PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20554857-10 2010 Orexin neurons show an indirect concentration-dependent sensitivity to glucose below 1 mm, responding by hyperpolarization, which is mediated by ATP-sensitive potassium channels composed of Kir6.1 and SUR1 subunits. Glucose 71-78 ATP binding cassette subfamily C member 8 Homo sapiens 201-205 19498446-1 2009 The genes (ABCC8 and KCNJ11) have a key role in glucose-stimulated insulin secretion and thus have always been considered as excellent susceptibility candidates for involvement in type 2 diabetes. Glucose 48-55 ATP binding cassette subfamily C member 8 Homo sapiens 11-16 19766903-5 2009 The aim of this study was to determine a relationship between SUR-1 [exon 16 (-3C/T), exon 31 (Arg1273Arg; AGG-->AGA) and exon 33 (S1369A)] and KCNJ11 (E23K) polymorphisms and the following parameters of metabolic control in T2D: fasting plasma glucose (FPG), postprandial glucose (PPG) and HbA1c in Caucasian T2D of European origin. Glucose 248-255 ATP binding cassette subfamily C member 8 Homo sapiens 62-67 19766903-5 2009 The aim of this study was to determine a relationship between SUR-1 [exon 16 (-3C/T), exon 31 (Arg1273Arg; AGG-->AGA) and exon 33 (S1369A)] and KCNJ11 (E23K) polymorphisms and the following parameters of metabolic control in T2D: fasting plasma glucose (FPG), postprandial glucose (PPG) and HbA1c in Caucasian T2D of European origin. Glucose 276-283 ATP binding cassette subfamily C member 8 Homo sapiens 62-67 19151370-1 2009 The beta-cell ATP-sensitive potassium (K(ATP)) channel composed of sulfonylurea receptor SUR1 and potassium channel Kir6.2 serves a key role in insulin secretion regulation by linking glucose metabolism to cell excitability. Glucose 184-191 ATP binding cassette subfamily C member 8 Homo sapiens 89-93 18758683-4 2009 Diabetic carriers of the ABCC8 G/G variant had reduced 2 h glucose compared to A/A+A/G (P=0.031). Glucose 59-66 ATP binding cassette subfamily C member 8 Homo sapiens 25-30 18796522-10 2008 CONCLUSIONS: We conclude that variation marked by the Kir6.2 E23K and SUR1 A1369S mutations is associated with alterations in glucose-stimulated insulin secretion but not with other measures of glucose homeostasis in an African-American population. Glucose 126-133 ATP binding cassette subfamily C member 8 Homo sapiens 70-74 18346985-0 2008 A rare mutation in ABCC8/SUR1 leading to altered ATP-sensitive K+ channel activity and beta-cell glucose sensing is associated with type 2 diabetes in adults. Glucose 97-104 ATP binding cassette subfamily C member 8 Homo sapiens 19-24 18635551-4 2008 Similar to the human condition, the SUR-1(-/-) mouse is hypoglycemic when fasted and hyperglycemic when glucose-loaded. Glucose 104-111 ATP binding cassette subfamily C member 8 Homo sapiens 36-41 18511848-1 2008 OBJECTIVE: A selective rise in hypothalamic lipid metabolism and the subsequent activation of SUR1/Kir6.2 ATP-sensitive K(+) (K(ATP)) channels inhibit hepatic glucose production. Glucose 159-166 ATP binding cassette subfamily C member 8 Homo sapiens 94-98 18346985-0 2008 A rare mutation in ABCC8/SUR1 leading to altered ATP-sensitive K+ channel activity and beta-cell glucose sensing is associated with type 2 diabetes in adults. Glucose 97-104 ATP binding cassette subfamily C member 8 Homo sapiens 25-29 18346985-10 2008 Overexpression of SUR1-Y356C in INS1(832/13) cells impaired glucose-induced cell depolarization and increased in intracellular free Ca(2+) concentration, albeit more weakly than neonatal diabetes-associated SUR1 mutants. Glucose 60-67 ATP binding cassette subfamily C member 8 Homo sapiens 18-22 18346985-11 2008 CONCLUSIONS: An ABCC8/SUR1 mutation with relatively minor effects on K(ATP) channel activity and beta-cell glucose sensing causes diabetes in adulthood. Glucose 107-114 ATP binding cassette subfamily C member 8 Homo sapiens 16-21 18346985-11 2008 CONCLUSIONS: An ABCC8/SUR1 mutation with relatively minor effects on K(ATP) channel activity and beta-cell glucose sensing causes diabetes in adulthood. Glucose 107-114 ATP binding cassette subfamily C member 8 Homo sapiens 22-26 16475928-2 2006 In pancreatic beta cells the K(ATP) channels, which are formed by 4 ion channels (Kir6.2) and 4 regulatory sulfonylurea receptors (SUR1), control the glucose stimulated release of insulin. Glucose 150-157 ATP binding cassette