PROC (Vitamin K-dependent protein C) variants and mutations

PROC (also known as Vitamin K-dependent protein C) is a human protein-coding gene encoding a vitamin K-dependent protein C protein. After activation, protein C limits coagulation by proteolytically inactivating factors Va and VIIIa with protein S as a cofactor. Heterozygous deficiency increases venous-thrombosis risk, while severe biallelic deficiency can cause neonatal purpura fulminans. This analysis covers 880 PROC variants and mutations. Of these, 79% have computational variant effect predictions. Disease context includes hereditary thrombophilia due to congenital protein C deficiency, venous thromboembolism, and deep vein thrombosis. Example PROC variants include M1?, W2*, and Q3P.

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, MaveDB, LitVar.

Notable PROC variants

Examples include M1?, W2*, Q3P, Q3*, Q3Q, L4L, T5R, S6I. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.