Noggin is involved in numerous developmental processes, such as neural tube fusion and joint formation. The morphogenesis of organs is initiated by a downgrowth from a layer of epithelial stem cells. This process is achieved through the receipt of signals from 1) a WNT protein (WNT3A) to stabilize beta-catenin; and 2) Noggin, which is a bone morphogenetic protein inhibitor. Noggin mutations in unrelated families with proximal symphalangism (SYM1) and multiple synostoses syndrome (SYNS1) have been identified, which have multiple joint fusion as their principal defect.
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