subfamily C member 8 Homo sapiens 131-135 18416191-3 2008 Sulfonylurea drugs lowering a level of glucose in blood which use for treatment of a 2 type diabetes,--influence, contacting SUR 1 subunit and oppressing thus a K(ATP) current. Glucose 39-46 ATP binding cassette subfamily C member 8 Homo sapiens 125-130 17956278-1 2007 K(ATP) channels (ATP-sensitive potassium channels), comprising four subunits each of Kir6.2 (inwardly rectifying potassium channel 6.2) and the SUR1 (sulfonylurea receptor 1), play a central role in glucose-stimulated insulin secretion by the pancreatic beta-cell. Glucose 199-206 ATP binding cassette subfamily C member 8 Homo sapiens 144-148 17956278-1 2007 K(ATP) channels (ATP-sensitive potassium channels), comprising four subunits each of Kir6.2 (inwardly rectifying potassium channel 6.2) and the SUR1 (sulfonylurea receptor 1), play a central role in glucose-stimulated insulin secretion by the pancreatic beta-cell. Glucose 199-206 ATP binding cassette subfamily C member 8 Homo sapiens 150-173 16475928-9 2006 NN414 has been shown to be a potent and Kir6.2/SUR1 selective K(ATP) channels opener, which inhibits glucose stimulated insulin release in vitro and in vivo and which has beneficial effects on glucose homeostasis in preclinical and clinical studies. Glucose 101-108 ATP binding cassette subfamily C member 8 Homo sapiens 47-51 15842514-0 2005 Common variants in the ATP-sensitive K+ channel genes KCNJ11 (Kir6.2) and ABCC8 (SUR1) in relation to glucose intolerance: population-based studies and meta-analyses. Glucose 102-109 ATP binding cassette subfamily C member 8 Homo sapiens 74-79 15842514-0 2005 Common variants in the ATP-sensitive K+ channel genes KCNJ11 (Kir6.2) and ABCC8 (SUR1) in relation to glucose intolerance: population-based studies and meta-analyses. Glucose 102-109 ATP binding cassette subfamily C member 8 Homo sapiens 81-85 15842514-8 2005 For the ABCC8 exon 18 and the KCNJ11 variant, associations were stronger for studies of clinical diabetes than newly detected glucose intolerance. Glucose 126-133 ATP binding cassette subfamily C member 8 Homo sapiens 8-13 15220194-0 2004 Glucose- and interleukin-1beta-induced beta-cell apoptosis requires Ca2+ influx and extracellular signal-regulated kinase (ERK) 1/2 activation and is prevented by a sulfonylurea receptor 1/inwardly rectifying K+ channel 6.2 (SUR/Kir6.2) selective potassium channel opener in human islets. Glucose 0-7 ATP binding cassette subfamily C member 8 Homo sapiens 225-228 15501029-1 2004 2-(4-Methoxyphenoxy)-5-nitro-N-(4-sulfamoylphenyl)benzamide and close analogues inhibit glucose stimulated insulin release through activation of Kir6.2/SUR1 K(ATP) channels of beta cells. Glucose 88-95 ATP binding cassette subfamily C member 8 Homo sapiens 152-156 12606519-1 2003 With ATP sites on K(ir)6.2 that inhibit activity and ADP sites on SUR1 that antagonize the inhibition, ATP-sensitive potassium channels (K(ATP) channels) are designed as exquisite sensors of adenine nucleotide levels that signal changes in glucose metabolism. Glucose 240-247 ATP binding cassette subfamily C member 8 Homo sapiens 66-70 14764798-0 2004 Induction of beta-cell rest by a Kir6.2/SUR1-selective K(ATP)-channel opener preserves beta-cell insulin stores and insulin secretion in human islets cultured at high (11 mM) glucose. Glucose 175-182 ATP binding cassette subfamily C member 8 Homo sapiens 40-44 11697420-12 2001 CONCLUSION: Transient, possibly focal, HI with paternal SUR1 mutation was associated with a gradual, but complete normalization of the in vivo beta-cell function; in the diffuse type HI, a blunted beta-cell response to glucose and glucagon stimulation persisted. Glucose 219-226 ATP binding cassette subfamily C member 8 Homo sapiens 56-60 12559865-5 2003 FINDINGS: Four people who were heterozygous for the SUR1 E1506K mutation had diabetes, five had impaired glucose tolerance, one had impaired fasting glucose, and one had normal glucose tolerance. Glucose 149-156 ATP binding cassette subfamily C member 8 Homo sapiens 52-56 12879777-4 2003 SUR1 also enhances a physiological secretion of insulin induced by an increase of glucose concentration. Glucose 82-89 ATP binding cassette subfamily C member 8 Homo sapiens 0-4 11272143-2 2001 We hypothesized that SUR1 mutations would render the beta-cell insensitive to sulfonylureas and to glucose. Glucose 