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Gene Information
Gene symbol: ABCC8
Gene name: ATP-binding cassette, sub-family C (CFTR/MRP), member 8
HGNC ID: 59
Synonyms: HI, PHHI, SUR1, MRP8, ABC36, HHF1, TNDM2
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | GSTA1 | 1 hits |
| 2 | HNF1A | 1 hits |
| 3 | HNF1B | 1 hits |
| 4 | HNF4A | 1 hits |
| 5 | INS | 1 hits |
| 6 | INSR | 1 hits |
| 7 | ISL1 | 1 hits |
| 8 | KCNJ11 | 1 hits |
| 9 | NEUROD1 | 1 hits |
| 10 | NEUROG3 | 1 hits |
| 11 | NKX2-2 | 1 hits |
| 12 | NKX6-1 | 1 hits |
| 13 | PAX6 | 1 hits |
| 14 | PDX1 | 1 hits |
| 15 | POMC | 1 hits |
| 16 | RHOD | 1 hits |
| 17 | TCF7 | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 21814221 | Variants in USF1, ABCC8, ISL1 and KCNJ11 showed nominal association, while haplotypes in these genes were significantly associated. rs3812704 upstream of NEUROG3 significantly increased risk for type 2 diabetes in normal-weight/lean subjects (OR=1.68 (95%CI 1.25-2.24), P=4.9 × 10(-4)). |
| 2 | 11289470 | In this study, we tested the primary hypotheses that previously described variants in the pancreatic sulfonylurea receptor gene (SUR1 or ABCC8), glucokinase (GCK) gene, or hepatocyte nuclear factor 1alpha (TCF1 or HNF1alpha) gene contribute to the inherited deficiencies of insulin secretion and beta-cell compensation to insulin resistance, as well as the secondary hypotheses that these variants altered insulin sensitivity. |
| 3 | 11289470 | The exon 16 variant of the ABCC8 gene reduced beta-cell compensation to the decreased insulin sensitivity in the heterozygous state. |
| 4 | 15840308 | It suggests that the defect in SUR1 gene (cc and AA) may contribute to insulin hypersecretion, which might be the cause of increased body weight and decreased insulin sensitivity and genotype cc of SUR1 is connected with severe type of GDM. |
| 5 | 16873704 | We examined the association of variants in genes encoding several transcription factors (TCF1, TCF2, HNF4A, ISL1, IPF1, NEUROG3, PAX6, NKX2-2, NKX6-1, and NEUROD1) and genes encoding the ATP-sensitive K(+) channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) with type 2 diabetes in a Japanese cohort of 2,834 subjects. |
| 6 | 16885549 | The ATP-sensitive potassium (K(ATP)) channel, composed of the beta-cell proteins sulfonylurea receptor (SUR1) and inward-rectifying potassium channel subunit Kir6.2, is a key regulator of insulin release. |
| 7 | 17496234 | Dialysis of GST-syntaxin-1A into the cell cytoplasm reduced both potency and efficacy of extracellularly perfused NNC55-0462 in a HEK cell line stably expressing Kir6.2/SUR1 (BA8 cells) and in rat islet beta-cells. |
| 8 | 18776135 | These studies demonstrate in a variety of rodent models that systemic delivery of Kir6.2/SUR-1-selective KCOs enhance the glucose counterregulatory response to insulin-induced hypoglycemia. |
| 9 | 19933268 | The conformation of the interface between these two subunits can be monitored using a rhodamine 123 (Rho) protection assay because Rho blocks Kir6.2 with an efficiency that depends on the relative position of transmembrane domain (TMD) 0 of the associated SUR (Hosy, E., Dérand, R., Revilloud, J., and Vivaudou, M. (2007) J. |
| 10 | 19933998 | Surprisingly, POMC-specific InsR knock-in increased energy expenditure and locomotor activity, exacerbated insulin resistance and increased HGP, associated with decreased expression of the ATP-sensitive K(+) channel (K(ATP) channel) sulfonylurea receptor 1 subunit, and decreased inhibitory synaptic contacts on POMC neurons. |
| 11 | 21411514 | Congenital hyperinsulinism in infancy (CHI) is characterized by unregulated insulin secretion from pancreatic ?-cells; severe forms are associated with defects in ABCC8 and KCNJ11 genes encoding sulfonylurea receptor 1 (SUR1) and Kir6.2 subunits, which form ATP-sensitive K(+) (K(ATP)) channels in ?-cells. |
| 12 | 10931418 | The acute insulin response to intravenous calcium stimulation (CaAIR) was determined in 9 patients <20 years with diffuse hyperinsulinism caused by defective beta-cell sulfonylurea receptor (SUR1(-/-)), 3 patients with focal congenital hyperinsulinism (6 weeks to 18 months), a 10-year-old with insulinoma, 5 with hyperinsulinism/hyperammonemia syndrome caused by defective glutamate dehydrogenase (6 months to 28 years), 4 SUR1(+/-) heterozygotes with no symptoms, and 9 normal adults. |
| 13 | 15631623 | Molecular analyses have demonstrated that Foxa2 is an important regulator of the genes encoding Sur1, Kir6.2 and Schad (short chain L-3-hydroxyacyl-CoA dehydrogenase), mutation of which causes PHHI in humans. |