Peter Proks

• The value of in vitro studies in a case of neonatal diabetes with a novel Kir6.2-W68G mutation.

  O'Connell SM. et al, (2015), Clin Case Rep, 3, 884 - 887

• Molecular action of sulphonylureas on KATP channels: a real partnership between drugs and nucleotides.

  de Wet H. and Proks P., (2015), Biochem Soc Trans, 43, 901 - 907

• ATP-sensitive potassium channels in health and disease

  Proks P. and Clark R., (2015), Islets of Langerhans, Second Edition, 305 - 336

• Sulfonylureas suppress the stimulatory action of Mg-nucleotides on Kir6.2/SUR1 but not Kir6.2/SUR2A KATP channels: a mechanistic study.

  Proks P. et al, (2014), J Gen Physiol, 144, 469 - 486

• Reversible changes in pancreatic islet structure and function produced by elevated blood glucose

  Brereton MF. et al, (2014), DIABETOLOGIA, 57, S93 - S93

• Reversible changes in pancreatic islet structure and function produced by elevated blood glucose.

  Brereton MF. et al, (2014), Nat Commun, 5

• Molecular mechanism of sulphonylurea block of K(ATP) channels carrying mutations that impair ATP inhibition and cause neonatal diabetes.

  Proks P. et al, (2013), Diabetes, 62, 3909 - 3919

• A mouse model of human hyperinsulinism produced by the E1506K mutation in the sulphonylurea receptor SUR1.

  Shimomura K. et al, (2013), Diabetes, 62, 3797 - 3806

• Neonatal diabetes caused by activating mutations in the sulphonylurea receptor.

  Proks P., (2013), Diabetes Metab J, 37, 157 - 164

• Development of postpartum Graves' disease and type 1 diabetes after delivery in a patient with gestational diabetes.

  Negishi M. et al, (2011), J Diabetes Investig, 2, 328 - 330

• Erratum: Effects of mitiglinide (S 21403) on Kir6.2/SUR1, Kir6.2/SUR2A and Kir6.2/SUR2B types of ATP-sensitive potassium channel (British Journal of Pharmacology (2001) 132 (1542-1548))

  Reimann F. et al, (2011), British Journal of Pharmacology, 162

• Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1.

  Proks P. et al, (2010), J Gen Physiol, 136, 389 - 405

• Sepsis and gas-forming splenic abscess by Clostridium septicum in a patient with type 2 diabetes.

  Imamura M. et al, (2010), J Diabetes Complications, 24, 142 - 144

• ATP-sensitive potassium channels in health and disease.

  Clark R. and Proks P., (2010), Adv Exp Med Biol, 654, 165 - 192

• An obese patient with slowly progressive type 1 diabetes diagnosed by ketoacidosis.

  Negishi M. et al, (2010), Intern Med, 49, 393 - 395

• Review. SUR1: a unique ATP-binding cassette protein that functions as an ion channel regulator.

  Aittoniemi J. et al, (2009), Philos Trans R Soc Lond B Biol Sci, 364, 257 - 267

• Modeling K(ATP) channel gating and its regulation.

  Proks P. and Ashcroft FM., (2009), Prog Biophys Mol Biol, 99, 7 - 19

• Mechanism of disopyramide-induced hypoglycaemia in a patient with Type 2 diabetes.

  Negishi M. et al, (2009), Diabet Med, 26, 76 - 78

• Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic beta cells recapitulates neonatal diabetes.

  Girard CA. et al, (2009), J Clin Invest, 119, 80 - 90

• A proposal of combined evaluation of waist circumference and BMI for the diagnosis of metabolic syndrome.

  Takahashi M. et al, (2009), Endocr J, 56, 1079 - 1082

• ATP-sensitive potassium channels in health and disease

  Proks P. and Ashcroft FM., (2008), Pancreatic Beta Cell in Health and Disease, 431 - 450

• A mouse model of neonatal diabetes caused by the K-ATP channel mutation Kir6.2-V59M

  Girard CA. et al, (2008), DIABETOLOGIA, 51, S54 - S54

• Alpha glucosidase inhibitor voglibose can prevent pioglitazone-induced body weight gain in Type 2 diabetic patients.

  Negishi M. et al, (2008), Br J Clin Pharmacol, 66, 318 - 319

• How ATP inhibits the open K(ATP) channel.

