C3 (Complement C3) variants and mutations

C3 (also known as Complement C3) is a human protein-coding gene encoding a complement protein. It is cleaved during complement activation to generate C3a and C3b, which amplify inflammation, opsonize targets, and drive formation of downstream complement complexes. Deficiency causes severe susceptibility to bacterial infection, while dysregulated activation contributes to complement-mediated kidney and inflammatory diseases. This analysis covers 2,032 C3 variants and mutations. Of these, 72% have computational variant effect predictions. Disease context includes atypical hemolytic-uremic syndrome with C3 anomaly, complement component 3 deficiency, and age-related macular degeneration. Example C3 variants include G2E, G2R, and P3L.

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 C3 variants

Examples include G2E, G2R, P3L, P3S, T4N, G6C, P7L, P7S. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.