Papers associated with kcnj11

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	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.
	Kir6.2 channel gating by intracellular protons: subunit stoichiometry for ligand binding and channel gating., Wang R, Su J, Zhang X, Shi Y, Cui N, Onyebuchi VA, Jiang C., J Membr Biol. January 1, 2006; 213 (3): 155-64.
	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 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.
	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.
	Scavenging of 14-3-3 proteins reveals their involvement in the cell-surface transport of ATP-sensitive K+ channels., Heusser K, Yuan H, Neagoe I, Tarasov AI, Ashcroft FM, Schwappach B., J Cell Sci. October 15, 2006; 119 (Pt 20): 4353-63.
	The N-terminal transmembrane domain (TMD0) and a cytosolic linker (L0) of sulphonylurea receptor define the unique intrinsic gating of KATP channels., Fang K, Csanády L, Chan KW., J Physiol. October 15, 2006; 576 (Pt 2): 379-89.
	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.
	Subunit-stoichiometric evidence for kir6.2 channel gating, ATP binding, and binding-gating coupling., Wang R, Zhang X, Cui N, Wu J, Piao H, Wang X, Su J, Jiang C., Mol Pharmacol. June 1, 2007; 71 (6): 1646-56.
	The Kir6.2-F333I mutation differentially modulates KATP channels composed of SUR1 or SUR2 subunits., Tammaro P, Ashcroft F., J Physiol. June 15, 2007; 581 (Pt 3): 1259-69.
	Remodelling of the SUR-Kir6.2 interface of the KATP channel upon ATP binding revealed by the conformational blocker rhodamine 123., Hosy E, Dérand R, Revilloud J, Vivaudou M., J Physiol. July 1, 2007; 582 (Pt 1): 27-39.
	Iptakalim, a vascular ATP-sensitive potassium (KATP) channel opener, closes rat pancreatic beta-cell KATP channels and increases insulin release., Misaki N, Mao X, Lin YF, Suga S, Li GH, Liu Q, Chang Y, Wang H, Wakui M, Wu J., J Pharmacol Exp Ther. August 1, 2007; 322 (2): 871-8.
	Single residue (K332A) substitution in Kir6.2 abolishes the stimulatory effect of long-chain acyl-CoA esters: indications for a long-chain acyl-CoA ester binding motif., Bränström R, Leibiger IB, Leibiger B, Klement G, Nilsson J, Arhem P, Aspinwall CA, Corkey BE, Larsson O, Berggren PO., Diabetologia. August 1, 2007; 50 (8): 1670-7.
	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 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 mutation in the ATP-binding site of the Kir6.2 subunit of the KATP channel alters coupling with the SUR2A subunit., Tammaro P, Ashcroft FM., J Physiol. November 1, 2007; 584 (Pt 3): 743-53.
	Sulfonylurea receptors type 1 and 2A randomly assemble to form heteromeric KATP channels of mixed subunit composition., Chan KW, Wheeler A, Csanády L., J Gen Physiol. January 1, 2008; 131 (1): 43-58.
	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. May 1, 2008; 51 (5): 802-10.
	Three C-terminal residues from the sulphonylurea receptor contribute to the functional coupling between the K(ATP) channel subunits SUR2A and Kir6.2., Dupuis JP, Revilloud J, Moreau CJ, Vivaudou M., J Physiol. July 1, 2008; 586 (13): 3075-85.
	How ATP inhibits the open K(ATP) channel., Craig TJ, Ashcroft FM, Proks P., J Gen Physiol. July 1, 2008; 132 (1): 131-44.
	Effects of sodium azide, barium ion, d-amphetamine and procaine on inward rectifying potassium channel 6.2 expressed in Xenopus oocytes., Kung FL, Tsai JL, Lee CH, Lee CH, Lou KL, Tang CY, Liou HH, Lu KL, Chen YH, Wang WJ, Tsai MC., J Formos Med Assoc. August 1, 2008; 107 (8): 600-8.
	A cytosolic factor that inhibits KATP channels expressed in Xenopus oocytes by impairing Mg-nucleotide activation by SUR1., Tammaro P, Ashcroft FM., J Physiol. April 15, 2009; 587 (Pt 8): 1649-56.
	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.
	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.
