Associated Papers
Phenotypic features, prevalence of KCNJ11-MODY in Chinese patients with early-onset diabetes and a literature review.
Ba T et al.
Clinical Endocrinology, 2024
Epilepsy genetics in the paediatric population of the Eastern Anatolia region of Turkey.
Yarali O et al.
Journal of Neurogenetics, 2024
MODY in China: two families carrying the KCNJ11 E229K variant.
Xiao B et al.
Acta Diabetologica, 2023
Determinants of trafficking, conduction, and disease within a K+ channel revealed through multiparametric deep mutational scanning.
Coyote-Maestas W et al.
Elife, 2022
35639599 (PubMed )
Supplement: elife-76903-data1.zip › SourceData › input_data › KCNJ_Clinvar_0325322_edited_annotations_.xlsx › clinvar_KCNJx_0325322
A novel mutation KCNJ11 R136C caused KCNJ11-MODY.
Chen Y et al.
Diabetology & Metabolic Syndrome, 2021
New insights into KATP channel gene mutations and neonatal diabetes mellitus.
Pipatpolkai T et al.
Nature Reviews. Endocrinology, 2020
KCNJ11, ABCC8 and TCF7L2 polymorphisms and the response to sulfonylurea treatment in patients with type 2 diabetes: a bioinformatics assessment.
Song J et al.
Bmc Medical Genetics, 2017
Mutations in KCNJ11 are associated with the development of autosomal dominant, early-onset type 2 diabetes.
Liu L et al.
Diabetologia, 2013
Glucokinase (GCK) mutations in hyper- and hypoglycemia: maturity-onset diabetes of the young, permanent neonatal diabetes, and hyperinsulinemia of infancy.
Gloyn AL
Human Mutation, 2003
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