ATP-sensitive K+ channels and disease: From molecule to malady

American Journal of Physiology - Endocrinology and Metabolism

Volumn 293, Issue 4, 2007, Pages

  Ashcroft, Frances M ^a  

^a UNIVERSITY OF OXFORD   (United Kingdom)

Author keywords

Hyperinsulinism; Kir6.2; Neonatal diabetes; SUR1

Indexed keywords

ADENOSINE TRIPHOSPHATE SENSITIVE POTASSIUM CHANNEL; AMINO ACID; GLUCOSE; INSULIN; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR6.2; SULFONYLUREA RECEPTOR 1; ADENOSINE TRIPHOSPHATE; INWARDLY RECTIFYING POTASSIUM CHANNEL; POTASSIUM CHANNEL;

ABCC8 GENE; AMINO ACID SEQUENCE; CHANNEL GATING; CLINICAL FEATURE; DIABETES MELLITUS; DISEASE MODEL; GENE MUTATION; GLUCOSE HOMEOSTASIS; HUMAN; HYPERGLYCEMIA; INSULIN RELEASE; KCNJ11 GENE; NEWBORN DISEASE; PANCREAS ISLET BETA CELL; PATCH CLAMP; PATHOPHYSIOLOGY; PERSISTENT HYPERINSULINEMIC HYPOGLYCEMIA OF INFANCY; PRIORITY JOURNAL; PROTEIN FUNCTION; PUBLICATION; REVIEW; RISK FACTOR; SEQUENCE ANALYSIS; STRUCTURE ANALYSIS; SYMPTOM; ANIMAL; ARTICLE; BIOLOGICAL MODEL; CHANNELOPATHY; CHEMICAL STRUCTURE; CHEMISTRY; GENETICS; HOMEOSTASIS; METABOLISM; MUTATION; PHYSIOLOGY;

ADENOSINE TRIPHOSPHATE; ANIMALS; CHANNELOPATHIES; DIABETES MELLITUS; GLUCOSE; HOMEOSTASIS; HUMANS; MODELS, BIOLOGICAL; MODELS, MOLECULAR; MUTATION; POTASSIUM CHANNELS; POTASSIUM CHANNELS, INWARDLY RECTIFYING;

EID: 35148826457     PISSN: 01931849     EISSN: 15221555     Source Type: Journal    
DOI: 10.1152/ajpendo.00348.2007     Document Type: Review

References (93)

