Open AccessNeonatal Diabetes Caused by Mutations in Sulfonylurea Receptor 1: Interplay between Expression and Mg-Nucleotide Gating Defects of ATP-Sensitive Potassium Channels
Author(s) -
Qing Zhou,
Intza Garin,
Luís Castaño,
Jesús Argente,
Ma. Teresa Muñoz-Calvo,
Guiomar Pérez de Nanclares,
ShowLing Shyng
Publication year - 2010
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2010-1231
Subject(s) - sulfonylurea receptor , gating , potassium channel , kir6.2 , mutation , inward rectifier potassium ion channel , biology , mutant , microbiology and biotechnology , endocrinology , medicine , protein subunit , chemistry , receptor , ion channel , biochemistry , diabetes mellitus , glibenclamide , biophysics , gene
ATP-sensitive potassium (KATP) channels regulate insulin secretion by coupling glucose metabolism to β-cell membrane potential. Gain-of-function mutations in the sulfonylurea receptor 1 (SUR1) or Kir6.2 channel subunit underlie neonatal diabetes.
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