Associated Papers
Focusing on Rare Variants Related to Maturity-Onset Diabetes of the Young in Children.
Ding Y et al.
Pediatric Diabetes, 2025
GCK Mutation Analysis and Clinical Profiles of Chinese Pediatric Patients with MODY2: Insights into Screening and Diagnosis.
Su C et al.
Pediatric Health, Medicine and Therapeutics, 2025
Underestimated risk of secondary complications in pathogenic and glucose-elevating GCK variant carriers with type 2 diabetes.
Schiabor Barrett KM et al.
Communications Medicine, 2024
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
Glucokinase Variant Proteins Are Resistant to Fasting-Induced Uridine Diphosphate Glucose-Dependent Degradation in Maturity-Onset Diabetes of the Young Type 2 Patients.
Cho J et al.
International Journal of Molecular Sciences, 2023
A comprehensive map of human glucokinase variant activity.
Gersing S et al.
Genome Biology, 2023
Reduced penetrance of MODY-associated HNF1A/HNF4A variants but not GCK variants in clinically unselected cohorts.
Mirshahi UL et al.
American Journal of Human Genetics, 2022
Search for a time- and cost-saving genetic testing strategy for maturity-onset diabetes of the young.
Dusatkova P et al.
Acta Diabetologica, 2022
Study of ten causal genes in Turkish patients with clinically suspected maturity-onset diabetes of the young (MODY) using a targeted next-generation sequencing panel.
Doğan M et al.
Molecular Biology Reports, 2022
A Comprehensive Analysis of Hungarian MODY Patients-Part II: Glucokinase MODY Is the Most Prevalent Subtype Responsible for about 70% of Confirmed Cases.
Gaál Z et al.
Life (basel, Switzerland), 2021
How Heterogeneity in Glucokinase and Gap-Junction Coupling Determines the Islet [Ca2+] Response.
Dwulet JM et al.
Biophysical Journal, 2019
High Prevalence of Diabetes-Predisposing Variants in MODY Genes Among Danish Women With Gestational Diabetes Mellitus.
Gjesing AP et al.
Journal of the Endocrine Society, 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
GCK-MODY diabetes as a protein misfolding disease: the mutation R275C promotes protein misfolding, self-association and cellular degradation.
Negahdar M et al.
Molecular and Cellular Endocrinology, 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
GCK-MODY diabetes associated with protein misfolding, cellular self-association and degradation.
Negahdar M et al.
Biochimica Et Biophysica Acta, 2012
Susceptibility of glucokinase-MODY mutants to inactivation by oxidative stress in pancreatic β-cells.
Cullen KS et al.
Diabetes, 2011
Mutations in pancreatic ß-cell Glucokinase as a cause of hyperinsulinaemic hypoglycaemia and neonatal diabetes mellitus.
Hussain K
Reviews in Endocrine & Metabolic Disorders, 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
Permanent neonatal diabetes caused by a homozygous nonsense mutation in the glucokinase gene.
Rubio-Cabezas O et al.
Pediatric Diabetes, 2008
Glucokinase (GCK) and other susceptibility genes for beta-cell dysfunction: the candidate approach.
Gloyn AL et al.
Biochemical Society Transactions, 2008
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
From clinicogenetic studies of maturity-onset diabetes of the young to unraveling complex mechanisms of glucokinase regulation.
Sagen JV et al.
Diabetes, 2006
Effects of novel maturity-onset diabetes of the young (MODY)-associated mutations on glucokinase activity and protein stability.
Galán M et al.
The Biochemical Journal, 2006
Clinical characteristics of mutation carriers in a large family with glucokinase diabetes (MODY2).
Shehadeh N et al.
Diabetic Medicine : a Journal of the British Diabetic Association, 2005
Insights into the structure and regulation of glucokinase from a novel mutation (V62M), which causes maturity-onset diabetes of the young.
Gloyn AL et al.
The Journal of Biological Chemistry, 2005
Glucokinase and glucose homeostasis: proven concepts and new ideas.
Zelent D et al.
Biochemical Society Transactions, 2005
Permanent neonatal diabetes in an Asian infant.
Porter JR et al.
The Journal of Pediatrics, 2005
Permanent neonatal diabetes.
Bakri D et al.
The Israel Medical Association Journal : Imaj, 2004
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
Permanent neonatal diabetes caused by glucokinase deficiency: inborn error of the glucose-insulin signaling pathway.
Njølstad PR et al.
Diabetes, 2003