MPL (Thrombopoietin receptor) variants and mutations

MPL (also known as Thrombopoietin receptor) is a human protein-coding gene encoding a thrombopoietin receptor protein. Thrombopoietin signaling through this pathway drives megakaryocyte maturation, platelet production, and hematopoietic stem-cell maintenance. Activating variants can cause myeloproliferative neoplasms or hereditary thrombocytosis, whereas loss-of-function variants cause congenital amegakaryocytic thrombocytopenia. This analysis covers 1,464 MPL variants and mutations. Of these, 81% have computational variant effect predictions. Disease context includes congenital amegakaryocytic thrombocytopenia 1, thrombocythemia 2, and congenital amegakaryocytic thrombocytopenia. Example MPL variants include P2A, P2L, and P2S.

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 MPL variants

Examples include P2A, P2L, P2S, P2H, P2P, S3F, S3Y, S3S. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.