Recombinant Human Sclerostin/SOST Protein

Synonym

SOST, VBCH

Source

Recombinant Human Sclerostin /SOST Protein (rhSOST) Gln24-Tyr213 (Accession # AAI01087.1)was produced in human 293 cells (HEK293) at ACRObiosystems.

Molecular Characterization

rhSOST, fused with 6×his tag at the N-terminus, has a calculated MW of 22.5 kDa expressed. The predicted N-terminus is Gln24. Protein migrates as 28 kDa in reduced SDS-PAGE resulting from glycosylation.

Endotoxin

Less than 1.0 EU per μg of the rhSOST by the LAL method.

Purity

>95% as determined by SDS-PAGE.

Formulation

Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4. Normally Mannitol or Trehalose are added as protectants before lyophilization.

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Reconstitution

See Certificate of Analysis for details of reconstitution instruction and specific concentration.

Storage

Avoid repeated freeze-thaw cycles.

No activity loss was observed after storage at:
In lyophilized state for 1 year (4^oC-8^oC); After reconstitution under sterile conditions for 1 month (4^oC-8^oC) or 3 months (-20^oC to -70^oC).

Background

Sclerostin (SOST) also known as Sclerosteosis, VBCH, is a secreted glycoprotein with a signal peptide for secretion and a C-terminal cysteine knot-like (CTCK) domain and belongs to the Cerberus/DAN family of bone morphogenetic protein (BMP) antagonists. Sclerostin is produced by the osteocyte and has anti-anabolic effects on bone formation. More recently Sclerostin has been identified as binding to LRP5/6 receptors and inhibiting the Wnt signalling pathway. Wnt pathway inhibition under these circumstances is antagonistic to bone formation (meaning Sclerostin antagonizes bone formation).[1] It has been shown that SOST binds BMP-5, -6, and -7 with high affinity and BMP-2 and -4 with low affinity. Sclerostin production by osteocytes is inhibited by parathyroid hormone, mechanical loading and cytokines including oncostatin M, cardiotrophin-1 and leukemia inhibitory factor. Sclerostin production is increased by calcitonin. Thus, osteoblast activity is self regulated by a negative feedback system. Mutations of Sclerostin is associated with the syndrome Sclerosteosis, and reduced sclerostin expression results in a milder form of the disorder called van Buchem disease. [2-3]

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References