sulfonylurea receptors

Summary

Summary: ATP-BINDING CASSETTE PROTEINS that are highly conserved and widely expressed in nature. They form an integral part of the ATP-sensitive potassium channel complex which has two intracellular nucleotide folds that bind to sulfonylureas and their analogs.

Top Publications

  1. Emdin C, Klarin D, Natarajan P, Florez J, Kathiresan S, Khera A. Genetic Variation at the Sulfonylurea Receptor, Type 2 Diabetes, and Coronary Heart Disease. Diabetes. 2017;66:2310-2315 pubmed publisher
    ..98; 95% CI 0.96, 0.99; P = 5.9 × 10-4). These results suggest that, despite a known association with increased weight, long-term sulfonylurea therapy may reduce the risk of coronary heart disease. ..
  2. Li C, Ackermann A, Boodhansingh K, Bhatti T, Liu C, Schug J, et al. Functional and Metabolomic Consequences of KATP Channel Inactivation in Human Islets. Diabetes. 2017;66:1901-1913 pubmed publisher
    ..These findings demonstrate that the pathophysiology of KATPHI is complex, and they provide a framework for the identification of new potential therapeutic targets for this devastating condition. ..
  3. Katanić D, Vorgucin I, Hattersley A, Ellard S, Houghton J, Obreht D, et al. A successful transition to sulfonylurea treatment in male infant with neonatal diabetes caused by the novel abcc8 gene mutation and three years follow-up. Diabetes Res Clin Pract. 2017;129:59-61 pubmed publisher
    ..A case of two months aged male infant with life threatening diabetic ketoacidosis is presented with novel ABCC8 gene mutation (p.F577L), successful transition from insulin to sulfonylurea and follow-up of three years. ..
  4. Kane C, Shepherd R, Squires P, Johnson P, James R, Milla P, et al. Loss of functional KATP channels in pancreatic beta-cells causes persistent hyperinsulinemic hypoglycemia of infancy. Nat Med. 1996;2:1344-7 pubmed
    ..As a consequence, PHHI beta-cells are spontaneously electrically active with high basal cytosolic Ca2+ concentrations due to Ca2+ influx. Our findings define the pathogenesis of this disease as a novel K+ channel disorder. ..
  5. Grady B, Torstenson E, McLaren P, de Bakker P, Haas D, Robbins G, et al. Use of biological knowledge to inform the analysis of gene-gene interactions involved in modulating virologic failure with efavirenz-containing treatment regimens in ART-naïve ACTG clinical trials participants. Pac Symp Biocomput. 2011;:253-64 pubmed
  6. Lin Z, Huang H, Gu Y, Huang K, Hu Y, Ji Z, et al. Glibenclamide ameliorates cerebral edema and improves outcomes in a rat model of status epilepticus. Neuropharmacology. 2017;121:1-11 pubmed publisher
    ..The salutary effects of GBC were correlated to the alleviation of cerebral edema and reduction in neurological injury via down-regulation of SUR1-TRPM4 channel. ..
  7. Stancill J, Cartailler J, Clayton H, O Connor J, Dickerson M, Dadi P, et al. Chronic ?-Cell Depolarization Impairs ?-Cell Identity by Disrupting a Network of Ca2+-Regulated Genes. Diabetes. 2017;66:2175-2187 pubmed publisher
  8. Song J, Yang Y, Mauvais Jarvis F, Wang Y, Niu T. KCNJ11, ABCC8 and TCF7L2 polymorphisms and the response to sulfonylurea treatment in patients with type 2 diabetes: a bioinformatics assessment. BMC Med Genet. 2017;18:64 pubmed publisher
    ..Our study indicates that a personalized medicine approach by tailoring sulfonylurea therapy of T2D patients according to their genotypes of KCNJ11, ABCC8, and TCF7L2 could attain an optimal treatment efficacy. ..
  9. Jain V, Satapathy A, Yadav J, Sharma R, Radha V, Mohan V, et al. Clinical and Molecular Characterization of Children with Neonatal Diabetes Mellitus at a Tertiary Care Center in Northern India. Indian Pediatr. 2017;54:467-471 pubmed
    ..Neonatal diabetes mellitus is a heterogeneous disorder. Identification of genetic cause guides clinical management. ..
  10. Ibrahim M, Eissa I, Alesawy M, Metwaly A, Radwan M, ElSohly M. Design, synthesis, molecular modeling and anti-hyperglycemic evaluation of quinazolin-4(3H)-one derivatives as potential PPAR? and SUR agonists. Bioorg Med Chem. 2017;25:4723-4744 pubmed publisher
    ..Also, two QSAR models were generated to explore the structural requirements controlling the different biological activities of the synthesized compounds against PPAR? and SUR. ..

