Bone Morphogenetic Proteins (BMPs) belong to the TGF-β (Transforming Growth Factor) superfamily of structurally related signaling proteins. BMP2 is a potent osteoinductive cytokine, capable of inducing bone and cartilage formation in association with osteoconductive carriers such as collagen and synthetic hydroxyapatite. In addition, BMP2 plays an important role in cardiac morphogenesis and is expressed in a variety of tissues; including the lung, spleen, brain, liver, prostate, ovary and small intestine. The functional form of BMP2 is a 26kDa protein composed of two identical 115 amino acid polypeptide chains linked by a single disulfide bond.

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Bone Morphogenetic Proteins (BMPs) belong to the TGF-β (Transforming Growth Factor) superfamily of structurally related signaling proteins. BMP7 is one of at least 15 structurally and functionally related BMPs, originally identified as protein regulators of cartilage and bone formation which have since been shown to be involved in embryogenesis and morphogenesis of various tissues and organs. BMPs have been shown to regulate the growth, differentiation, chemotaxis and apoptosis of a variety of cell types; including mesenchymal cells, epithelial cells, hematopoietic cells and neuronal cells. The active form of BMP7 can consist of a dimer of two identical proteins or a heterodimer of two related BMPs. BMP7 is expressed highest in the kidneys and is genetically linked in mice to eye, skeletal and kidney development.

Noggin belongs to a group of diffusible proteins that bind to ligands of the TGF-β (Transforming Growth Factor) family and regulate their activity by inhibiting their access to signaling receptors. Noggin was originally identified as a BMP4 antagonist whose action is critical for proper formation of the head and other dorsal structures. Noggin has been shown to modulate the activities of other BMPs including BMP2, 7, 13, and 14. Targeted deletion of noggin in mice results in prenatal death and recessive phenotype displaying a severely malformed skeletal system. Transgenic mice over-expressing noggin in mature osteoblasts display impaired osteoblastic differentiation, reduced bone formation and severe osteoporosis.

Noggin belongs to a group of diffusible proteins that bind to ligands of the TGF-β (Transforming Growth Factor) family and regulate their activity by inhibiting their access to signaling receptors. Noggin was originally identified as a BMP4 antagonist whose action is critical for proper formation of the head and other dorsal structures. Noggin has been shown to modulate the activities of other BMPs including BMP2, 7, 13 and 14. Targeted deletion of noggin in mice results in prenatal death and recessive phenotype displaying a severely malformed skeletal system. Transgenic mice overexpressing noggin in mature osteoblasts display impaired osteoblastic differentiation, reduced bone formation, and severe osteoporosis.