1. Aguilar-Bryan L, Nichols CG, Wechsler SW, Clement JP 4th, Boyd AE 3rd, Gonzalez Herrerasosa H, Nguy K, Bryan J, Nelson DA. Cloning of the beta-cell high-affinity sulphonylurea receptor: a regulator of insulin secretion. Science 268: 423-425, 1995.
2. ATP channel Kir6.2 subunit. EMBO J 24: 229-239, 2005.
3. Ashcroft FM. ATP-sensitive potassium channelopathies: focus on insulin secretion. J Clin Invest 115: 2047-2058, 2005.
4. Ashcroft FM, Harrison DE, Ashcroft SJH. Glucose induces closure of single potassium channels in isolated rat pancreatic β-cells. Nature 312: 446-448, 1984.
5. 2+ ions. J Physiol 416, 349-367, 1989.
6. Ashcroft FM, Rorsman P. Electrophysiology of the pancreatic β-cell. Prog Biophys Mol Biol 54: 87-143, 1989.
7. Ashcroft SJ. Glucoreceptor mechanisms and the control of insulin release and biosynthesis. Diabetologia 18: 5-15, 1980.
8. Babenko AP, Polak M, Cavé H, Busiah K, Czernichow P, Scharfmann R, Bryan J, Aguilar-Bryan L, Vaxillaire M, Froguel P. Activating mutations in the ABCC8 gene in neonatal diabetes mellitus. New Engl J Med 355: 456-466, 2006.
9. ATP channels: Linker between phospholipid metabolism and excitability. Biochem Pharmacol 60: 735-740, 2000.
10. + channels in pancreatic β-cells. Nature 311: 271-273, 1984.
11. Detimary P, Dejonghe S, Ling Z, Pipeleers D, Schuit F, Henquin JC. The changes in adenine nucleotides measured in glucose-stimulated rodent islets occur in beta cells but not in alpha cells and are also observed in human islets. J Biol Chem 273: 33905-33908, 1998.
12. Diabetes Control, and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 329: 977-986, 1993.
13. Dunne MJ, Cosgrove KE, Shepherd RM, Aynsley-Green A, Lindley KJ. Hyperinsulinism in infancy: from basic science to clinical disease. Physiol Rev 84: 239-275, 2004.
14. Dunne MJ, Petersen OH. Intracellular ADP activates ATP-sensitive K+ channels in an insulin-secreting cell line. FEBS Lett 208: 59-62, 1986.
15. Edghill EL, Gloyn AL, Gillespie KM, Lambert AP, Raymond NT, Swift PG, Ellard S, Gale EA, Hattersley AT. Activating mutations in the KCNJ11 gene encoding the ATP-sensitive K+ channel subunit Kir6.2 are rare in clinically defined type 1 diabetes diagnosed before 2 years. Diabetes 5:2998 -3001, 2004.
16. Ellard E, Flanagan SE, Girard CA, Patch AM, Harries LW, Parrish A, Edghill EL, Mackay DJG, Proks P, Shimomura K, Haberland H, Carson DJ, Shield JPH, Hattersley AT, Ashcroft FM. Permanent neonatal diabetes caused by dominant, recessive or compound heterozygous SUR1 mutations with opposite functional effects. Am J Hum Genetics. 81:375-382, 2007.
17. Fan Z, Makielski JC. Anionic phospholipids activate ATP-sensitive potassium channels. J Biol Chem 272: 5388-5395, 1997.
18. ATP channels: what do we really know? J Mol Cell Cardiol 39: 61-70, 2005.
19. Flanagan SE, Patch AM, Mackay DJ, Edghill EL, Gloyn AL, Robinson D, Shield JP, Temple K, Ellard S, Hattersley AT. Mutations in ATP-sensitive K+ channel genes cause Transient Neonatal Diabetes and Permanent Diabetes in Childhood or Adulthood. Diabetes 56: 1930-1937, 2007.
20. Frayling TM, Timpson NJ, Weedon MN, Zeggini E, Freathy RM, Lindgren CM, Perry JR, Elliott KS, Lango H, Rayner NW, Shields B, Harries LW, Barrett JC, Ellard S, Groves CJ, Knight B, Patch AM, Ness AR, Ebrahim S, Lawlor DA, Ring SM, Ben-Shlomo Y, Jarvelin MR, Sovio U, Bennett AJ, Melzer D, Ferrucci L, Loos RJ, Barroso I, Wareham NJ, Karpe F, Owen KR, Cardon LR, Walker M, Hitman GA, Palmer CN, Doney AS, Morris AD, Davey-Smith G, The Wellcome Trust Case Control Consortium; Hattersley AT, McCarthy MI. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science 316: 889-894, 2007.
