Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions.
ATP-sensitive K(+) (K(ATP)) channels, comprised of pore-forming Kir6.2 and regulatory SUR1 subunits, play a critical role in regulating insulin secretion. Binding of ATP to Kir6.2 inhibits, whereas interaction of MgATP with SUR1 activates, K(ATP) channels. We tested the functional effects of two Kir...
| Main Authors: | , , , , |
|---|---|
| Formato: | Journal article |
| Idioma: | English |
| Publicado em: |
2005
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