	Targeting hypertension with a new adenosine triphosphate-sensitive potassium channel opener iptakalim., Pan Z, Huang J, Cui W, Long C, Zhang Y, Wang H., J Cardiovasc Pharmacol. September 1, 2010; 56 (3): 215-28.
	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.
	Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1., Proks P, de Wet H, Ashcroft FM., J Gen Physiol. October 1, 2010; 136 (4): 389-405.
	β2-Adrenergic ion-channel coupled receptors as conformational motion detectors., Caro LN, Moreau CJ, Revilloud J, Vivaudou M., PLoS One. March 9, 2011; 6 (3): e18226.
	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.
	A conserved tryptophan at the membrane-water interface acts as a gatekeeper for Kir6.2/SUR1 channels and causes neonatal diabetes when mutated., Männikkö R, Stansfeld PJ, Ashcroft AS, Hattersley AT, Sansom MS, Ellard S, Ashcroft FM., J Physiol. July 1, 2011; 589 (Pt 13): 3071-83.
	Forced gating motions by a substituted titratable side chain at the bundle crossing of a potassium channel., Khurana A, Shao ES, Kim RY, Vilin YY, Huang X, Yang R, Kurata HT., J Biol Chem. October 21, 2011; 286 (42): 36686-93.
	Engineering of an artificial light-modulated potassium channel., Caro LN, Moreau CJ, Estrada-Mondragón A, Ernst OP, Vivaudou M., PLoS One. January 1, 2012; 7 (8): e43766.
	A universally conserved residue in the SUR1 subunit of the KATP channel is essential for translating nucleotide binding at SUR1 into channel opening., de Wet H, Shimomura K, Aittoniemi J, Ahmad N, Lafond M, Sansom MS, Ashcroft FM., J Physiol. October 15, 2012; 590 (20): 5025-36.
	Molecular mechanism of sulphonylurea block of K(ATP) channels carrying mutations that impair ATP inhibition and cause neonatal diabetes., Proks P, de Wet H, Ashcroft FM., Diabetes. November 1, 2013; 62 (11): 3909-19.
	The unusual stoichiometry of ADP activation of the KATP channel., Hosy E, Vivaudou M., Front Physiol. January 28, 2014; 5 11.
	Intracellular ATP does not inhibit Slo2.1 K+ channels., Garg P, Sanguinetti MC., Physiol Rep. September 11, 2014; 2 (9):
	Recessive mutations in PCBD1 cause a new type of early-onset diabetes., Simaite D, Kofent J, Gong M, Rüschendorf F, Jia S, Arn P, Bentler K, Ellaway C, Kühnen P, Hoffmann GF, Blau N, Spagnoli FM, Hübner N, Raile K., Diabetes. October 1, 2014; 63 (10): 3557-64.
	Sulfonylureas suppress the stimulatory action of Mg-nucleotides on Kir6.2/SUR1 but not Kir6.2/SUR2A KATP channels: a mechanistic study., Proks P, de Wet H, Ashcroft FM., J Gen Physiol. November 1, 2014; 144 (5): 469-86.
	Distinct action of the α-glucosidase inhibitor miglitol on SGLT3, enteroendocrine cells, and GLP1 secretion., Lee EY, Kaneko S, Jutabha P, Zhang X, Seino S, Jomori T, Anzai N, Miki T., J Endocrinol. March 1, 2015; 224 (3): 205-14.
	Kir6.2 activation by sulfonylurea receptors: a different mechanism of action for SUR1 and SUR2A subunits via the same residues., Principalli MA, Dupuis JP, Moreau CJ, Vivaudou M, Revilloud J., Physiol Rep. September 1, 2015; 3 (9):
	Sensitivity of KATP channels to cellular metabolic disorders and the underlying structural basis., Li CG, Cui WY, Wang H., Acta Pharmacol Sin. January 1, 2016; 37 (1): 134-42.
	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.
	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.
	Bioelectric signalling via potassium channels: a mechanism for craniofacial dysmorphogenesis in KCNJ2-associated Andersen-Tawil Syndrome., Adams DS, Uzel SG, Akagi J, Wlodkowic D, Andreeva V, Yelick PC, Devitt-Lee A, Pare JF, Levin M., J Physiol. June 15, 2016; 594 (12): 3245-70.
	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.
	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;
	Modeling endoderm development and disease in Xenopus., Edwards NA, Zorn AM., Curr Top Dev Biol. January 1, 2021; 145 61-90.
	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.

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