GCK (Hexokinase-4) variants and mutations

GCK (also known as Hexokinase-4) is a human protein-coding gene encoding a hexokinase-4 protein. It sets the glucose threshold for insulin secretion in pancreatic beta cells and controls hepatic glucose phosphorylation after meals. Heterozygous loss-of-function variants cause GCK-MODY, stronger loss can cause neonatal diabetes, and activating variants can cause hyperinsulinemic hypoglycemia. This analysis covers 1,184 GCK variants and mutations. Of these, 76% have computational variant effect predictions. Disease context includes Alzheimer disease, Parkinson disease, and neurodegenerative disease. Example GCK variants include M1I, M1L, and D3Y.

Variant analysis overview

Variant and mutation evidence

Clinical, disease, and population context

Protein structure and variant hotspots

Data sources

Evidence in this analysis draws on EBI Proteins Variation, UniProt, gnomAD v4, EuropePMC, 3D Hotspot Analysis, Interaction Network Analysis, Protein Data Bank, AlphaFold DB, gnomAD constraint, Open Targets, ClinGen, MaveDB, LitVar.

Notable GCK variants

Examples include M1I, M1L, D3Y, D4G, D4N, R5G, R5K, A6T. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.