Is a positive regulator of the BMP signaling pathway, required for proper chondrogenesis, osteogenesis and skeletal development (PubMed:33308444). It acts as coreceptor for BMP ligands, particularly BMP2 and BMP4, facilitating their interactions with BMP type I receptors (By similarity). It is required for ligand-induced recruitment of BMP receptors to lipid rafts (PubMed:33308444). Binds to TGFBR2 and activates TGFB signaling (By similarity). Forms homooligomers. Forms heterooligomers with SCUBE1 and SCUBE2. Interacts with TGFBR2 through the CUB domain; this interaction does not affect TGFB1-binding to TGFBR2. Interacts with BMP2, BMP4 and BMP7; the interaction is mediated by the CUB domain. Interacts with BMPR1A, BMPR1B and BMPR2; the interaction with BMPR1A and BMPR1B is BMP2- and BMP4-dependent. Highly expressed in femur and humerus with little or no expression in non-bone tissues. N-glycosylated. Proteolytic cleavage produces a CUB-containing C-terminal fragment that retains the ability to bind to TGFBR2. This reaction is catalyzed in vitro by MMP2 and, to a lesser extent, by MMP9 (By similarity). Knockout mice are viable and do not show any macroscopically visible abnormality at birth. At day P1, however, knockout mice are shorter than their control littermates, and show misaligned upper/lower incisors and altered craniofacial development. All appendicular (forelimbs and hindlimbs) and axial (skull, vertebral column, and rib cage) skeletal elements are smaller than in control animals. The defective skeletal growth persists up to adulthood.