HRAS (GTPase HRas) variants and mutations

HRAS (also known as GTPase HRas) is a human protein-coding gene encoding a GTPase protein. Its GTP-bound state activates RAF-MEK-ERK and other pathways downstream of growth-factor receptors. Somatic activating variants drive several cancers, while germline activating variants cause Costello syndrome. This analysis covers 949 HRAS variants and mutations. Of these, 60% have computational variant effect predictions. Disease context includes Costello syndrome, linear nevus sebaceous syndrome, and Linear nevus sebaceus syndrome. Example HRAS variants include T2A, T2K, and T2M.

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 HRAS variants

Examples include T2A, T2K, T2M, T2R, T2S, E3*, E3G, E3K. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.