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The molecular mechanisms and pharmacotherapy of ATP-sensitive potassium channel gene mutations underlying neonatal diabetes

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Figure

Figure 1 Glucose-stimulated insulin secretion in pancreatic β-cells. (Left) when plasma glucose is low, the decreased ratio of ATP/Mg-ADP will increase KATP channel opening
Figure 2  channel is a hetero-octameric complex composed of four pore Kir6.2 subunits and four ATPof MgATP within the SUR1 subunit nucleotide-binding domains (NBDs) leads to generation of stimulatory MgADP
Table 1 Mutations in KATP channel genes KCNJ11 and ABCC8 causing hyperinsulinism of infancy
Table 1 (Continued)
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