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Summary Expression Phenotypes Gene Literature (112) GO Terms (6) Nucleotides (46) Proteins (32) Interactants (165) Wiki
XB--6084576

Papers associated with kcnj11



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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.

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.

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.

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.

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.

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 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.

Ligand-dependent linkage of the ATP site to inhibition gate closure in the KATP channel., Li L, Geng X, Yonkunas M, Su A, Densmore E, Tang P, Drain P., J Gen Physiol. September 1, 2005; 126 (3): 285-99.                  

Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions., Tammaro P, Girard C, Molnes J, Njølstad PR, Ashcroft FM., EMBO J. July 6, 2005; 24 (13): 2318-30.

A gating mutation at the internal mouth of the Kir6.2 pore is associated with DEND syndrome., Proks P, Girard C, Haider S, Gloyn AL, Hattersley AT, Sansom MS, Ashcroft FM., EMBO Rep. May 1, 2005; 6 (5): 470-5.

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.

Determinant role of membrane helices in K ATP channel gating., Wang R, Rojas A, Wu J, Piao H, Adams CY, Xu H, Shi Y, Shi Y, Wang Y, Jiang C., J Membr Biol. March 1, 2005; 204 (1): 1-10.

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. December 14, 2004; 101 (50): 17539-44.

Molecular basis of inward rectification: polyamine interaction sites located by combined channel and ligand mutagenesis., Kurata HT, Phillips LR, Rose T, Loussouarn G, Herlitze S, Fritzenschaft H, Enkvetchakul D, Nichols CG, Baukrowitz T., J Gen Physiol. November 1, 2004; 124 (5): 541-54.                

Arylcyanoguanidines as activators of Kir6.2/SUR1K ATP channels and inhibitors of insulin release., Tagmose TM, Schou SC, Mogensen JP, Nielsen FE, Arkhammar PO, Wahl P, Hansen BS, Worsaae A, Boonen HC, Antoine MH, Lebrun P, Hansen JB., J Med Chem. June 3, 2004; 47 (12): 3202-11.

Mapping the architecture of the ATP-binding site of the KATP channel subunit Kir6.2., Dabrowski M, Tarasov A, Ashcroft FM., J Physiol. June 1, 2004; 557 (Pt 2): 347-54.

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.

Concerted gating mechanism underlying KATP channel inhibition by ATP., Drain P, Geng X, Li L., Biophys J. April 1, 2004; 86 (4): 2101-12.

Na(+) current through KATP channels: consequences for Na(+) and K(+) fluxes during early myocardial ischemia., Bollensdorff C, Knopp A, Biskup C, Zimmer T, Benndorf K., Am J Physiol Heart Circ Physiol. January 1, 2004; 286 (1): H283-95.

Pyridine nucleotide regulation of the KATP channel Kir6.2/SUR1 expressed in Xenopus oocytes., Dabrowski M, Trapp S, Ashcroft FM., J Physiol. July 15, 2003; 550 (Pt 2): 357-63.

Identification of residues contributing to the ATP binding site of Kir6.2., Trapp S, Haider S, Jones P, Sansom MS, Ashcroft FM., EMBO J. June 16, 2003; 22 (12): 2903-12.

Identification of domains that control the heteromeric assembly of Kir5.1/Kir4.0 potassium channels., Konstas AA, Korbmacher C, Tucker SJ., Am J Physiol Cell Physiol. April 1, 2003; 284 (4): C910-7.

A threonine residue (Thr71) at the intracellular end of the M1 helix plays a critical role in the gating of Kir6.2 channels by intracellular ATP and protons., Cui N, Wu J, Xu H, Wang R, Rojas A, Piao H, Mao J, Abdulkadir L, Li L, Jiang C., J Membr Biol. March 15, 2003; 192 (2): 111-22.

K(ATP) channel activity is required for hatching in Xenopus embryos., Cheng SM, Chen I, Levin M., Dev Dyn. December 1, 2002; 225 (4): 588-91.        

Protons activate homomeric Kir6.2 channels by selective suppression of the long and intermediate closures., Wu J, Xu H, Yang Z, Wang Y, Mao J, Jiang C., J Membr Biol. November 15, 2002; 190 (2): 105-16.

Allosteric modulation of the mouse Kir6.2 channel by intracellular H+ and ATP., Wu J, Cui N, Piao H, Wang Y, Xu H, Mao J, Jiang C., J Physiol. September 1, 2002; 543 (Pt 2): 495-504.

The novel diazoxide analog 3-isopropylamino-7-methoxy-4H-1,2,4-benzothiadiazine 1,1-dioxide is a selective Kir6.2/SUR1 channel opener., Dabrowski M, Ashcroft FM, Ashfield R, Lebrun P, Pirotte B, Egebjerg J, Bondo Hansen J, Wahl P., Diabetes. June 1, 2002; 51 (6): 1896-906.

