The first clinical case of a mutation at residue K185 of Kir6.2 (KCNJ11): a major ATP-binding residue.
BACKGROUND: Closure of the adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel plays a key role in insulin secretion from the pancreatic beta-cells. Many mutations in KCNJ11 and ABCC8, which respectively encode the pore-forming (Kir6.2) and regulatory (SUR1) subunits of the K(ATP) cha...
| المؤلفون الرئيسيون: | , , , , , |
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| التنسيق: | Journal article |
| اللغة: | English |
| منشور في: |
2010
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