Associated Papers
Mechanistic Insights into the Function of 14-3-3 Proteins as Negative Regulators of Brassinosteroid Signaling in Arabidopsis.
Obergfell E et al.
Plant & Cell Physiology, 2024
Non-surgical Treatment May be Appropriate for Most Chinese Children With Monogenic Congenital Hyperinsulinism Based on a Retrospective Study of 121 Patients.
Cheng M et al.
Pediatric Diabetes, 2024
40302972 (PubMed )
Supplement: 3961900.f1.docx
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
Statistical evidence for high-penetrance MODY-causing genes in a large population-based cohort.
Billings LK et al.
Endocrinology, Diabetes & Metabolism, 2022
36208030 (PubMed )
Supplement: EDM2-5-e372-s001.xlsx › eTable_1
A novel mutation KCNJ11 R136C caused KCNJ11-MODY.
Chen Y et al.
Diabetology & Metabolic Syndrome, 2021
GLP-1 receptor antagonist exendin-(9-39) elevates fasting blood glucose levels in congenital hyperinsulinism owing to inactivating mutations in the ATP-sensitive K+ channel.
Calabria AC et al.
Diabetes, 2012
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
Molecular and immunohistochemical analyses of the focal form of congenital hyperinsulinism.
Suchi M et al.
Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 2006
Genotype-phenotype correlations in children with congenital hyperinsulinism due to recessive mutations of the adenosine triphosphate-sensitive potassium channel genes.
Henwood MJ et al.
The Journal of Clinical Endocrinology and Metabolism, 2005
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