99-106 ATP binding cassette subfamily C member 8 Homo sapiens 21-25 11343328-1 2001 The high affinity sulfonylurea receptor 1 (SUR1) is involved in the metabolism of glucose in pancreatic beta-cells. Glucose 82-89 ATP binding cassette subfamily C member 8 Homo sapiens 18-41 11343328-1 2001 The high affinity sulfonylurea receptor 1 (SUR1) is involved in the metabolism of glucose in pancreatic beta-cells. Glucose 82-89 ATP binding cassette subfamily C member 8 Homo sapiens 43-47 11289470-12 2001 However, combined genotypes of ABCC8 exon 16 and 18 variants again significantly predicted both indexes of glucose and tolbutamide-stimulated insulin secretion. Glucose 107-114 ATP binding cassette subfamily C member 8 Homo sapiens 31-36 11246895-0 2001 Decreased fasting and oral glucose stimulated C-peptide in nondiabetic subjects with sequence variants in the sulfonylurea receptor 1 gene. Glucose 27-34 ATP binding cassette subfamily C member 8 Homo sapiens 110-133 11272143-8 2001 The greater response to glucose than to tolbutamide indicates that ATP-sensitive potassium (KATP) channel-independent pathways are involved in glucose-mediated insulin release in patients with diffuse SUR1 defects. Glucose 24-31 ATP binding cassette subfamily C member 8 Homo sapiens 201-205 11272143-9 2001 The diminished glucose responsiveness suggests that SUR1 mutations and lack of KATP channel activity may contribute to the late development of diabetes in patients with hyperinsulinism independently of subtotal pancreatectomy. Glucose 15-22 ATP binding cassette subfamily C member 8 Homo sapiens 52-56 10866047-4 2000 Here, we report that the NES2Y beta-cells that are transfected with the genes encoding the components of KATP channels in beta-cells, sulfonylurea receptor (SUR) 1 and Kir6.2, have operational KATP channels and show normal intracellular Ca2+ and secretory responses to glucose. Glucose 269-276 ATP binding cassette subfamily C member 8 Homo sapiens 134-163 10748090-11 2000 Glucose effects on the IAPP promoter were observed only in the presence of PDX1 when normal calcium signaling was restored by overexpression of the two K(ATP) channel subunits SUR1 and Kir6.2. Glucose 0-7 ATP binding cassette subfamily C member 8 Homo sapiens 176-180 10570926-1 1999 Pancreatic beta-cell ATP-sensitive potassium channels, composed of SUR1 and Kir6.2 subunits, serve as a sensor for intracellular nucleotides and regulate glucose-induced insulin secretion. Glucose 154-161 ATP binding cassette subfamily C member 8 Homo sapiens 67-71 9075812-1 1997 The sulfonylurea receptor (SUR) is a key component in glucose-stimulated insulin secretion. Glucose 54-61 ATP binding cassette subfamily C member 8 Homo sapiens 4-25 9075812-1 1997 The sulfonylurea receptor (SUR) is a key component in glucose-stimulated insulin secretion. Glucose 54-61 ATP binding cassette subfamily C member 8 Homo sapiens 27-30 30637228-1 2018 Sulfonylurea (SUR) agents are the second and most used oral hypoglycemic drugs after metformin and they still as an imperative tool for most favorable of glucose control. Glucose 154-161 ATP binding cassette subfamily C member 8 Homo sapiens 14-17 33341896-11 2021 This study supports the hypothesis that an effective paracrine interaction exists between IMEC and beta cells and modulates glucose-induced insulin secretion via TPI- sulfonylurea receptor- KATP channel (SUR1-Kir6.2) complex attenuating interactions. Glucose 124-131 ATP binding cassette subfamily C member 8 Homo sapiens 204-208 8635661-3 1996 The two nucleotide-binding fold (NBF) regions of SUR are known to be critical for normal glucose regulation of insulin secretion. Glucose 89-96 ATP binding cassette subfamily C member 8 Homo sapiens 49-52 34099169-4 2021 In pancreatic beta-cells, channels comprising SUR1 and Kir6.2 mediate glucose-stimulated insulin secretion and are the targets of antidiabetic sulfonylureas. Glucose 70-77 ATP binding cassette subfamily C member 8 Homo sapiens 46-50 31821855-3 2020 In pancreatic beta-cells, KATP channels composed of Kir6.2 and SUR1, encoded by KCNJ11 and ABCC8, respectively, play a key role in coupling blood glucose concentration to insulin secretion. Glucose 146-153 ATP binding cassette subfamily C member 8 Homo sapiens 63-67 31821855-3 2020 In pancreatic beta-cells, KATP channels composed of Kir6.2 and SUR1, encoded by KCNJ11 and ABCC8, respectively, play a