21. Girard C, Shimomura K, Proks P, Absalom N, de Nanclares PG, Ashcroft FM. Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes. Pflügers Arch 453: 323-332, 2006.
22. Gloyn AL. Glucokinase (GCK) mutations in hyper- and hypoglycemia: maturity-onset diabetes of the young, permanent neonatal diabetes, and hyperinsulinemia of infancy. Hum Mut 22: 353-362, 2003.
23. Gloyn AL, Pearson ER, Antcliff JF, Proks P, Bruining JG, Slingerland AS, Howard N, Srinivasan S, Silva JMCL, Molnes J, Edghill EL, Frayling TM, Temple IK, Deborah Mackay D, Shield JPH, Sumnik Z, van Rhijn A, Wales JKH, Clark P, Gorman S, Aisenberg J, Ellard S, Njølstad PR, Ashcroft FM, Hattersley AT. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med 350: 1838-1849, 2004.
24. ATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mut 27: 220-231, 2006.
25. ATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) confirm that the KCNJ11 E23K variant is associated with type 2 diabetes Diabetes 52: 568-572, 2003.
26. ATP channel activation by oleyol-CoA. J Biol Chem 273: 26383-26387, 1998.
27. Gribble FM, Reimann F. Sulphonylurea action revisited: the postcloning era. Diabetologia 46: 875-891, 2003.
28. ATP channel activation by Mg-ADP and diazoxide. EMBO J 16: 1145-1152, 1997.
29. ATP channel by interaction with its SUR1 subunit. Proc Natl Acad Sci USA 95: 7185-7190, 1998.
30. Haider S, Antcliff JF, Proks P, Sansom MSP, Ashcroft FM. Focus on Kir6.2: a key component of the ATP-sensitive potassium channel. J Mol Cell Cardiol 38: 927-936, 2005.
31. Hamill OP, Marty A, Neher E, Sakmann B, Sigworth FJ. Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches. Pflügers Arch 391: 85-100, 1981.
32. Hattersley AT, Ashcroft FM. Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy. Diabetes 54: 2503-2513, 2005.
33. Henquin JC. D-Glucose inhibits potassium efflux from pancreatic islet cells. Nature 271: 271-273, 1978.
34. Henquin JC. The fiftieth anniversary of hypoglycaemic sulphonamides. How did the mother compound work? Diabetologia 35: 907-912, 1992.
35. Henquin JC, Meissner HP. Significance of ionic fluxes and changes in membrane potential for stimulus-secretion coupling in pancreatic β-cells. Experientia 40: 1043-1052, 1984.
36. Huopio H, Otonkoski T, Vauhkonen I, Reimann F, Ashcroft Laakso M FM. A new subtype of autosomal dominant diabetes due to the E1506K substitution in the sulfonylurea receptor 1 gene. Lancet 361: 301-307, 2003.
37. KATP: An inward rectifier subunit plus the sulfonylurea receptor. Science 270: 1166-1169, 1995.
38. + channel. FEBS Lett 409: 232-236, 1997.
39. ATP channels in health and disease. J Mol Cell Cardiol 38: 937-43, 2005.
40. + channels in rat pancreatic β-cells is modulated by ADP. FEBS Lett 208: 63-66, 1986.
41. ATP channel-forming Kir6.2 subunit and the sulfonylurea receptor SUR1 in rodent brain. FEBS Lett 401: 59-64, 1997.
42. King H, Aubert RE, Herman WH. Global burden of diabetes, 1995-2025: prevalence, numerical estimates, and projections. Diabetes Care 21: 1414-1431, 1998.
43. Koster JC, Knopp A, Flagg TP, Markova KP, Sha Q, Enkvetchakul D, Betsuyaku T, Yamada KA, Nichols CG. Tolerance for ATP-insensitive K-ATP channels in transgenic mice. Circ Res 89: 1022-1029, 2001.
44. ATP channels induces profound neonatal diabetes. Cell 100: 645-654, 2000.
