 27118464
    [Abstract] [Full Text] [Related]

  • 2. A loss-of-function mutation in KCNJ11 causing sulfonylurea-sensitive diabetes in early adult life.
    Vedovato N, Salguero MV, Greeley SAW, Yu CH, Philipson LH, Ashcroft FM.
    Diabetologia; 2024 May; 67(5):940-951. PubMed ID: 38366195
    [Abstract] [Full Text] [Related]

  • 3. Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy.
    Proks P, Girard C, Baevre H, Njølstad PR, Ashcroft FM.
    Diabetes; 2006 Jun; 55(6):1731-7. PubMed ID: 16731836
    [Abstract] [Full Text] [Related]

  • 4. Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features.
    Proks P, Antcliff JF, Lippiat J, Gloyn AL, Hattersley AT, Ashcroft FM.
    Proc Natl Acad Sci U S A; 2004 Dec 14; 101(50):17539-44. PubMed ID: 15583126
    [Abstract] [Full Text] [Related]

  • 5. A Kir6.2 mutation causing severe functional effects in vitro produces neonatal diabetes without the expected neurological complications.
    Tammaro P, Flanagan SE, Zadek B, Srinivasan S, Woodhead H, Hameed S, Klimes I, Hattersley AT, Ellard S, Ashcroft FM.
    Diabetologia; 2008 May 14; 51(5):802-10. PubMed ID: 18335204
    [Abstract] [Full Text] [Related]

  • 6. Mutations at the same residue (R50) of Kir6.2 (KCNJ11) that cause neonatal diabetes produce different functional effects.
    Shimomura K, Girard CA, Proks P, Nazim J, Lippiat JD, Cerutti F, Lorini R, Ellard S, Hattersley AT, Barbetti F, Ashcroft FM.
    Diabetes; 2006 Jun 14; 55(6):1705-12. PubMed ID: 16731833
    [Abstract] [Full Text] [Related]

  • 7. 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 14; 58(10):2419-24. PubMed ID: 19587354
    [Abstract] [Full Text] [Related]

  • 8. 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 14; 60(6):1813-22. PubMed ID: 21617188
    [Abstract] [Full Text] [Related]

  • 9. An in-frame deletion in Kir6.2 (KCNJ11) causing neonatal diabetes reveals a site of interaction between Kir6.2 and SUR1.
    Craig TJ, Shimomura K, Holl RW, Flanagan SE, Ellard S, Ashcroft FM.
    J Clin Endocrinol Metab; 2009 Jul 14; 94(7):2551-7. PubMed ID: 19351728
    [Abstract] [Full Text] [Related]

  • 10. Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes.
    Girard CA, Shimomura K, Proks P, Absalom N, Castano L, Perez de Nanclares G, Ashcroft FM.
    Pflugers Arch; 2006 Dec 14; 453(3):323-32. PubMed ID: 17021801
    [Abstract] [Full Text] [Related]

  • 11. The first clinical case of a mutation at residue K185 of Kir6.2 (KCNJ11): a major ATP-binding residue.
    Shimomura K, de Nanclares GP, Foutinou C, Caimari M, Castaño L, Ashcroft FM.
    Diabet Med; 2010 Feb 14; 27(2):225-9. PubMed ID: 20546268
    [Abstract] [Full Text] [Related]

  • 12. Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations.
    Pearson ER, Flechtner I, Njølstad PR, Malecki MT, Flanagan SE, Larkin B, Ashcroft FM, Klimes I, Codner E, Iotova V, Slingerland AS, Shield J, Robert JJ, Holst JJ, Clark PM, Ellard S, Søvik O, Polak M, Hattersley AT, Neonatal Diabetes International Collaborative Group.
    N Engl J Med; 2006 Aug 03; 355(5):467-77. PubMed ID: 16885550
    [Abstract] [Full Text] [Related]

  • 13. Relapsing diabetes can result from moderately activating mutations in KCNJ11.
    Gloyn AL, Reimann F, Girard C, Edghill EL, Proks P, Pearson ER, Temple IK, Mackay DJ, Shield JP, Freedenberg D, Noyes K, Ellard S, Ashcroft FM, Gribble FM, Hattersley AT.
    Hum Mol Genet; 2005 Apr 01; 14(7):925-34. PubMed ID: 15718250
    [Abstract] [Full Text] [Related]

  • 14. Functional analysis of two Kir6.2 (KCNJ11) mutations, K170T and E322K, causing neonatal diabetes.
    Tarasov AI, Girard CA, Larkin B, Tammaro P, Flanagan SE, Ellard S, Ashcroft FM.
    Diabetes Obes Metab; 2007 Nov 01; 9 Suppl 2():46-55. PubMed ID: 17919178
    [Abstract] [Full Text] [Related]

  • 15. Congenital hyperinsulinism and glucose hypersensitivity in homozygous and heterozygous carriers of Kir6.2 (KCNJ11) mutation V290M mutation: K(ATP) channel inactivation mechanism and clinical management.
    Loechner KJ, Akrouh A, Kurata HT, Dionisi-Vici C, Maiorana A, Pizzoferro M, Rufini V, de Ville de Goyet J, Colombo C, Barbetti F, Koster JC, Nichols CG.
    Diabetes; 2011 Jan 01; 60(1):209-17. PubMed ID: 20980454
    [Abstract] [Full Text] [Related]

  • 16. Successful transfer to sulfonylureas in KCNJ11 neonatal diabetes is determined by the mutation and duration of diabetes.
    Babiker T, Vedovato N, Patel K, Thomas N, Finn R, Männikkö R, Chakera AJ, Flanagan SE, Shepherd MH, Ellard S, Ashcroft FM, Hattersley AT.
    Diabetologia; 2016 Jun 01; 59(6):1162-6. PubMed ID: 27033559
    [Abstract] [Full Text] [Related]

  • 17. 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 Jun 01; 6(2):133-8. PubMed ID: 22562119
    [Abstract] [Full Text] [Related]

  • 18. The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy.
    Koster JC, Cadario F, Peruzzi C, Colombo C, Nichols CG, Barbetti F.
    J Clin Endocrinol Metab; 2008 Mar 01; 93(3):1054-61. PubMed ID: 18073297
    [Abstract] [Full Text] [Related]

  • 19. 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 01; 15(11):1793-800. PubMed ID: 16613899
    [Abstract] [Full Text] [Related]

  • 20. Molecular Genetics, Clinical Characteristics, and Treatment Outcomes of KATP-Channel Neonatal Diabetes Mellitus in Vietnam National Children's Hospital.
    Ngoc CTB, Dien TM, De Franco E, Ellard S, Houghton JAL, Lan NN, Thao BP, Khanh NN, Flanagan SE, Craig ME, Dung VC.
    Front Endocrinol (Lausanne); 2021 Jun 01; 12():727083. PubMed ID: 34566892
    [Abstract] [Full Text] [Related]

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