Upon ligand binding, BMPR1A forms a receptor complex 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 mixed polyposis syndrome 2, which lead to gastrointestinal, breast, thyroid, endometrial and colon cancers.

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