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SOST // Sclerostin

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Scleroteosis is a genetic disorder caused by the loss of the SOST gen product. Studies of this disease characterized, among other clinical features, by progressive bone overgrowth, facial distortion, entrapment of cranial nerves and high intracranial pressure have allowed the identification of the Sclerostin (SOST) protein, which is implicated in the regulation of bone mass (Balemans et al., 2001). SOST is a glycoprotein with a cysteine-knot motif which belongs to the DAN/Cerberus family and is secreted mainly by bone dwelling osteocytes (Veverka et al., 2009). SOST inhibits bone forming activity of osteoblast in vitro, with a mechanism different from the Bone Morphogenetic Protein antagonists (van Bezooijen et al., 2004). Since, SOST have been found to be an endogenous antagonist of the Wnt/β-catenin pathway in the regulation of bone mass (Lin et al., 2009).

Bioclinica Lab employs a manual sandwich immunoassay for the measurement of human SOST in serum.

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