RET (P07949) variants and mutations

RET (also known as P07949) is a human protein-coding gene encoding a proto-oncogene tyrosine-protein kinase receptor protein. Its activation by GDNF-family ligands guides development of the enteric nervous system, kidney, and other tissues. Activating variants cause multiple endocrine neoplasia type 2 and can drive cancer, whereas loss-of-function variants are an important cause of Hirschsprung disease. This analysis covers 4,409 RET variants and mutations. Of these, 51% have computational variant effect predictions. Disease context includes medullary thyroid gland carcinoma, multiple endocrine neoplasia type 2A, and multiple endocrine neoplasia type 2B. Example RET variants include M1?, A2E, and A2G.

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 RET variants

Examples include M1?, A2E, A2G, A2V, A2T, A2S, A2A, K3E. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.