Associated Papers
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
Association of KCNJ11 (E23K) gene polymorphism with susceptibility to type 2 diabetes in Iranian patients.
Rastegari A et al.
Advanced Biomedical Research, 2015
Association of KCNJ11 with impaired glucose regulation in essential hypertension.
Wang Y et al.
Genetics and Molecular Research : Gmr, 2011
Origin of de novo KCNJ11 mutations and risk of neonatal diabetes for subsequent siblings.
Edghill EL et al.
The Journal of Clinical Endocrinology and Metabolism, 2007
Genotypes of the pancreatic beta-cell K-ATP channel and clinical phenotypes of Japanese patients with persistent hyperinsulinaemic hypoglycaemia of infancy.
Ohkubo K et al.
Clinical Endocrinology, 2005
Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes.
Gloyn AL et al.
The New England Journal of Medicine, 2004
KCNJ11 polymorphisms and sudden cardiac death in patients with acute myocardial infarction.
Jeron A et al.
Journal of Molecular and Cellular Cardiology, 2004
Diabetes and insulin secretion: whither KATP?
Nichols CG et al.
American Journal of Physiology. Endocrinology and Metabolism, 2002
Intragenic single nucleotide polymorphism haplotype analysis of SUR1 mutations in familial hyperinsulinism.
Glaser B et al.
Human Mutation, 1999
Missense mutations in the pancreatic islet beta cell inwardly rectifying K+ channel gene (KIR6.2/BIR): a meta-analysis suggests a role in the polygenic basis of Type II diabetes mellitus in Caucasians.
Hani EH et al.
Diabetologia, 1998
Sequence variants in the pancreatic islet beta-cell inwardly rectifying K+ channel Kir6.2 (Bir) gene: identification and lack of role in Caucasian patients with NIDDM.
Inoue H et al.
Diabetes, 1997
Sequence variations in the human Kir6.2 gene, a subunit of the beta-cell ATP-sensitive K-channel: no association with NIDDM in while Caucasian subjects or evidence of abnormal function when expressed in vitro.
Sakura H et al.
Diabetologia, 1996
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