GLA (Alpha-galactosidase A) variants and mutations

GLA (also known as Alpha-galactosidase A) is a human protein-coding gene encoding an alpha-galactosidase A protein. It removes terminal alpha-galactose residues from glycosphingolipids during lysosomal degradation. Loss-of-function variants cause Fabry disease, with progressive accumulation of globotriaosylceramide-related lipids in vascular, renal, cardiac, and nervous tissues. This analysis covers 1,077 GLA variants and mutations. Of these, 77% have computational variant effect predictions. Disease context includes Fabry disease, cardiomyopathy, and Angiokeratoma corporis diffusum. Example GLA variants include M1A, M1I, and M1K.

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 GLA variants

Examples include M1A, M1I, M1K, M1L, M1T, M1V, Q2*, Q2H. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.