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.
- 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. ..
- 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. ..
- 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. ..
- 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. ..
- 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
- 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. ..
- 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. ..
- 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. ..
- 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. ..