Associated Papers
Glucokinase (GCK) in diabetes: from molecular mechanisms to disease pathogenesis.
Abu Aqel Y et al.
Cellular & Molecular Biology Letters, 2024
Endophenotype effect sizes support variant pathogenicity in monogenic disease susceptibility genes.
Halford JL et al.
Nature Communications, 2022
36042188 (PubMed )
Supplement: 41467_2022_32009_MOESM4_ESM.xlsx › Supplementary_Data_2
Evidence-based tailoring of bioinformatics approaches to optimize methods that predict the effects of nonsynonymous amino acid substitutions in glucokinase.
Šimčíková D et al.
Scientific Reports, 2017
28842611 (PubMed )
Supplement: 41598_2017_9810_MOESM1_ESM.pdf
Evolution- and structure-based computational strategy reveals the impact of deleterious missense mutations on MODY 2 (maturity-onset diabetes of the young, type 2).
George DC et al.
Theranostics, 2014
The glucokinase mutation p.T206P is common among MODY patients of Jewish Ashkenazi descent.
Gozlan Y et al.
Pediatric Diabetes, 2012
Stress hyperglycemia: a sign of familial diabetes in children.
Oron T et al.
Pediatrics, 2011
GCK-MODY (MODY 2) Caused by a Novel p.Phe330Ser Mutation.
Bonfig W et al.
Isrn Pediatrics, 2011
Biochemical characterization of novel glucokinase mutations isolated from Spanish maturity-onset diabetes of the young (MODY2) patients.
Estalella I et al.
Journal of Human Genetics, 2008
Mutations in GCK and HNF-1alpha explain the majority of cases with clinical diagnosis of MODY in Spain.
Estalella I et al.
Clinical Endocrinology, 2007
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