Anti-BMP2, clone 2H6D12

Bone morphogenetic protein-2 (BMP-2) is a member of the transforming growth factor-beta (TGFB) superfamily. BMP2 is synthesized as a 60 kDa precursor that is processed in the secretory pathway to a small 18 kDa monomer, 2 monomers then associate to form the active 30 kDa homodimer,which binds to its receptor. There is also a 40-45 kDa form of BMP2,as an amino-terminal propeptide. BMP2 can induce bone formation and regeneration during early embryonic development. It is involved in the hedgehog pathway,TGF beta signaling pathway,and cytokine-cytokine receptor interaction. Protein function: Growth factor of the TGF-beta superfamily that plays essential roles in many developmental processes, including cardiogenesis, neurogenesis, and osteogenesis (PubMed:18436533, PubMed:31019025, PubMed:24362451). Induces cartilage and bone formation (PubMed:3201241). Initiates the canonical BMP signaling cascade by associating with type I receptor BMPR1A and type II receptor BMPR2 (PubMed:15064755, PubMed:17295905, PubMed:18436533). Once all three components are bound together in a complex at the cell surface, BMPR2 phosphorylates and activates BMPR1A (PubMed:7791754). In turn, BMPR1A propagates signal by phosphorylating SMAD1/5/8 that travel to the nucleus and act as activators and repressors of transcription of target genes. Also acts to promote expression of HAMP, via the interaction with its receptor BMPR1A/ALK3 (PubMed:31800957). Can also signal through non-canonical pathways such as ERK/MAP kinase signaling cascade that regulates osteoblast differentiation (PubMed:20851880, PubMed:16771708). Also stimulates the differentiation of myoblasts into osteoblasts via the EIF2AK3-EIF2A-ATF4 pathway by stimulating EIF2A phosphorylation which leads to increased expression of ATF4 which plays a central role in osteoblast differentiation (PubMed:24362451). Acts as a positive regulator of odontoblast differentiation during mesenchymal tooth germ formation, expression is repressed during the bell stage by MSX1-mediated inhibition of CTNNB1 signaling. [The UniProt Consortium]