Associated Papers
Sex-dependent additive effects of dorzagliatin and incretin on insulin secretion in a novel mouse model of GCK-MODY.
Salazar S et al.
Biorxiv : the Preprint Server for Biology, 2024
Glucokinase (GCK) in diabetes: from molecular mechanisms to disease pathogenesis.
Abu Aqel Y et al.
Cellular & Molecular Biology Letters, 2024
Quantitative profiling and diagnostic potential of one-carbon and central metabolism pools in MODY2 and T1DM.
Liu J et al.
Diabetology & Metabolic Syndrome, 2023
Localized increases in CEPT1 and ATGL elevate plasmalogen phosphatidylcholines in HDLs contributing to atheroprotective lipid profiles in hyperglycemic GCK-MODY.
Wang X et al.
Redox Biology, 2021
MODY2 in Asia: analysis of GCK mutations and clinical characteristics.
Zhou Y et al.
Endocrine Connections, 2020
How Heterogeneity in Glucokinase and Gap-Junction Coupling Determines the Islet [Ca2+] Response.
Dwulet JM et al.
Biophysical Journal, 2019
Identification and functional analysis of GCK gene mutations in 12 Chinese families with hyperglycemia.
Wang Z et al.
Journal of Diabetes Investigation, 2019
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
Lack of glibenclamide response in a case of permanent neonatal diabetes caused by incomplete inactivation of glucokinase.
Oriola J et al.
Jimd Reports, 2015
Phenotypic severity of homozygous GCK mutations causing neonatal or childhood-onset diabetes is primarily mediated through effects on protein stability.
Raimondo A et al.
Human Molecular Genetics, 2014
Analysis of transcription factors key for mouse pancreatic development establishes NKX2-2 and MNX1 mutations as causes of neonatal diabetes in man.
Flanagan SE et al.
Cell Metabolism, 2014
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
Variability in the age at diagnosis of diabetes in two unrelated patients with a homozygous glucokinase gene mutation.
Durmaz E et al.
Journal of Pediatric Endocrinology & Metabolism : Jpem, 2012
MODY type 2 in Greig cephalopolysyndactyly syndrome (GCPS) as part of a contiguous gene deletion syndrome.
Zung A et al.
American Journal of Medical Genetics. Part A, 2011
[Long-term follow-up of permanent neonatal diabetes in Tunisian infant].
Ben Hamouda H et al.
Annales D'endocrinologie, 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
Update on mutations in glucokinase (GCK), which cause maturity-onset diabetes of the young, permanent neonatal diabetes, and hyperinsulinemic hypoglycemia.
Osbak KK et al.
Human Mutation, 2009
RD Lawrence Lecture 2009. Old genes, new tricks: learning about blood glucose regulation from naturally occurring genetic variation in humans.
Gloyn AL
Diabetic Medicine : a Journal of the British Diabetic Association, 2009
Permanent neonatal diabetes mellitus caused by a novel homozygous (T168A) glucokinase (GCK) mutation: initial response to oral sulphonylurea therapy.
Turkkahraman D et al.
The Journal of Pediatrics, 2008
Permanent neonatal diabetes caused by a homozygous nonsense mutation in the glucokinase gene.
Rubio-Cabezas O et al.
Pediatric Diabetes, 2008
Glucokinase gene mutations: structural and genotype-phenotype analyses in MODY children from South Italy.
Tinto N et al.
Plos One, 2008