Ontology highlight
ABSTRACT:
SUBMITTER: Camden M Driggers
PROVIDER: EMPIAR-13517 | biostudies-other |
REPOSITORIES: biostudies-other

eLife 20250326
Pancreatic K<sub>ATP</sub> channel trafficking defects underlie congenital hyperinsulinism (CHI) cases unresponsive to the K<sub>ATP</sub> channel opener diazoxide, the mainstay medical therapy for CHI. Current clinically used K<sub>ATP</sub> channel inhibitors have been shown to act as pharmacochaperones and restore surface expression of trafficking mutants; however, their therapeutic utility for K<sub>ATP</sub> trafficking-impaired CHI is hindered by high affinity binding, which limits functio ...[more]