Rat SOST / Sclerostin 단백질(Protein) (His Tag)

Rat SOST / Sclerostin Datasheet

SOST / Sclerostin Protein Product Information

• Synonym: SOST
• Protein Construction: A DNA sequence encoding the rat SOST ( NP_085073.1 ) ( Met 1 - Tyr 213 ) was expressed, fused with a polyhistidine tag at the C-terminus
• Source: Rat
• Expression Host: Human Cells

SOST / Sclerostin Protein QC Testing

• Purity: > 97 % as determined by SDS-PAGE
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method
• Stability: Samples are stable for up to twelve months from date of receipt at -70℃
• Predicted N terminal: Gln 24
• Molecular Mass: The recombinant rat SOST comprises 201 amino acids and predicts a molecular mass of 23 kDa. The apparent molecular mass of the rat SOST is approximately 33 kDa in SDS-PAGE under reducing conditions due to glycosylation
• Formulation: Lyophilized from sterile PBS , pH 7.4
  1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
  2. Please contact us for any concerns or special requirements.

• SDS-PAGE: SOST protein

SOST / Sclerostin Protein Usage Guide

• Storage: Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Reconstitution: A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

SOST / Sclerostin Protein Description

Rat SOST, also known as sclerostin, is a 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 including Dan, Cerberus, Gremlin, PRDC, and Caronte. SOST is expressed at significant levels in bone, cartilage, kidney, and liver, and was originally identified as an important regulator of bone remodeling, homeostasis, and links bone resorption and bone apposition. It negatively regulates the formation of bone by repressing the differentiation and/or function of osteoblasts induced by BMPs. It has been shown that SOST binds BMP-5, -6, and -7 with high affinity and BMP-2 and -4 with low affinity. Recent studies have revealed that SOST inhibits the bone growth probably by binding to the extracellular domain of the Wnt coreceptors LRP5 and LRP6 and disrupts the Wnt signaling. Loss-of-function mutations of SOST are associated with sclerosteosis which is an autosomal-recessive bone dysplasia characterized by progressive skeletal overgrowth, and reduced sclerostin expression results in a milder form of the disorder called van Buchem disease.

References

1. Brunkow, M.E. et al., 2001, Am. J. Hum. Genet. 68: 577-589.
2. Balemans, W. et al., 2001, Hum. Mol. Genet. 10: 537-543.
3. Naoki, K. et al., 2003, J. Biol. Chem. 278: 24113-24117.
4. Balemans, W. et al., 2002, J. Med. Genet. 39:91-97.
5. Semennov, M. et al., 2005, J. Biol. Chem. 280: 26770-26775.