Detail Information

Publications10

  1. Emdin C, Klarin D, Natarajan P, Florez J, Kathiresan S, Khera A. Genetic Variation at the Sulfonylurea Receptor, Type 2 Diabetes, and Coronary Heart Disease. Diabetes. 2017;66:2310-2315 pubmed publisher
    ..98; 95% CI 0.96, 0.99; P = 5.9 × 10-4). These results suggest that, despite a known association with increased weight, long-term sulfonylurea therapy may reduce the risk of coronary heart disease. ..
  2. Li C, Ackermann A, Boodhansingh K, Bhatti T, Liu C, Schug J, et al. Functional and Metabolomic Consequences of KATP Channel Inactivation in Human Islets. Diabetes. 2017;66:1901-1913 pubmed publisher
    ..These findings demonstrate that the pathophysiology of KATPHI is complex, and they provide a framework for the identification of new potential therapeutic targets for this devastating condition. ..
  3. Katanić D, Vorgucin I, Hattersley A, Ellard S, Houghton J, Obreht D, et al. A successful transition to sulfonylurea treatment in male infant with neonatal diabetes caused by the novel abcc8 gene mutation and three years follow-up. Diabetes Res Clin Pract. 2017;129:59-61 pubmed publisher
    ..A case of two months aged male infant with life threatening diabetic ketoacidosis is presented with novel ABCC8 gene mutation (p.F577L), successful transition from insulin to sulfonylurea and follow-up of three years. ..
  4. Kane C, Shepherd R, Squires P, Johnson P, James R, Milla P, et al. Loss of functional KATP channels in pancreatic beta-cells causes persistent hyperinsulinemic hypoglycemia of infancy. Nat Med. 1996;2:1344-7 pubmed
    ..As a consequence, PHHI beta-cells are spontaneously electrically active with high basal cytosolic Ca2+ concentrations due to Ca2+ influx. Our findings define the pathogenesis of this disease as a novel K+ channel disorder. ..
  5. Grady B, Torstenson E, McLaren P, de Bakker P, Haas D, Robbins G, et al. Use of biological knowledge to inform the analysis of gene-gene interactions involved in modulating virologic failure with efavirenz-containing treatment regimens in ART-naïve ACTG clinical trials participants. Pac Symp Biocomput. 2011;:253-64 pubmed
  6. Lin Z, Huang H, Gu Y, Huang K, Hu Y, Ji Z, et al. Glibenclamide ameliorates cerebral edema and improves outcomes in a rat model of status epilepticus. Neuropharmacology. 2017;121:1-11 pubmed publisher
    ..The salutary effects of GBC were correlated to the alleviation of cerebral edema and reduction in neurological injury via down-regulation of SUR1-TRPM4 channel. ..
  7. Stancill J, Cartailler J, Clayton H, O Connor J, Dickerson M, Dadi P, et al. Chronic ?-Cell Depolarization Impairs ?-Cell Identity by Disrupting a Network of Ca2+-Regulated Genes. Diabetes. 2017;66:2175-2187 pubmed publisher
  8. Song J, Yang Y, Mauvais Jarvis F, Wang Y, Niu T. KCNJ11, ABCC8 and TCF7L2 polymorphisms and the response to sulfonylurea treatment in patients with type 2 diabetes: a bioinformatics assessment. BMC Med Genet. 2017;18:64 pubmed publisher
    ..Our study indicates that a personalized medicine approach by tailoring sulfonylurea therapy of T2D patients according to their genotypes of KCNJ11, ABCC8, and TCF7L2 could attain an optimal treatment efficacy. ..
  9. Jain V, Satapathy A, Yadav J, Sharma R, Radha V, Mohan V, et al. Clinical and Molecular Characterization of Children with Neonatal Diabetes Mellitus at a Tertiary Care Center in Northern India. Indian Pediatr. 2017;54:467-471 pubmed
    ..Neonatal diabetes mellitus is a heterogeneous disorder. Identification of genetic cause guides clinical management. ..
  10. Ibrahim M, Eissa I, Alesawy M, Metwaly A, Radwan M, ElSohly M. Design, synthesis, molecular modeling and anti-hyperglycemic evaluation of quinazolin-4(3H)-one derivatives as potential PPAR? and SUR agonists. Bioorg Med Chem. 2017;25:4723-4744 pubmed publisher
    ..Also, two QSAR models were generated to explore the structural requirements controlling the different biological activities of the synthesized compounds against PPAR? and SUR. ..