Open state destabilization by ATP occupancy is mechanism speeding burst exit underlying KATP channel inhibition by ATP., Li L, Geng X, Drain P., J Gen Physiol. January 1, 2002; 119 (1): 105-16.                    

Distinct histidine residues control the acid-induced activation and inhibition of the cloned K(ATP) channel., Xu H, Wu J, Cui N, Abdulkadir L, Wang R, Mao J, Giwa LR, Chanchevalap S, Jiang C., J Biol Chem. October 19, 2001; 276 (42): 38690-6.

Amiloride derivatives are potent blockers of KATP channels., Bollensdorff C, Zimmer T, Benndorf K., Naunyn Schmiedebergs Arch Pharmacol. October 1, 2001; 364 (4): 351-8.

Mutations within the P-loop of Kir6.2 modulate the intraburst kinetics of the ATP-sensitive potassium channel., Proks P, Capener CE, Jones P, Ashcroft FM., J Gen Physiol. October 1, 2001; 118 (4): 341-53.                    

Structural basis for the interference between nicorandil and sulfonylurea action., Reimann F, Ashcroft FM, Gribble FM., Diabetes. October 1, 2001; 50 (10): 2253-9.

Requirement of multiple protein domains and residues for gating K(ATP) channels by intracellular pH., Piao H, Cui N, Xu H, Mao J, Rojas A, Wang R, Abdulkadir L, Li L, Wu J, Jiang C., J Biol Chem. September 28, 2001; 276 (39): 36673-80.

Identification and pharmacological correction of a membrane trafficking defect associated with a mutation in the sulfonylurea receptor causing familial hyperinsulinism., Partridge CJ, Beech DJ, Sivaprasadarao A., J Biol Chem. September 21, 2001; 276 (38): 35947-52.

Glimepiride block of cloned beta-cell, cardiac and smooth muscle K(ATP) channels., Song DK, Ashcroft FM., Br J Pharmacol. May 1, 2001; 133 (1): 193-9.

Phospholipids as modulators of K(ATP) channels: distinct mechanisms for control of sensitivity to sulphonylureas, K(+) channel openers, and ATP., Krauter T, Ruppersberg JP, Baukrowitz T., Mol Pharmacol. May 1, 2001; 59 (5): 1086-93.

Effects of mitiglinide (S 21403) on Kir6.2/SUR1, Kir6.2/SUR2A and Kir6.2/SUR2B types of ATP-sensitive potassium channel., Reimann F, Proks P, Ashcroft FM., Br J Pharmacol. April 1, 2001; 132 (7): 1542-8.

Interaction of stilbene disulphonates with cloned K(ATP) channels., Proks P, Jones P, Ashcroft FM., Br J Pharmacol. March 1, 2001; 132 (5): 973-82.

Direct interaction of Na-azide with the KATP channel., Trapp S, Ashcroft FM., Br J Pharmacol. November 1, 2000; 131 (6): 1105-12.

Identification of molecular regions responsible for the membrane trafficking of Kir6.2., Hough E, Beech DJ, Sivaprasadarao A., Pflugers Arch. July 1, 2000; 440 (3): 481-7.

Direct photoaffinity labeling of Kir6.2 by [gamma-(32)P]ATP-[gamma]4-azidoanilide., Tanabe K, Tucker SJ, Ashcroft FM, Proks P, Kioka N, Amachi T, Ueda K., Biochem Biophys Res Commun. June 7, 2000; 272 (2): 316-9.

Sensitivity of Kir6.2-SUR1 currents, in the absence and presence of sodium azide, to the K(ATP) channel inhibitors, ciclazindol and englitazone., McKay NG, Kinsella JM, Campbell CM, Ashford ML., Br J Pharmacol. June 1, 2000; 130 (4): 857-66.

Nucleotide modulation of pinacidil stimulation of the cloned K(ATP) channel Kir6.2/SUR2A., Gribble FM, Reimann F, Ashfield R, Ashcroft FM., Mol Pharmacol. June 1, 2000; 57 (6): 1256-61.

Altered functional properties of KATP channel conferred by a novel splice variant of SUR1., Sakura H, Trapp S, Liss B, Ashcroft FM., J Physiol. December 1, 1999; 521 Pt 2 337-50.

In vitro mechanism of action on insulin release of S-22068, a new putative antidiabetic compound., Le Brigand L, Virsolvy A, Manechez D, Godfroid JJ, Guardiola-Lemaître B, Gribble FM, Ashcroft FM, Bataille D., Br J Pharmacol. November 1, 1999; 128 (5): 1021-6.

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