Papers associated with kcnj21

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	Beneficial actions of the [A14K] analog of the frog skin peptide PGLa-AM1 in mice with obesity and degenerative diabetes: A mechanistic study., Musale V, Moffett RC, Conlon JM, Flatt PR, Abdel-Wahab YH., Peptides. February 1, 2021; 136 170472.
	Permanent neonatal diabetes: combining sulfonylureas with insulin may be an effective treatment., Misra S, Vedovato N, Cliff E, De Franco E, Hattersley AT, Ashcroft FM, Oliver NS., Diabet Med. June 13, 2018;
	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. July 1, 2016; 59 (7): 1430-1436.
	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. June 1, 2016; 59 (6): 1162-6.
	Xenopus as a model system for studying pancreatic development and diabetes., Kofent J, Spagnoli FM., Semin Cell Dev Biol. March 1, 2016; 51 106-16.
	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. June 1, 2011; 60 (6): 1813-22.
	Disease progression and search for monogenic diabetes among children with new onset type 1 diabetes negative for ICA, GAD- and IA-2 Antibodies., Pörksen S, Laborie LB, Nielsen L, Louise Max Andersen M, Sandal T, de Wet H, Schwarcz E, Aman J, Swift P, Kocova M, Schönle EJ, de Beaufort C, Hougaard P, Ashcroft F, Molven A, Knip M, Mortensen HB, Hansen L, Njølstad PR, Hvidøre Study Group on Childhood Diabetes., BMC Endocr Disord. September 23, 2010; 10 16.
	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. February 1, 2010; 27 (2): 225-9.
	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. July 1, 2009; 94 (7): 2551-7.
	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. November 1, 2007; 9 Suppl 2 46-55.
	A novel mutation causing DEND syndrome: a treatable channelopathy of pancreas and brain., Shimomura K, Hörster F, de Wet H, Flanagan SE, Ellard S, Hattersley AT, Wolf NI, Ashcroft F, Ebinger F., Neurology. September 25, 2007; 69 (13): 1342-9.
	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. December 1, 2006; 453 (3): 323-32.
	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. August 3, 2006; 355 (5): 467-77.
	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. June 1, 2006; 55 (6): 1731-7.
	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. June 1, 2006; 55 (6): 1705-12.
	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. June 1, 2006; 15 (11): 1793-800.
	Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels., Tammaro P, Proks P, Ashcroft FM., J Physiol. February 15, 2006; 571 (Pt 1): 3-14.
	Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP., Proks P, Girard C, Ashcroft FM., Hum Mol Genet. September 15, 2005; 14 (18): 2717-26.
	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. April 1, 2005; 14 (7): 925-34.
	Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes., Gloyn AL, Pearson ER, Antcliff JF, Proks P, Bruining GJ, Slingerland AS, Howard N, Srinivasan S, Silva JM, Molnes J, Edghill EL, Frayling TM, Temple IK, Mackay D, Shield JP, Sumnik Z, van Rhijn A, Wales JK, Clark P, Gorman S, Aisenberg J, Ellard S, Njølstad PR, Ashcroft FM, Hattersley AT., N Engl J Med. April 29, 2004; 350 (18): 1838-49.

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