CG Nichols - Nature, 2006 - nature.com Even in the absence of ATP, the single-channel kinetics of K ATP are complex,
but certain key features are clearly discernible and can be modelled by assuming
a single 'fast' gate and ligand-operated 'slow' gates within each subunit ... Cited by 136 - Related articles - BL Direct - All 8 versions
- ►shouxi.net ER Pearson, I Flechtner, PR Njolstad, MT … - New England Journal of Medicine, 2006 - content.nejm.org Background Heterozygous activating mutations in KCNJ11, encoding the Kir6.2
subunit of the ATP-sensitive potassium (K ATP ) channel, cause 30 to 58 percent
of cases of diabetes diagnosed in patients under six months of age. ... Cited by 127 - Related articles - BL Direct - All 13 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 ... Cited by 43 - Related articles - BL Direct - All 5 versions
- ►shouxi.net AI Tarasov, HJ Welters, S Senkel, GU Ryffel, … - 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 ... Cited by 17 - Related articles - BL Direct - All 5 versions
- ►shouxi.net R Masia, JC Koster, S Tumini, F Chiarelli, C … - 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 ... Cited by 17 - Related articles - BL Direct - All 6 versions
G Tonini, C Bizzarri, R Bonfanti, M Vanelli, F … - Diabetologia, 2006 - Springer To the Editor, Activating missense mutations in the gene encoding potassium
inwardly rectifying channel, subfamily J, mem- ber 11 (KCNJ11) represent the
most common cause (40 to 64%, depending on populations) of permanent ... Cited by 16 - Related articles - BL Direct - All 3 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 ... Cited by 15 - Related articles - BL Direct - All 6 versions
MS Remedi, JV Rocheleau, A Tong, BL Patton … - Diabetologia, 2006 - Springer Abstract Aims/hypothesis ATP-sensitive K + (K ATP ) channels couple glucose
metabolism to insulin secretion in pancreatic beta cells. In humans,
loss-of-function mutations of beta cell K ATP subunits (SUR1, encoded by ... Cited by 13 - Related articles - BL Direct - All 4 versions
- ►shouxi.net CW Lin, YW Lin, FF Yan, J Casey, M Kochhar, … - Diabetes, 2006 - Am Diabetes Assoc Heterozygous missense mutations in the pore-forming subunit Kir6.2 of
ATP-sensitive K + channels (K ATP channels) have recently been shown to cause
permanent neonatal diabetes mellitus (PNDM). Functional studies ... Cited by 12 - Related articles - BL Direct - All 5 versions
- ►endojournals.org JC Koster, F Cadario, C Peruzzi, C Colombo, … - Journal of Clinical Endocrinology & Metabolism, 2008 - Endocrine Soc Context: Mutations in the Kir6.2 subunit (KCNJ11) of the ATP-sensitive potassium
channel (K ATP ) underlie neonatal diabetes mellitus. In severe cases, Kir6.2
mutations underlie developmental delay, epilepsy, and neonatal diabetes ... Cited by 12 - Related articles - BL Direct - All 5 versions