45. ATP channels. Proc Natl Acad Sci USA 99: 16992-16997, 2002.
46. Koster JC, Remedi MS, Masia R, Patton B, Tong A, Nichols CG. Expression of ATP-insensitive KATP channels in pancreatic beta-cells underlies a spectrum of diabetic phenotypes. Diabetes 55: 2957-2964, 2006.
47. Kuo AL, Gulbis JM, Antcliff JF, Rahman T, Lowe ED, Zimmer J, Cuthbertson J, Ashcroft FM, Ezaki T, Doyle DA. Crystal structure of the potassium channel KirBac1.1 in the closed state Science 300: 1922-1926, 2003.
48. + channels by long chain acyl-CoA. J Biol Chem 271: 10623-10626, 1996.
49. ATP channels by SUR1 and SUR2A. J Mol Cell Cardiol 39: 491-501, 2005.
50. Masia R, Koster JC, Tumini S, Chiarelli F, Colombo C, Nichols CG, Barbetti F. An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetes. Diabetes 56: 328-336, 2007.
51. Matsuo M, Tanabe K, Kioka N, Amachi T, Ueda K. Different binding properties and affinities for ATP and ADP among sulfonylurea receptor subtypes, SUR1, SUR2A, and SUR2B. J Biol Chem 275: 28757-28763, 2002.
52. + channels. Circ Res 87: 873-880, 2000.
53. ATP channel complex Kir6.2-SUR1. EMBO J 24: 4166-4175, 2005.
54. ATP channels as metabolic sensors in acute metabolic changes. J Mol Cell Cardiol 38: 917-925, 2005.
55. ATP channel-deficient mice. Proc Natl Acad Sci USA 95: 10402-10406, 1998.
56. ATP channel. Proc Natl Acad Sci USA 94: 11969-71193, 1997.
57. Nestorowicz A, Inagaki N, Gonoi T, Schoor KP, Wilson BA, Glaser B, Landau H, Stanley CA, Thornton PS, Seino S, Permutt MA. A nonsense mutation in the inward rectifier potassium channel gene, Kir6.2, is associated with familial hyperinsulinism. Diabetes 46: 1743-1748, 1997.
58. ATP channels as molecular sensors of cellular metabolism. Nature 440: 470-476, 2006.
59. Nichols CG, Shyng SL, Nestorowicz A. Adenosine diphosphate as an intracellular regulator of insulin secretion. Science 272: 1785-1787, 1996.
60. Nishida M, MacKinnon R. Structural basis of inward rectification: cytoplasmic pore of the G protein-gated inward rectifier GIRK1 at 1.8Å resolution. Cell 111: 957-965, 2002.
61. + channels in cardiac muscle. Nature 305: 147-148, 1983.
62. Pearson ER, Flechtner I, Njølståd PR, Neonatal Diabetes International Collaborative Group, Malecki MT, Flanagan S, Larkin B, Ashcroft FM, Klimes I, Codner E, Iotova V, Slingerland AS, Shield J, Robert JJ, Holst JJ, Clark PM, Ellard S, Sovik O, Polak M, Hattersley AT. The successful transfer of insulin treated patients with diabetes due to Kir62 (KCNJ11) mutations to sulphonylurea tablets. N Eng J Med 355: 467-477, 2006.
63. 2+, cAMP, and phospholipid-derived messengers in coupling mechanisms of insulin secretion. Physiol Rev 67: 1185-1248, 1987.
64. Proks P, Antcliff JF, Lippiat J, Gloyn A, Hattersley AT, Ashcroft FM. Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features. Proc Natl Acad Sci USA 101: 17539-17544, 2004.
65. Proks P, Arnold A, Bruining J, Girard C, Flanagan SE, Larkin B, Colclough K, Hattersley AT, Ashcroft FM, Ellard SE. A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes. Hum Mol Genet 15: 1793-1800, 2006.
66. Proks P, Girard C, Ashcroft FM. Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP. Hum Mol Genet 14: 2717-2726, 2005.
67. 2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulphonylurea therapy. Diabetes 55: 1731-1737, 2006.
68. Proks P, Girard C, Haider S, Gloyn AL, Hattersley AT, Sansom MSP, Ashcroft FM. A novel gating mutation at the internal mouth of the Kir6.2 pore is associated with DEND syndrome. EMBO Rep 6: 470-475, 2005.
