ADA (Adenosine deaminase) variants and mutations

ADA (also known as Adenosine deaminase) is a human protein-coding gene encoding an adenosine deaminase protein. It degrades adenosine and deoxyadenosine, preventing accumulation of metabolites that are particularly toxic to developing lymphocytes. Biallelic deficiency causes severe combined immunodeficiency, while partial deficiency can present later with immune dysfunction. This analysis covers 700 ADA variants and mutations. Of these, 78% have computational variant effect predictions. Disease context includes Severe combined immunodeficiency due to adenosine deaminase deficiency, severe combined immunodeficiency, autosomal recessive, T cell-negative, B cell-n, and severe combined immunodeficiency. Example ADA variants include M1R, M1V, and M1I.

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 ADA variants

Examples include M1R, M1V, M1I, A2V, Q3*, T4K, P5S, A6P. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.