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
Clinical and genetic characteristics of maturity-onset diabetes of the young type 13: A systematic review of the literature.
Chen Y et al.
Journal of Diabetes, 2024
Continuous spectrum of glucose dysmetabolism due to the KCNJ11 gene mutation-Case reports and review of the literature.
He B et al.
Journal of Diabetes, 2021
Neonatal diabetes due to potassium channel mutation: Response to sulfonylurea according to the genotype.
Garcin L et al.
Pediatric Diabetes, 2020
New insights into KATP channel gene mutations and neonatal diabetes mellitus.
Pipatpolkai T et al.
Nature Reviews. Endocrinology, 2020
Synergistic gene editing in human iPS cells via cell cycle and DNA repair modulation.
Maurissen TL et al.
Nature Communications, 2020
Molecular and clinical features of KATP -channel neonatal diabetes mellitus in Japan.
Hashimoto Y et al.
Pediatric Diabetes, 2017
KATP Channel Mutations and Neonatal Diabetes.
Shimomura K et al.
Internal Medicine (tokyo, Japan), 2017
Neonatal diabetes caused by a homozygous KCNJ11 mutation demonstrates that tiny changes in ATP sensitivity markedly affect diabetes risk.
Vedovato N et al.
Diabetologia, 2016
27118464 (PubMed )
Supplement: 125_2016_3964_MOESM1_ESM.pdf
Successful transfer to sulfonylureas in KCNJ11 neonatal diabetes is determined by the mutation and duration of diabetes.
Babiker T et al.
Diabetologia, 2016
The value of in vitro studies in a case of neonatal diabetes with a novel Kir6.2-W68G mutation.
O'Connell SM et al.
Clinical Case Reports, 2015
Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11.
Edghill EL et al.
Reviews in Endocrine & Metabolic Disorders, 2010
Interaction between mutations in the slide helix of Kir6.2 associated with neonatal diabetes and neurological symptoms.
Männikkö R et al.
Human Molecular Genetics, 2010
The molecular mechanisms and pharmacotherapy of ATP-sensitive potassium channel gene mutations underlying neonatal diabetes.
Lang V et al.
Pharmacogenomics and Personalized Medicine, 2010
Adjacent mutations in the gating loop of Kir6.2 produce neonatal diabetes and hyperinsulinism.
Shimomura K et al.
Embo Molecular Medicine, 2009
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