69. Riedel MJ, Boora P, Steckley D, de Vries G, Light Kir6 PE.2. polymorphisms sensitize beta-cell ATP-sensitive potassium channels to activation by acyl CoAs: a possible cellular mechanism for increased susceptibility to type 2 diabetes? Diabetes 52: 2630-2635, 2003.
70. +-channels in pancreatic beta-cells are regulated by intracellular ATP. Pflügers Arch 405: 305-309, 1985.
71. Sakura H, Ämmalä C, Smith PA, Gribble FM, Ashcroft FM. Cloning and functional expression of the cDNA encoding a novel ATP-sensitive potassium channel subunit expressed in pancreatic beta cells, brain, heart and skeletal muscle. FEBS Lett 377: 338-344, 1995.
72. Sakura H, Wat N, Horton V, Millns H, Turner RC, Ashcroft FM. Sequence variations in the human Kir6.2 gene, a subunit of the β-cell ATP-sensitive K-channel: no association with non-insulin dependent diabetes in white Caucasian subjects or evidence of abnormal function when expressed in vitro. Diabetologia 39: 1233-1237, 1996.
73. ATP channel-independent regulation of insulin secretion. J Biol Chem 275: 9270-9277, 2000.
74. + permeability in pancreatic beta cells. Nature 253: 635-636, 1975.
75. + channels. Diabetes 51: 875-879, 2002.
76. Shih DQ, Stoffel M. Molecular etiologies of MODY and other early-onset forms of diabetes. Curr Diab Rep 2: 125-134, 2002.
77. Shimomura K, Girard CAJ, Proks P, Nazim J, Lippiat JD, Cerutti F, Lorini R, Ellard S, Hattersely A, Barbetti F, Ashcroft FM. Mutations at the same residue (R50) of Kir6.2 (KCNJ11) produce different functional effects. Diabetes 55: 1705-1712, 2006.
78. Shimomura K, Hörster F, de Wet H, Flanagan SE, Ellard S, Hattersley AT, Wolf NI, Ashcroft FM, Ebinger F. A novel mutation causing DEND syndrome - a treatable channelopathy of pancreas and brain. Neurology 2007 [Published on-line July 25, PMID 17652641].
79. ATP channels. Science 282: 1138-1141, 1998.
80. Sladek R, Rocheleau G, Rung J, Dina C, Shen L, Serre D, Boutin P, Vincent D, Belisle A, Hadjadj S, Balkau B, Heude B, Charpentier G, Hudson TJ, Montpetit A, Pshezhetsky AV, Prentki M, Posner BI, Balding DJ, Meyre D, Polychronakos C, Froguel P. A genome-wide association study identifies novel risk loci for type 2 diabetes. Nature 445: 881-885, 2007.
81. Slingerland AS, Nuboer R, Hadders-Algra M, Hattersley AT, Bruining GJ. Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation in the KCNJ11 gene. Diabetologia 49: 2559-2563, 2006.
82. Tammaro P, Girard C, Molnes J, Njølstad PR, Ashcroft Kir6 FM.2. mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions. EMBO J 24: 2318-2330, 2005.
83. ATP channels. J Physiol 571: 3-14, 2006.
84. ATP channel: a pas de deux. Diabetes 53: S123-S127, 2004.
85. Tarasov A, Welters HJ, Senkel S, Ryffel GU, Hattersley AT, Morgan NG, Ashcroft Kir6 FMA.2. mutation causing neonatal diabetes impairs electrical activity and insulin secretion from INS-1 beta cells. Diabetes 55: 3075-3082, 2006.
86. Thomas PM, Cote GJ, Wohllk N, Haddad B, Mathew PM, Rabl W, Aguilar-Bryan L, Gagel RF, Bryan J. Mutations in the sulfonylurea receptor gene in familial persistent hyperinsulinemic hypoglycemia of infancy. Science 268: 426-429, 1995.
87. + channel in mouse pancreatic beta-cells. Pflügers Arch 407: 493-499, 1986.
88. Tucker SJ, Gribble FM, Zhao C, Trapp S, Ashcroft Truncation of Kir6 FM.2. produces ATP-sensitive K channels in the absence of the sulphonylurea receptor. Nature 387: 179-181, 1997.
89. UK Prospective Diabetes Study (UKPDS) Group. Intensive bloodglucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 352: 837-853, 1998.
