Upon ligand binding, BMPR1A forms a receptor comple, Xenopus/Amphibian, consisting of two type II and two type I transmembrane Ser/Thr kinases. The type I receptors are activated by the type II receptors by using a phosphorylation mechanism, and subsequently bind SMAD transcriptional regulators. Defects in BMPR1A are the cause of juvenile polyposis syndrome, Cowden disease and hereditary mi, Xenopus/Amphibian,ed polyposis syndrome 2, which lead to gastrointestinal, breast, thyroid, endometrial and colon cancers.