FGA (Fibrinogen alpha chain) variants and mutations

FGA (also known as Fibrinogen alpha chain) is a human protein-coding gene encoding a fibrinogen alpha chain protein. It contributes the alpha chains of fibrinogen, which thrombin converts into fibrin to form the structural mesh of blood clots. Pathogenic variants can cause afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia, thrombosis, or certain hereditary amyloidoses. This analysis covers 1,569 FGA variants and mutations. Of these, 72% have computational variant effect predictions. Disease context includes familial dysfibrinogenemia, Familial renal amyloidosis, and familial visceral amyloidosis. Example FGA variants include M1?, F2L, and F2S.

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, Interaction Network Analysis, Protein Data Bank, AlphaFold DB, gnomAD constraint, Open Targets, MaveDB, LitVar.

Notable FGA variants

Examples include M1?, F2L, F2S, S3F, S3Y, M4L, M4V, R5K. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.