ACTA2 (Actin, aortic smooth muscle) variants and mutations

ACTA2 (also known as Actin, aortic smooth muscle) is a human protein-coding gene encoding an actin, aortic smooth muscle protein. Its smooth-muscle actin filaments generate contractile force in arteries and visceral organs and help maintain vascular-wall structure. Pathogenic variants are an important cause of familial thoracic aortic aneurysm and dissection and can also produce occlusive vascular disease. This analysis covers 668 ACTA2 variants and mutations. Of these, 78% have computational variant effect predictions. Disease context includes aortic aneurysm, familial thoracic 6, multisystemic smooth muscle dysfunction syndrome, and Moyamoya disease 5. Example ACTA2 variants include M1I, M1V, and C2S.

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, AlphaFold DB, gnomAD constraint, Open Targets, ClinGen, MaveDB, LitVar.

Notable ACTA2 variants

Examples include M1I, M1V, C2S, C2Y, E3K, E5A, E5K, E5Q. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.