Noggin belongs to a group of diffusible proteins which bind to ligands of the TGF-α family and regulate their activity by inhibiting their access to signaling receptors. Noggin was originally identified as a BMP-4 antagonist whose action is critical for proper formation of the head and other dorsal structures. Consequently, Noggin has been shown to modulate the activities of other BMPs including BMP-2,-7,-13, and -14. Targeted deletion of Noggin in mice results in prenatal death and recessive phenotype displaying a severely malformed skeletal system. Conversely, transgenic mice over-expressing Noggin in mature osteoblasts display impaired osteoblastic differentiation, reduced bone formation, and severe osteoporosis. The amino acid sequence of human noggin is highly homologous to that of Xenopus, rat and mouse.

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