Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy.

Closure of ATP-sensitive K(+) channels (K(ATP) channels) in response to metabolically generated ATP or binding of sulfonylurea drugs stimulates insulin release from pancreatic beta-cells. Heterozygous gain-of-function mutations in the KCJN11 gene encoding the Kir6.2 subunit of this channel are found...

Cur síos iomlán

Sonraí bibleagrafaíochta
Príomhchruthaitheoirí: Hattersley, A, Ashcroft, F
Formáid: Journal article
Teanga:English
Foilsithe / Cruthaithe: 2005