Associated Papers
Glucokinase (GCK) in diabetes: from molecular mechanisms to disease pathogenesis.
Abu Aqel Y et al.
Cellular & Molecular Biology Letters, 2024
Characterizing glucokinase variant mechanisms using a multiplexed abundance assay.
Gersing S et al.
Genome Biology, 2024
Characterizing glucokinase variant mechanisms using a multiplexed abundance assay.
Gersing S et al.
Biorxiv : the Preprint Server for Biology, 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
Not quite type 1 or type 2, what now? Review of monogenic, mitochondrial, and syndromic diabetes.
Yeung RO et al.
Reviews in Endocrine & Metabolic Disorders, 2018
Genetic Confirmation Rate in Clinically Suspected Maturity-Onset Diabetes of the Young.
Brahm AJ et al.
Canadian Journal of Diabetes, 2016
Phenotypic heterogeneity in monogenic diabetes: the clinical and diagnostic utility of a gene panel-based next-generation sequencing approach.
Alkorta-Aranburu G et al.
Molecular Genetics and Metabolism, 2014
Analysis of the co-operative interaction between the allosterically regulated proteins GK and GKRP using tryptophan fluorescence.
Zelent B et al.
The Biochemical Journal, 2014
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
Mutational analysis of allosteric activation and inhibition of glucokinase.
Zelent B et al.
The Biochemical Journal, 2011
Generation of N-ethyl-N-nitrosourea (ENU) diabetes models in mice demonstrates genotype-specific action of glucokinase activators.
Fenner D et al.
The Journal of Biological Chemistry, 2011
GCK-MODY (MODY 2) Caused by a Novel p.Phe330Ser Mutation.
Bonfig W et al.
Isrn Pediatrics, 2011
Extremes of clinical and enzymatic phenotypes in children with hyperinsulinism caused by glucokinase activating mutations.
Sayed S et al.
Diabetes, 2009
Cell biology assessment of glucokinase mutations V62M and G72R in pancreatic beta-cells: evidence for cellular instability of catalytic activity.
Arden C et al.
Diabetes, 2007
Functional analysis of human glucokinase gene mutations causing MODY2: exploring the regulatory mechanisms of glucokinase activity.
García-Herrero CM et al.
Diabetologia, 2007
From clinicogenetic studies of maturity-onset diabetes of the young to unraveling complex mechanisms of glucokinase regulation.
Sagen JV et al.
Diabetes, 2006
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
Spectrum of HNF1A and GCK mutations in Canadian families with maturity-onset diabetes of the young (MODY).
McKinney JL et al.
Clinical and Investigative Medicine. Medecine Clinique Et Experimentale, 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
GCK and HNF1A mutations in Canadian families with maturity onset diabetes of the young (MODY).
Cao H et al.
Human Mutation, 2002