key role in coupling blood glucose concentration to insulin secretion. Glucose 146-153 ATP binding cassette subfamily C member 8 Homo sapiens 91-96 29546446-8 2018 Genotype of ABCC8 T-3C was associated with fasting serum glucose in both NODAT and non-NODAT patients (p < 0.05). Glucose 57-64 ATP binding cassette subfamily C member 8 Homo sapiens 12-17 26504125-4 2015 We report here the case of an 8-year-old boy affected by a severe form of CHI due to a biallelic heterozygous ABCC8 mutation who responded to sirolimus with a dramatic improvement in his glucose blood level regulation and quality of life, with no serious adverse events after 6 months of follow-up. Glucose 187-194 ATP binding cassette subfamily C member 8 Homo sapiens 110-115 27188453-12 2016 Notably, patients with ABCC8 mutations were diagnosed earlier, with lower blood glucose levels and required higher doses of diazoxide than those without a genetic diagnosis. Glucose 80-87 ATP binding cassette subfamily C member 8 Homo sapiens 23-28 28346775-6 2017 In contrast, SUR1 mutations that disrupt trafficking and/or decrease gating of KATP channels cause congenital hyperinsulinism, where oversecretion of insulin occurs even in the presence of low glucose levels. Glucose 193-200 ATP binding cassette subfamily C member 8 Homo sapiens 13-17 23736775-6 2013 Differentiated CD34(+) cells also expressed glucokinase, glucagon-like peptide 1 receptor (GLP1R), sulfonylurea receptor-1 (SUR1) and phogrin-all essential for glucose sensitivity and insulin secretion. Glucose 160-167 ATP binding cassette subfamily C member 8 Homo sapiens 124-128 22311976-1 2012 ATP-sensitive potassium (K(ATP)) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2 regulate insulin secretion by linking glucose metabolism with membrane potential. Glucose 134-141 ATP binding cassette subfamily C member 8 Homo sapiens 54-77 22381691-10 2012 Expression of MRP8/14 was also elevated in EC exposed to high glucose conditions. Glucose 62-69 ATP binding cassette subfamily C member 8 Homo sapiens 14-21 22381691-11 2012 EC function was impaired by high glucose concentrations, and this effect could be mimicked by MRP8 over-expression. Glucose 33-40 ATP binding cassette subfamily C member 8 Homo sapiens 94-98 22381691-12 2012 MRP8 knockdown by shRNA significantly restored EC function after exposure to high glucose concentrations. Glucose 82-89 ATP binding cassette subfamily C member 8 Homo sapiens 0-4 22381691-13 2012 MRP8 expression in glucose exposed cells was also inhibited using pharmacological blockade of glucose-induced pathways. Glucose 19-26 ATP binding cassette subfamily C member 8 Homo sapiens 0-4 22381691-13 2012 MRP8 expression in glucose exposed cells was also inhibited using pharmacological blockade of glucose-induced pathways. Glucose 94-101 ATP binding cassette subfamily C member 8 Homo sapiens 0-4 22381691-14 2012 CONCLUSIONS: EC dysfunction caused by elevated glucose levels could be mimicked by MRP8/14 over-expression and reversed/prevented by MRP8 knockdown. Glucose 47-54 ATP binding cassette subfamily C member 8 Homo sapiens 83-87 22381691-14 2012 CONCLUSIONS: EC dysfunction caused by elevated glucose levels could be mimicked by MRP8/14 over-expression and reversed/prevented by MRP8 knockdown. Glucose 47-54 ATP binding cassette subfamily C member 8 Homo sapiens 133-137 22311976-1 2012 ATP-sensitive potassium (K(ATP)) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2 regulate insulin secretion by linking glucose metabolism with membrane potential. Glucose 134-141 ATP binding cassette subfamily C member 8 Homo sapiens 79-83 22210575-6 2012 RESULTS: ABCC8 mutation carriers exhibited glucose intolerance, frank diabetes, or insulin-requiring diabetes since diagnosis. Glucose 43-50 ATP binding cassette subfamily C member 8 Homo sapiens 9-14 22083559-1 2012 The pancreatic K(ATP) channel, SUR1/Kir6.2, couples insulin secretion to the plasma glucose level. Glucose 84-91 ATP binding cassette subfamily C member 8 Homo sapiens 31-35 22927833-1 2012 AIM: The aim of this study is to investigate the relationship between the common C49620T polymorphism in the sulfonylurea receptor (SUR1) gene and glucose metabolism, beta-cell secretory function and insulin resistance in women with a history of gestational diabetes (GDM). Glucose 147-154 ATP binding cassette subfamily C member 8 Homo sapiens 132-136