90. Zeggini E, Weedon MN, Lindgren CM, Frayling TM, Elliott KS, Lango H, Timpson NJ, Perry JR, Rayner NW, Freathy RM, Barrett JC, Shields B, Morris AP, Ellard S, Groves CJ, Harries LW, Marchini JL, Owen KR, Knight B, Cardon LR, Walker M, Hitman GA, Morris AD, Doney AS; Wellcome Trust Case Control Consortium (WTCCC), Burton PR, Clayton DG, Craddock N, Deloukas P, Duncanson A, Kwiatkowski DP, Ouwehand WH, Samani NJ, Todd JA, Donnelly P, Davison D, Easton D, Evans D, Leung HT, Spencer CC, Tobin MD, Attwood AP, Boorman JP, Cant B, Everson U, Hussey JM, Jolley JD, Knight AS, Koch K, Meech E, Nutland S, Prowse CV, Stevens HE, Taylor NC, Walters GR, Walker NM, Watkins NA, Winzer T, Jones RW, McArdle WL, Ring SM, Strachan DP, Pembrey M, Breen G, St Clair D, Caesar S, Gordon-Smith K, Jones L, Fraser C, Green EK, Grozeva D, Hamshere ML, Holmans PA, Jones IR, Kirov G, Moskvina V, Nikolov I, O'donovan MC, Owen MJ, Collier DA, Elkin A, Farmer A, Williamson R, McGuffin P, Young AH, Ferrier IN, Ball SG, Balmforth AJ, Barrett JH, Bishop DT, Iles MM, Maqbool A, Yuldasheva N, Hall AS, Braund PS, Dixon RJ, Mangino M, Stevens S, Thompson JR, Bredin F, Tremelling M, Parkes M, Drummond H, Lees CW, Nimmo ER, Satsangi J, Fisher SA, Forbes A, Lewis CM, Onnie CM, Prescott NJ, Sanderson J, Mathew CG, Barbour J, Mohiuddin MK, Todhunter CE, Mansfield JC, Ahmad T, Cummings FR, Jewell DP, Webster J, Brown MJ, Lathrop GM, Connell J, Dominiczak A, Braga Marcano CA, Burke B, Dobson R, Gungadoo J, Lee KL, Munroe PB, Newhouse SJ, Onipinla A, Wallace C, Xue M, Caulfield M, Farrall M, Barton A, Bruce IN, Donovan H, Eyre S, Gilbert PD, Hider SL, Hinks AM, John SL, Potter C, Silman AJ, Symmons DP, Thomson W, Worthington J, Dunger DB, Widmer B, Newport M, Sirugo G, Lyons E, Vannberg F, Hill AV, Bradbury LA, Farrar C, Pointon JJ, Wordsworth P, Brown MA, Franklyn JA, Heward JM, Simmonds MJ, Gough SC, Seal S, Stratton MR, Rahman N, Ban M, Goris A, Sawcer SJ, Compston A, Conway D, Jallow M, Rockett KA, Bumpstead SJ, Chaney A, Downes K, Ghori MJ, Gwilliam R, Hunt SE, Inouye M, Keniry A, King E, McGinnis R, Potter S, Ravindrarajah R, Whittaker P, Widden C, Withers D, Cardin NJ, Ferreira T, Pereira-Gale J, Hallgrimsdóttir IB, Howie BN, Su Z, Teo YY, Vukcevic D, Bentley D, Compston A, Ouwehand NJ, Samani MR, Isaacs JD, Morgan AW, Wilson GD, Ardern-Jones A, Berg J, Brady A, Bradshaw N, Brewer C, Brice G, Bullman B, Campbell J, Castle B, Cetnarsryj R, Chapman C, Chu C, Coates N, Cole T, Davidson R, Donaldson A, Dorkins H, Douglas F, Eccles D, Eeles R, Elmslie F, Evans DG, Goff S, Goodman S, Goudie D, Gray J, Greenhalgh L, Gregory H, Hodgson SV, Homfray T, Houlston RS, Izatt L, Jackson L, Jeffers L, Johnson-Roffey V, Kavalier F, Kirk C, Lalloo F, Langman C, Locke I, Longmuir M, Mackay J, Magee A, Mansour S, Miedzybrodzka Z, Miller J, Morrison P, Murday V, Paterson J, Pichert G, Porteous M, Rahman N, Rogers M, Rowe S, Shanley S, Saggar A, Scott G, Side L, Snadden L, Steel M, Thomas M, Thomas S, McCarthy MI, Hattersley AT. Replication of genome-wide association signals in UK samples reveals risk loci for type 2 diabetes. Science 316: 1336-1341, 2007.
91. ATP channels. Neuron 22: 537-548, 1999.
92. + conductance. Neuron 31: 233-245, 2001.
93. Zung A, Glaser B, Nimri R, Zadik Z. Glibenclamide treatment in permanent neonatal diabetes mellitus due to an activating mutation in Kir6.2. J Clin Endocrinol Metab 89: 5504-5507, 2004.