R Murphy, S Ellard, AT Hattersley - Nature Clinical Practice Endocrinology …, 2008 - nature.com Sian Ellard is Professor of Human Molecular Genetics, Peninsula Medical School, Exeter,
UK. Following research training at the University of Swansea (UK), she set up the Molecular
Genetics Laboratory in Exeter with Professor Andrew Hattersley in 1995. Her research is ... Cited by 31 - Related articles - BL Direct - All 6 versions
CAJ Girard, K Shimomura, P Proks, N Absalom, L … - Pflügers Archiv European …, 2006 - Springer Abstract ATP-sensitive potassium (K ATP ) channels, com- posed of pore-forming Kir6.2 and
regulatory sulphonylurea receptor (SUR) subunits, play an essential role in insulin secretion
from pancreatic beta cells. Binding of ATP to Kir6.2 inhibits, whereas interaction of Mg- ... Cited by 20 - Related articles - BL Direct - All 4 versions
- ►shouxi.net AI Tarasov, HJ Welters, S Senkel, GU Ryffel, AT … - Diabetes, 2006 - Am Diabetes Assoc ATP-sensitive K + channels (K ATP channels) couple ß-cell metabolism to electrical activity and
thereby play an essential role in the control of insulin secretion. Gain-of-function mutations in
Kir6.2 (KCNJ11), the pore-forming subunit of this channel, cause neonatal diabetes. We ... Cited by 17 - Related articles - BL Direct - All 5 versions
R Masia, JC Koster, S Tumini, F Chiarelli, C Colombo, … - Diabetes, 2007 - Am Diabetes Assoc Mutations in the pancreatic ATP-sensitive K + channel (K ATP channel) cause permanent neonatal
diabetes mellitus (PNDM) in humans. All of the K ATP channel mutations examined result in
decreased ATP inhibition, which in turn is predicted to suppress insulin secretion. Here ... Cited by 17 - Related articles - BL Direct - All 6 versions
- ►endojournals.org L Aguilar-Bryan, J Bryan - Endocrine Reviews, 2008 - Endocrine Soc An explosion of work over the last decade has produced insight into the multiple hereditary causes
of a nonimmunological form of diabetes diagnosed most frequently within the first 6 months of
life. These studies are providing increased understanding of genes involved in the entire ... Cited by 15 - Related articles - BL Direct - All 6 versions
- ►ox.ac.uk [PDF] S Haider, S Khalid, SJ Tucker, FM Ashcroft, MSP … - Biochemistry, 2007 - pubs.acs.org Inward rectifier potassium (Kir) channels regulate cell excitability and transport K + ions across
membranes. Homotetrameric models of three mammalian Kir channels (Kir1.1, Kir3.1, and
Kir6.2) have been generated, using the KirBac3.1 transmembrane and rat Kir3.1 ... Cited by 13 - Related articles - All 7 versions
- ►physiology.org FM Ashcroft - American Journal of Physiology- Endocrinology And …, 2007 - Am Physiological Soc This essay is based on a lecture given to the American Physiological Society in honor of Walter
B. Cannon, an advocate of homeostasis. It focuses on the role of the ATP-sensitive potassium
K + (K ATP ) channel in glucose homeostasis and, in particular, on its role in insulin ... Cited by 12 - Related articles - BL Direct - All 2 versions
- ►oxfordjournals.org P Proks, K Shimomura, TJ Craig, CAJ Girard, … - Human Molecular …, 2007 - Oxford Univ Press Activating mutations in the genes encoding the ATP-sensitive potassium (K ATP ) channel subunits
Kir6.2 and SUR1 are a common cause of neonatal diabetes. Here, we analyse the molecular
mechanism of action of the heterozygous mutation F132L, which lies in the first set of ... Cited by 13 - Related articles - BL Direct - All 4 versions
I Flechtner, P De Lonlay, M Polak - Diabetes and Metabolism, 2006 - Elsevier ATP-sensitive potassium channels (K ATP ) couple cell metabolism to electrical activity by regulating
potassium movement across the membrane. These channels are octameric complex with two
kind of subunits: four regulatory sulfonylurea receptor (SUR) embracing four poreforming ... Cited by 6 - Related articles - BL Direct - All 3 versions
- ►nih.gov P Tammaro, SE Flanagan, B Zadek, S Srinivasan, H … - Diabetologia, 2008 - Springer Abstract Aims/hypothesis Heterozygous activating mutations in the pancreatic ATP-sensitive
K+ channel cause permanent neonatal diabetes mellitus (PNDM). This results from a decrease
in the ability of ATP to close the channel, which thereby suppresses insulin secretion. ... Cited by 4 - Related articles - BL Direct - All 7 versions
