The Walter B. Cannon Physiology in Perspective Lecture, 2007. ATP-sensitive K+ channels and disease: from molecule to malady.

No abstract is available for this paper.

• Publication year

  2007

• Venue

  American Journal of Physiology. Endocrinology and Metabolism

• Publication date

  2007-07-24

• Fields of study

  Medicine, Chemistry

• Identifiers
  DOI 10.1152/AJPENDO.00348.2007PMID 17652156
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• The Wellcome Trust Case Control Consortium, U.K.

  2008cited by this paper
• Mutations in ATP-sensitive K+ channel genes cause transient neonatal diabetes and permanent diabetes in childhood or adulthood.

  2008cited by this paper
• Mutations in ATP-Sensitive K+ Channel Genes Cause Transient Neonatal Diabetes and Permanent Diabetes in Childhood or Adulthood

  2007cited by this paper
• An ATP-Binding Mutation (G334D) in KCNJ11 Is Associated With a Sulfonylurea-Insensitive Form of Developmental Delay, Epilepsy, and Neonatal Diabetes

  2007cited by this paper
• A genome-wide association study identifies novel risk loci for type 2 diabetes

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• A novel mutation causing DEND syndrome

  2007cited by this paper
• A Common Variant in the FTO Gene Is Associated with Body Mass Index and Predisposes to Childhood and Adult Obesity

  2007cited by this paper
• Permanent neonatal diabetes caused by dominant, recessive, or compound heterozygous SUR1 mutations with opposite functional effects.

  2007cited by this paper
• Replication of Genome-Wide Association Signals in UK Samples Reveals Risk Loci for Type 2 Diabetes

  2007cited by this paper
• Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes

  2006cited by this paper
• Activating mutations in the ABCC8 gene in neonatal diabetes mellitus.

  2006influential reference
• Expression of ATP-Insensitive K ATP Channels in Pancreatic -Cells Underlies a Spectrum of Diabetic

  2006cited by this paper
• Mutations in the genes encoding the pancreatic beta‐cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism

  2006cited by this paper
• KATP channels as molecular sensors of cellular metabolism

  2006cited by this paper
• A Kir6.2 Mutation Causing Neonatal Diabetes Impairs Electrical Activity and Insulin Secretion From INS-1 β-Cells

  2006cited by this paper
• A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes.

  2006cited by this paper
• Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations.

  2006cited by this paper
• Expression of ATP-Insensitive KATP Channels in Pancreatic β-Cells Underlies a Spectrum of Diabetic Phenotypes

  2006cited by this paper
• Functional Effects of Mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), Causing Neonatal Diabetes, and Response to Sulfonylurea Therapy

  2006cited by this paper
• Mutations at the Same Residue (R50) of Kir6.2 (KCNJ11) That Cause Neonatal Diabetes Produce Different Functional Effects

  2006cited by this paper
• 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

  2006cited by this paper
• Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels

  2006cited by this paper
• Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy.

  2005influential reference
• Focus on Kir6.2: a key component of the ATP-sensitive potassium channel.

  2005cited by this paper
• Glucoreceptor mechanisms and the control of insulin release and biosynthesis

  2005cited by this paper
• Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2–SUR1 interactions

  2005cited by this paper
• Differential nucleotide regulation of KATP channels by SUR1 and SUR2A.

  2005cited by this paper
• Sarcolemmal K(ATP) channels: what do we really know?

  2005cited by this paper
• Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP.

  2005cited by this paper
• Roles of KATP channels as metabolic sensors in acute metabolic changes.

  2005cited by this paper
• 3‐D structural and functional characterization of the purified KATP channel complex Kir6.2–SUR1

  2005cited by this paper
• Sarcolemmal KATP channels : what do we really know?

  2005cited by this paper
• ATP-sensitive potassium channelopathies: focus on insulin secretion.

  2005influential reference
• Cardiac KATP channels in health and disease.

  2005cited by this paper
• Functional analysis of a structural model of the ATP‐binding site of the KATP channel Kir6.2 subunit

  2005cited by this paper
• A gating mutation at the internal mouth of the Kir6.2 pore is associated with DEND syndrome

  2005cited by this paper
• Identification of a functionally important negatively charged residue within the second catalytic site of the SUR1 nucleotide-binding domains.

  2004cited by this paper
• Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features.

  2004cited by this paper
• 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.

  2004cited by this paper
• Hyperinsulinism in infancy: from basic science to clinical disease.

  2004cited by this paper
• Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes.

  2004influential reference
• Glibenclamide treatment in permanent neonatal diabetes mellitus due to an activating mutation in Kir6.2.

  2004cited by this paper
• Sulphonylurea action revisited: the post-cloning era

  2003cited by this paper
• Crystal structure of an inward rectifier potassium channel

  2003cited by this paper
• Crystal Structure of the Potassium Channel KirBac1.1 in the Closed State

  2003cited by this paper
• Large-scale association studies of variants in genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) confirm that the KCNJ11 E23K variant is associated with type 2 diabetes.

  2003cited by this paper
• Kir6.2 polymorphisms sensitize beta-cell ATP-sensitive potassium channels to activation by acyl CoAs: a possible cellular mechanism for increased susceptibility to type 2 diabetes?

  2003cited by this paper
• Glucokinase (GCK) mutations in hyper‐ and hypoglycemia: Maturity‐onset diabetes of the young, permanent neonatal diabetes, and hyperinsulinemia of infancy

  2003cited by this paper
• A new subtype of autosomal dominant diabetes attributable to a mutation in the gene for sulfonylurea receptor 1.

  2003cited by this paper
• K(IR)6.2 polymorphism predisposes to type 2 diabetes by inducing overactivity of pancreatic beta-cell ATP-sensitive K(+) channels.

