|Application ||WB, IHC-P, E|
|Calculated MW||24031 Da|
|Antigen Region||134-163 aa|
|Other Names||Sclerostin, SOST|
|Target/Specificity||This SOST antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 134-163 amino acids from the Central region of human SOST.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||SOST Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Negative regulator of bone growth that acts through inhibition of Wnt signaling and bone formation.|
|Cellular Location||Secreted, extracellular space, extracellular matrix|
|Tissue Location||Widely expressed at low levels with highest levels in bone, cartilage, kidney, liver, bone marrow and primary osteoblasts differentiated for 21 days. Detected in the subendothelial layer of the aortic intima (at protein level)|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Loss-of-function mutations in this gene are associated with an autosomal-recessive disorder, sclerosteosis, which causes progressive bone overgrowth. A deletion downstream of the sclerostin gene, which causes reduced sclerostin expression, is associated with a milder form of the disorder called van Buchem disease.
Semenov,M.V., J. Biol. Chem. 281 (50), 38276-38284 (2006)
Ellies,D.L., J. Bone Miner. Res. 21 (11), 1738-1749 (2006)
Balemans,W., J Musculoskelet Neuronal Interact 6 (4), 355-356 (2006)
Gardner,J.C., J. Clin. Endocrinol. Metab. 90 (12), 6392-6395 (2005)
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