ATM (Serine-protein kinase ATM) variants and mutations

ATM (also known as Serine-protein kinase ATM) is a human protein-coding gene encoding a serine-protein kinase protein. It is activated by DNA double-strand breaks and coordinates checkpoint arrest, repair, and apoptosis through phosphorylation of numerous targets. Biallelic loss causes ataxia-telangiectasia, while heterozygous pathogenic variants increase susceptibility to several cancers. This analysis covers 14,477 ATM variants and mutations. Of these, 55% have computational variant effect predictions. Disease context includes ataxia telangiectasia, Ataxia-telangiectasia, and cancer. Example ATM variants include M1?, M1I, and M1L.

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

Notable ATM variants

Examples include M1?, M1I, M1L, M1T, S2C, S2G, S2N, S2R. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.