  2002cited by this paper
• Structural basis of inward rectification: cytoplasmic pore of the G protein-gated inward rectifier GIRK1 at 1.8 A resolution.

  2002cited by this paper
• Hyperinsulinism induced by targeted suppression of beta cell KATP channels

  2002cited by this paper
• KIR6.2 Polymorphism Predisposes to Type 2 Diabetes by Inducing Overactivity of Pancreatic β-Cell ATP-Sensitive K+ Channels

  2002cited by this paper
• Molecular etiologies of mody and other early-onset forms of diabetes

  2002cited by this paper
• Signaling in channel/enzyme multimers: ATPase transitions in SUR module gate ATP-sensitive K+ conductance.

  2001cited by this paper
• Tolerance for ATP-Insensitive KATP Channels in Transgenic Mice

  2001cited by this paper
• C-Terminal Tails of Sulfonylurea Receptors Control ADP-Induced Activation and Diazoxide Modulation of ATP-Sensitive K+ Channels

  2000cited by this paper
• Targeted overactivity of beta cell K(ATP) channels induces profound neonatal diabetes.

  2000cited by this paper
• Different Binding Properties and Affinities for ATP and ADP among Sulfonylurea Receptor Subtypes, SUR1, SUR2A, and SUR2B*

  2000cited by this paper
• Sur1 Knockout Mice A MODEL FOR K ATP CHANNEL-INDEPENDENT REGULATION OF INSULIN SECRETION*

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• K(ATP) channels: linker between phospholipid metabolism and excitability.

  2000cited by this paper
• Sur1 Knockout Mice

  2000cited by this paper
• A new ER trafficking signal regulates the subunit stoichiometry of plasma membrane K(ATP) channels.

  1999cited by this paper
• Global Burden of Diabetes, 1995–2025: Prevalence, numerical estimates, and projections

  1998cited by this paper
• The Changes in Adenine Nucleotides Measured in Glucose-stimulated Rodent Islets Occur in β Cells but Not in α Cells and Are Also Observed in Human Islets*

  1998cited by this paper
• Defective insulin secretion and enhanced insulin action in KATP channel-deficient mice.

  1998cited by this paper
• MgATP activates the beta cell KATP channel by interaction with its SUR1 subunit.

  1998cited by this paper
• Membrane phospholipid control of nucleotide sensitivity of KATP channels.

  1998cited by this paper
• Mechanism of Cloned ATP-sensitive Potassium Channel Activation by Oleoyl-CoA*

  1998cited by this paper
• Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)

  1998cited by this paper
• Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group.

  1998cited by this paper
• Truncation of Kir6.2 produces ATP-sensitive K+ channels in the absence of the sulphonylurea receptor

  1997cited by this paper
• A Nonsense Mutation in the Inward Rectifier Potassium Channel Gene, Kir6.2, Is Associated With Familial Hyperinsulinism

  1997cited by this paper
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  1997cited by this paper
• The essential role of the Walker A motifs of SUR1 in K‐ATP channel activation by Mg‐ADP and diazoxide

  1997influential reference
• Overlapping distribution of KATP channel‐forming Kir6.2 subunit and the sulfonylurea receptor SUR1 in rodent brain

  1997cited by this paper
• Subunit stoichiometry of the pancreatic beta-cell ATP-sensitive K+ channel.

  1997cited by this paper
• Anionic Phospholipids Activate ATP-sensitive Potassium Channels*

  1997cited by this paper
• Subunit stoichiometry of the pancreatic β‐cell ATP‐sensitive K+ channel

  1997cited by this paper
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  1996cited by this paper
• Adenosine Diphosphate as an Intracellular Regulator of Insulin Secretion

  1996cited by this paper
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  1996cited by this paper
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  1995cited by this paper
• Cloning of the beta cell high-affinity sulfonylurea receptor: a regulator of insulin secretion.

  1995cited by this paper
• Reconstitution of IKATP: An Inward Rectifier Subunit Plus the Sulfonylurea Receptor

  1995influential reference
• 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.

  1995influential reference
• Mutations in the sulfonylurea receptor gene in familial persistent hyperinsulinemic hypoglycemia of infancy.

  1995cited by this paper
• The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.

  1993cited by this paper
• The fiftieth anniversary of hypoglycaemic sulphonamides. How did the mother compound work?

  1992cited by this paper
• ATP‐sensitive K+ channels in rat pancreatic beta‐cells: modulation by ATP and Mg2+ ions.

  1989cited by this paper
• Electrophysiology of the pancreatic beta-cell.

  1989cited by this paper
• Ca2+, cAMP, and phospholipid-derived messengers in coupling mechanisms of insulin secretion.

  1987cited by this paper
• Intracellular ADP activates K+ channels that are inhibited by ATP in an insulin‐secreting cell line

  1986cited by this paper
• Opposite effects of tolbutamide and diazoxide on the ATP-dependent K+ channel in mouse pancreatic β-cells

  1986cited by this paper
• The ATP‐sensitivity of K+ channels in rat pancreatic B‐cells is modulated by ADP

  1986cited by this paper
• Glucose dependent K+-channels in pancreaticβ-cells are regulated by intracellular ATP

  1985cited by this paper
• Significance of ionic fluxes and changes in membrane potential for stimulus-secretion coupling in pancreatic B-cells

  1984cited by this paper
• Glucose induces closure of single potassium channels in isolated rat pancreatic β-cells

  1984cited by this paper
• Intracellular ATP directly blocks K+ channels in pancreatic B-cells

  1984cited by this paper
• ATP-regulated K+ channels in cardiac muscle

  1983cited by this paper

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