  Craig TJ. et al, (2008), J Gen Physiol, 132, 131 - 144

• A mutation (R826W) in nucleotide-binding domain 1 of ABCC8 reduces ATPase activity and causes transient neonatal diabetes.

  de Wet H. et al, (2008), EMBO Rep, 9, 648 - 654

• Xenopus oocytes as a heterologous expression system for studying ion channels with the patch-clamp technique.

  Tammaro P. et al, (2008), Methods Mol Biol, 491, 127 - 139

• Mosaic paternal uniparental isodisomy and an ABCC8 gene mutation in a patient with permanent neonatal diabetes and hemihypertrophy.

  Shield JP. et al, (2008), Diabetes, 57, 255 - 258

• Mechanism of action of a sulphonylurea receptor SUR1 mutation (F132L) that causes DEND syndrome.

  Proks P. et al, (2007), Hum Mol Genet, 16, 2011 - 2019

• Permanent neonatal diabetes caused by dominant, recessive, or compound heterozygous SUR1 mutations with opposite functional effects.

  Ellard S. et al, (2007), Am J Hum Genet, 81, 375 - 382

• Erratum: Mutations at the same residue (R50) of Kir6.2 (KCNJ11) that cause neonatal diabetes produce different functional effects (Diabetes (2006) 55, (1705-1712))

  Shimomura K. et al, (2007), Diabetes, 56

• Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes.

  Girard CA. et al, (2006), Pflugers Arch, 453, 323 - 332

• Effect of peroxisome proliferator-activated receptor alpha ligand fenofibrate on K(v) channels in the insulin-secreting cell line HIT-T15.

  Shimomura K. et al, (2006), Gen Physiol Biophys, 25, 455 - 460

• Mutations at the same residue (R50) of Kir6.2 (KCNJ11) that cause neonatal diabetes produce different functional effects.

  Shimomura K. et al, (2006), Diabetes, 55, 1705 - 1712

• Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy.

  Proks P. et al, (2006), Diabetes, 55, 1731 - 1737

• A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes.

  Proks P. et al, (2006), Hum Mol Genet, 15, 1793 - 1800

• Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels.

  Tammaro P. et al, (2006), J Physiol, 571, 3 - 14

• Membrane ion channels and diabetes.

  Proks P. and Lippiat JD., (2006), Curr Pharm Des, 12, 485 - 501

• Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP.

  Proks P. et al, (2005), Hum Mol Genet, 14, 2717 - 2726

• Focus on Kir6.2: a key component of the ATP-sensitive potassium channel.

  Haider S. et al, (2005), J Mol Cell Cardiol, 38, 927 - 936

• A gating mutation at the internal mouth of the Kir6.2 pore is associated with DEND syndrome.

  Proks P. et al, (2005), EMBO Rep, 6, 470 - 475

• Relapsing diabetes can result from moderately activating mutations in KCNJ11.

  Gloyn AL. et al, (2005), Hum Mol Genet, 14, 925 - 934

• A genetic and physiological study of impaired glucose homeostasis control in C57BL/6J mice.

  Toye AA. et al, (2005), Diabetologia, 48, 675 - 686

• Functional analysis of a structural model of the ATP-binding site of the KATP channel Kir6.2 subunit.

  Antcliff JF. et al, (2005), EMBO J, 24, 229 - 239

• Molecular basis of Kir6.2 mutations causing neonatal diabetes and neonatal diabetes with neurological features

  Proks P. et al, (2005), BIOPHYSICAL JOURNAL, 88, 181A - 181A

• Modelling of the ATP-inhibitory mechanism in ATP-sensitive potassium (KATP) channels: Insights from computer simulations of wild-type and mutant channels.

  Shang LJ. et al, (2005), BIOPHYSICAL JOURNAL, 88, 284A - 284A

• A KCNJ11 mutation in the ATP-binding site of the K-ATP channel causes neonatal diabetes with epilepsy

  Shimomura K. et al, (2005), DIABETOLOGIA, 48, A113 - A113

• Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features.

  Proks P. et al, (2004), Proc Natl Acad Sci U S A, 101, 17539 - 17544

• Inhibition of ATP-sensitive potassium channels by haloperidol.

  Yang SB. et al, (2004), Br J Pharmacol, 143, 960 - 967

• Identification of a functionally important negatively charged residue within the second catalytic site of the SUR1 nucleotide-binding domains.

  Campbell JD. et al, (2004), Diabetes, 53 Suppl 3, S123 - S127

• Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes.

