- ►whiterose.ac.uk [PDF] AL Gloyn, ER Pearson, JF Antcliff, P Proks, … - The New England …, 2004 - nejm.highwire.org Results Six novel, heterozygous missense mutations were identified in 10 of the 29 patients.
In two patients the diabetes was familial, and in eight it arose from a spontaneous mutation. Their
neonatal diabetes was characterized by ketoacidosis or marked hyperglycemia and was ... Cited by 353 - Related articles - BL Direct - All 13 versions
- ►diabetesjournals.org JC Florez, N Burtt, PIW de Bakker, P Almgren, T Tuomi, … - Diabetes, 2004 - Am Diabetes Assoc The genes for the sulfonylurea receptor (SUR1; encoded by ABCC8) and its associated islet
ATP-sensitive potassium channel (Kir6.2; encoded by KCNJ11) are adjacent to one another
on human chromosome 11. Multiple studies have reported association of the E23K ... Cited by 148 - Related articles - BL Direct - All 7 versions
- ►nih.gov FM Ashcroft - Journal of Clinical Investigation, 2005 - Am Soc Clin Investig ATP-sensitive potassium (K ATP ) channels, so named because they are inhibited by intracellular
ATP , play key physiological roles in many tissues. In pancreatic β cells, these channels regulate
glucose-dependent insulin secretion and serve as the target for sulfonylurea drugs used ... Cited by 142 - Related articles - BL Direct - All 14 versions
AT Hattersley, FM Ashcroft - Diabetes, 2005 - Am Diabetes Assoc Closure of ATP-sensitive K + channels (K ATP channels) in response to metabolically generated
ATP or binding of sulfonylurea drugs stimulates insulin release from pancreatic β-cells. Heterozygous
gain-of-function mutations in the KCJN11 gene encoding the Kir6.2 subunit of this ... Cited by 138 - Related articles - BL Direct - All 10 versions
- ►nih.gov P Proks, JF Antcliff, J Lippiat, AL Gloyn, … - Proceedings of the …, 2004 - National Acad Sciences Inwardly rectifying potassium channels (Kir channels) control cell membrane K + fluxes and electrical
signaling in diverse cell types. Heterozygous mutations in the human Kir6.2 gene (KCNJ11),
the pore-forming subunit of the ATP-sensitive (K ATP ) channel, cause permanent ... Cited by 115 - Related articles - All 11 versions
- ►oxfordjournals.org AL Gloyn, F Reimann, C Girard, EL Edghill, P … - Human molecular …, 2005 - Oxford Univ Press Neonatal diabetes can either remit and hence be transient or else may be permanent. These
two phenotypes were considered to be genetically distinct. Abnormalities of 6q24 are the commonest
cause of transient neonatal diabetes (TNDM). Mutations in KCNJ11, which encodes ... Cited by 89 - Related articles - All 7 versions
- ►diabetesjournals.org A Tarasov, J Dusonchet, F Ashcroft - Diabetes, 2004 - Am Diabetes Assoc Closure of ATP-sensitive K + channels (K ATP channels) is a key step in glucose-stimulated
insulin secretion. The precise mechanism(s) by which glucose metabolism regulates K ATP channel
activity, however, remains controversial. It is widely believed that the principal ... Cited by 48 - Related articles - BL Direct - All 4 versions
- ►diabetesjournals.org JC Koster, MA Permutt, CG Nichols - Diabetes, 2005 - Am Diabetes Assoc The ATP-sensitive K + channel (K ATP channel) senses metabolic changes in the pancreatic
β-cell, thereby coupling metabolism to electrical activity and ultimately to insulin secretion. When
K ATP channels open, β-cells hyperpolarize and insulin secretion is suppressed. The ... Cited by 43 - Related articles - BL Direct - All 5 versions
J Bryan, WH Vila-Carriles, G Zhao, AP Babenko, L … - Diabetes, 2004 - Am Diabetes Assoc Advances in understanding the overall structural features of inward rectifiers and ATP-binding
cassette (ABC) transporters are providing novel insight into the architecture of ATP-sensitive
K + channels (K ATP channels) (K IR 6.0/SUR) 4 . The structure of the K IR pore has been ... Cited by 44 - Related articles - BL Direct - All 4 versions
- ►jbc.org YW Lin, C MacMullen, A Ganguly, CA Stanley, SL … - Journal of Biological …, 2006 - ASBMB The -cell ATP-sensitive potassium (K ATP ) channel controls insulin secretion by linking glucose
metabolism to membrane excitability. Loss of K ATP channel function due to mutations in ABCC8
or KCNJ11, genes that encode the sulfonylurea receptor 1 or the inward rectifier Kir6.2 ... Cited by 34 - Related articles - BL Direct - All 6 versions
