Associated Papers
CL-705G: a novel chemical Kir6.2-specific KATP channel opener.
Gando I et al.
Frontiers in Pharmacology, 2023
REVEL Is Better at Predicting Pathogenicity of Loss-of-Function than Gain-of-Function Variants.
Hopkins JJ et al.
Human Mutation, 2023
40225155 (PubMed )
Supplement: 8857940.f1.pdf
Engineered interaction between SUR1 and Kir6.2 that enhances ATP sensitivity in KATP channels.
Pratt EB et al.
The Journal of General Physiology, 2012
Adjacent mutations in the gating loop of Kir6.2 produce neonatal diabetes and hyperinsulinism.
Shimomura K et al.
Embo Molecular Medicine, 2009
The genetic basis of congenital hyperinsulinism.
James C et al.
Journal of Medical Genetics, 2009
Update of mutations in the genes encoding the pancreatic beta-cell K(ATP) channel subunits Kir6.2 (KCNJ11) and sulfonylurea receptor 1 (ABCC8) in diabetes mellitus and hyperinsulinism.
Flanagan SE et al.
Human Mutation, 2009
Clinical characteristics and biochemical mechanisms of congenital hyperinsulinism associated with dominant KATP channel mutations.
Pinney SE et al.
The Journal of Clinical Investigation, 2008
Destabilization of ATP-sensitive potassium channel activity by novel KCNJ11 mutations identified in congenital hyperinsulinism.
Lin YW et al.
The Journal of Biological Chemistry, 2008
Identification of the PIP2-binding site on Kir6.2 by molecular modelling and functional analysis.
Haider S et al.
The Embo Journal, 2007
A novel KCNJ11 mutation associated with congenital hyperinsulinism reduces the intrinsic open probability of beta-cell ATP-sensitive potassium channels.
Lin YW et al.
The Journal of Biological Chemistry, 2006
Exaggerated Mg2+ inhibition of Kir2.1 as a consequence of reduced PIP2 sensitivity in Andersen syndrome.
Ballester LY et al.
Channels (austin, Tex.), 0
Select a paper to view details