  Gloyn AL. et al, (2004), N Engl J Med, 350, 1838 - 1849

• Erratum: Characterisation of new KATP-channel mutations associated with congenital hyperinsulinism in the Finnish population (Diabetologia (2003) 46 (195-202))

  Reimann F. et al, (2004), Diabetologia, 47

• Characterisation of new K-ATP-channel mutations associated with congenital hyperinsulinism in the Finnish population (vol 46, pg 241, 2003)

  Reimann F. et al, (2004), DIABETOLOGIA, 47, 155 - 155

• Filter flexibility in a mammalian K channel: models and simulations of Kir6.2 mutants.

  Capener CE. et al, (2003), Biophys J, 84, 2345 - 2356

• Characterisation of new KATP-channel mutations associated with congenital hyperinsulinism in the Finnish population.

  Reimann F. et al, (2003), Diabetologia, 46, 241 - 249

• The ligand-sensitive gate of a potassium channel lies close to the selectivity filter.

  Proks P. et al, (2003), EMBO Rep, 4, 70 - 75

• The ligand-sensitive gate of a potassium channel lies close to the selectivity filter

  Proks P. et al, (2003), EMBO Reports, 4, 70 - 75

• Sulfonylurea stimulation of insulin secretion.

  Proks P. et al, (2002), Diabetes, 51 Suppl 3, S368 - S376

• The ligand-sensitive gate of a potassium channel lies close to the selectivity filter

  Proks P. et al, (2002), JOURNAL OF PHYSIOLOGY-LONDON, 544, 9P - 9P

• Inhibition of recombinant K(ATP) channels by the antidiabetic agents midaglizole, LY397364 and LY389382.

  Proks P. et al, (2002), Eur J Pharmacol, 452, 11 - 19

• Mutations within the P-loop of Kir6.2 modulate the intraburst kinetics of the ATP-sensitive potassium channel.

  Proks P. et al, (2001), J Gen Physiol, 118, 341 - 353

• Gliclazide produces high-affinity block of KATP channels in mouse isolated pancreatic beta cells but not rat heart or arterial smooth muscle cells.

  Lawrence CL. et al, (2001), Diabetologia, 44, 1019 - 1025

• Structure-function studies of the fast gating kinetics of the cloned ATP-sensitive potassium channel, Kir6.2/SUR1

  Proks P. et al, (2001), JOURNAL OF PHYSIOLOGY-LONDON, 533, 113P - 114P

• High-affinity block of K-ATP channels of mouse isolated pancreatic beta-cells but not rat heart or arterial smooth muscle cells by the sulphonylurea gliclazide

  Jones P. et al, (2001), JOURNAL OF PHYSIOLOGY-LONDON, 533, 116P - 116P

• Effects of mitiglinide (S 21403) on Kir6.2/SUR1, Kir6.2/SUR2A and Kir6.2/SUR2B types of ATP-sensitive potassium channel.

  Reimann F. et al, (2001), Br J Pharmacol, 132, 1542 - 1548

• Interaction of stilbene disulphonates with cloned K(ATP) channels.

  Proks P. et al, (2001), Br J Pharmacol, 132, 973 - 982

• Two types of gating in inward rectifiers: The case of the K-ATP channel.

  Proks P. et al, (2001), BIOPHYSICAL JOURNAL, 80, 512A - 512A

• Inhibition of cloned K-ATP channels by stilbene disulphonates

  Proks P. et al, (2000), JOURNAL OF PHYSIOLOGY-LONDON, 527, 114P - 114P

• Direct photoaffinity labeling of Kir6.2 by [gamma-(32)P]ATP-[gamma]4-azidoanilide.

  Tanabe K. et al, (2000), Biochem Biophys Res Commun, 272, 316 - 319

Recent Publications

• The value of in vitro studies in a case of neonatal diabetes with a novel Kir6.2-W68G mutation.

  O'Connell SM. et al, (2015), Clin Case Rep, 3, 884 - 887

• Molecular action of sulphonylureas on KATP channels: a real partnership between drugs and nucleotides.

  de Wet H. and Proks P., (2015), Biochem Soc Trans, 43, 901 - 907

• ATP-sensitive potassium channels in health and disease

  Proks P. and Clark R., (2015), Islets of Langerhans, Second Edition, 305 - 336

• Sulfonylureas suppress the stimulatory action of Mg-nucleotides on Kir6.2/SUR1 but not Kir6.2/SUR2A KATP channels: a mechanistic study.

  Proks P. et al, (2014), J Gen Physiol, 144, 469 - 486

• Reversible changes in pancreatic islet structure and function produced by elevated blood glucose

  Brereton MF. et al, (2014), DIABETOLOGIA, 57, S93 - S93