ATP binding cassette subfamily C member 8
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The ABCC8 gene provides instructions for making one part (subunit) of the ATP-sensitive potassium (KATP) channels that are found in specialized pancreas cells called beta cells. These KATP channels consist of eight subunits: four of these subunits are produced from the ABCC8 gene and four are produced from another gene called KCNJ11.
Normal function
The ABCC8 gene provides instructions for making one part (subunit) of the ATP-sensitive potassium (KATP) channels that are found in specialized pancreas cells called beta cells. These KATP channels consist of eight subunits: four of these subunits are produced from the ABCC8 gene and four are produced from another gene called KCNJ11.
These KATP channels span the cell membranes of the beta cells. Beta cells secrete the hormone insulin, which helps control the levels of glucose in the blood, also called blood sugar. Glucose is a simple sugar and the primary energy source for most cells in the body. When blood glucose levels are high, the KATP channels close, which triggers the beta cells to release insulin into the bloodstream. In this way, KATP channels help regulate insulin secretion and control blood glucose levels.
Conditions referring to this gene or chromosome
Other names
ABC36
ATP-binding cassette, sub-family C (CFTR/MRP), member 8
ATP-binding cassette, sub-family C, member 8
MRP8
sulfonylurea receptor
sulfonylurea receptor, beta cell high affinity
SUR1
TNDM2
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Leitura adicional e referências
- ATP binding cassette subfamily C member 8; MedlinePlus, National Library of Medicine.
- Bennett K, James C, Hussain K. Pancreatic beta-cell KATP channels: Hypoglycaemia and hyperglycaemia. Rev Endocr Metab Disord. 2010 Sep;11(3):157-63. doi: 10.1007/s11154-010-9144-2.
- De Leon DD, Pinney SE. Permanent Neonatal Diabetes Mellitus. 2008 Feb 8 [updated 2025 Sep 25]. In: Adam MP, Bick S, Mirzaa GM, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from http://www.ncbi.nlm.nih.gov/books/NBK1447/
- Edghill EL, Flanagan SE, Ellard S. Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11. Rev Endocr Metab Disord. 2010 Sep;11(3):193-8. doi: 10.1007/s11154-010-9149-x.
- Ellard S, Flanagan SE, Girard CA, Patch AM, Harries LW, Parrish A, Edghill EL, Mackay DJ, Proks P, Shimomura K, Haberland H, Carson DJ, Shield JP, Hattersley AT, Ashcroft FM. Permanent neonatal diabetes caused by dominant, recessive, or compound heterozygous SUR1 mutations with opposite functional effects. Am J Hum Genet. 2007 Aug;81(2):375-82. doi: 10.1086/519174. Epub 2007 Jun 29.
- Flanagan SE, Clauin S, Bellanne-Chantelot C, de Lonlay P, Harries LW, Gloyn AL, Ellard S. Update of mutations in the genes encoding the pancreatic beta-cell K(ATP) channel subunits Kir6.2 (KCNJ11) and sulfonylurea receptor 1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mutat. 2009 Feb;30(2):170-80. doi: 10.1002/humu.20838.
- Flanagan SE, Patch AM, Mackay DJ, Edghill EL, Gloyn AL, Robinson D, Shield JP, Temple K, Ellard S, Hattersley AT. Mutations in ATP-sensitive K+ channel genes cause transient neonatal diabetes and permanent diabetes in childhood or adulthood. Diabetes. 2007 Jul;56(7):1930-7. doi: 10.2337/db07-0043. Epub 2007 Apr 19.
- Gloyn AL, Siddiqui J, Ellard S. Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mutat. 2006 Mar;27(3):220-31. doi: 10.1002/humu.20292.
- Huopio H, Shyng SL, Otonkoski T, Nichols CG. K(ATP) channels and insulin secretion disorders. Am J Physiol Endocrinol Metab. 2002 Aug;283(2):E207-16. doi: 10.1152/ajpendo.00047.2002.
- Magge SN, Shyng SL, MacMullen C, Steinkrauss L, Ganguly A, Katz LE, Stanley CA. Familial leucine-sensitive hypoglycemia of infancy due to a dominant mutation of the beta-cell sulfonylurea receptor. J Clin Endocrinol Metab. 2004 Sep;89(9):4450-6. doi: 10.1210/jc.2004-0441.
- Pinney SE, MacMullen C, Becker S, Lin YW, Hanna C, Thornton P, Ganguly A, Shyng SL, Stanley CA. Clinical characteristics and biochemical mechanisms of congenital hyperinsulinism associated with dominant KATP channel mutations. J Clin Invest. 2008 Aug;118(8):2877-86. doi: 10.1172/JCI35414.
- Sandal T, Laborie LB, Brusgaard K, Eide SA, Christesen HB, Sovik O, Njolstad PR, Molven A. The spectrum of ABCC8 mutations in Norwegian patients with congenital hyperinsulinism of infancy. Clin Genet. 2009 May;75(5):440-8. doi: 10.1111/j.1399-0004.2009.01152.x.
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