Biolegend, 767308, Recombinant Human/Mouse/Rat BMP-2 (carrier-free)

Bone morphogenetic protein 2 (BMP-2) belongs to the TGF-β superfamily. Like other members of BMP family, BMP-2 is synthesized as an inactive propeptide precursor which dimerizes and then it is further processed into mature form by proprotein convertases (PCs). Some evidence indicated that PC5/6A and Factor VII-activating protease (FSAP) are involved in maturation of BMP-2. Mature BMP-2 is a 26 kD protein composed of 114 amino acids, forming three intramolecular and one intermolecular disulfide bond. BMP-2 forms homodimer or heterodimer with other BMP proteins, including BMP-4, BMP-6 and BMP-7. BMP-2 signal through heterodimeric serine/threonine kinase receptors composed of a type I (BMPR1a/ALK3, BMPR1b/ALK6, ActRIa/ALK2) and a type II (BMPR2, ACVR2a/ActRIIA, ACVR2b/ActRIIB). BMP-2 binds to the type I receptor with high affinity, in turn recruits the type II receptor. BMP-2 stimulation initiates receptor shutting, leading to receptor clustering and activation of the downstream signaling. BMP-2 signals via canonical Smad or other downstream kinase, such as p38 and JNK in a context-dependent manner. BMP-2 is involved in several processes, including cartilage and bone formation, differentiation, and embryogenesis. BMP-2 induces osteogenic differentiation in human mesenchymal stem cells and myogenic cells. BMP-2 induces cartilage repair and remodeling by stimulating chondrocyte proliferation and expression of matrix proteins. BMP-2/BMP-7 heterodimer is more potent in the induction of bone formation in vivo than BMP-2 homodimer. BMP-2-deficiency leads to embryonic lethality with abnormal cardiac development, malformation of the amnion/chorion, severe chondrodysplasia, and defects in myocardial patterning, suggesting that BMP-2 mediates organ morphogenesis. Noggin is an antagonist to reverse BMP-2-mediated effect and its expression is induced by BMP-2 in osteoblasts as a negative feedback loop. In addition, BMP-2 stimulates epithelial to mesenchymal cell transformation through TGF-β type III receptor.