On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP2, BMP4, GDF5 and GDF6. Positively regulates chondrocyte differentiation through GDF5 interaction. Mediates induction of adipogenesis by GDF6. ATP + L-threonyl-[receptor-protein] = ADP + H(+) + O-phospho-L-threonyl-[receptor-protein] ATP + L-seryl-[receptor-protein] = ADP + H(+) + O-phospho-L-seryl-[receptor-protein] Interacts with BMP2 (PubMed:10881198, PubMed:15064755, PubMed:17295905, PubMed:18937504). Interacts with low affinity with GDF5; positively regulates chondrocyte differentiation (PubMed:24098149). Interacts with BMP4 (PubMed:8006002). Interacts with SCUBE3 (PubMed:33308444). Highly expressed in skeletal muscle. Glycosylated. The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry. A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome. Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. TGFB receptor subfamily.