Recombinant Mouse Sclerostin (SOST) Protein (His&Myc)

Beta LifeScience SKU/CAT #: BLC-01365P
Greater than 85% as determined by SDS-PAGE.
Greater than 85% as determined by SDS-PAGE.

Recombinant Mouse Sclerostin (SOST) Protein (His&Myc)

Beta LifeScience SKU/CAT #: BLC-01365P
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Product Overview

Description Recombinant Mouse Sclerostin (SOST) Protein (His&Myc) is produced by our Baculovirus expression system. This is a full length protein.
Purity Greater than 85% as determined by SDS-PAGE.
Uniprotkb Q99P68
Target Symbol SOST
Species Mus musculus (Mouse)
Expression System Baculovirus
Tag N-10His&C-Myc
Target Protein Sequence QGWQAFRNDATEVIPGLGEYPEPPPENNQTMNRAENGGRPPHHPYDAKDVSEYSCRELHYTRFLTDGPCRSAKPVTELVCSGQCGPARLLPNAIGRVKWWRPNGPDFRCIPDRYRAQRVQLLCPGGAAPRSRKVRLVASCKCKRLTRFHNQSELKDFGPETARPQKGRKPRPGARGAKANQAELENAY
Expression Range 24-211aa
Protein Length Full Length of Mature Protein
Mol. Weight 25 kDa
Research Area Signal Transduction
Form Liquid or Lyophilized powder
Buffer Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage 1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target Function Negative regulator of bone growth that acts through inhibition of Wnt signaling and bone formation.
Subcellular Location Secreted, extracellular space, extracellular matrix.
Protein Families Sclerostin family
Database References

KEGG: mmu:74499

STRING: 10090.ENSMUSP00000001534

UniGene: PMID: 30041240

  • Since adipocytes do not produce sclerostin, these findings suggest an unexplored endocrine function for sclerostin that facilitates communication between the skeleton and adipose tissue. PMID: 29229807
  • A microtubule-dependent mechanotransduction pathway that linked fluid shear stress to reactive oxygen species and calcium (Ca2+) signals that led to a reduction in sclerostin abundance in cultured osteocytes. PMID: 29162742
  • osteoclast-derived LIF regulates bone turnover through sclerostin expression. PMID: 28543818
  • our study provided histological evidences that sclerostin tends to be secreted in osteocytes of remodeled mature bone, while FGF23 would be differently synthesized in osteoblasts and osteocytes according to the developmental stages PMID: 28794403
  • These results show that osteocytes and/or osteoblasts secrete factors regulating beige adipogenesis, at least in part, through the Wnt-signaling inhibitor sclerostin. PMID: 27653320
  • In vivo muCT analysis of cortical bone at age 1 and 3 months confirmed increased thickness in Sost-/-mice, but revealed no cortical abnormalities in single Gja1+/-or Sost+/-mice PMID: 29149200
  • loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL and SOST, leading to osteoclast inhibition and Wnt activation together. PMID: 27402532
  • humanized Multiple Myeloma xenograft mouse model bearing human MM cells (NOD-SCID.CB17 male mice injected intravenously with 2.5 million of MM1.S-Luc-GFP cells) demonstrated significantly higher concentrations of mouse-derived sclerostin, suggesting a microenvironmental source of sclerostin. PMID: 26763740
  • Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin PMID: 27163932
  • Osteocyte-derived molecule sclerostin drives bone marrow adipogenesis. PMID: 28460416
  • complete absence of sclerostin has only minor effects on chronic kidney disease-induced bone loss in mice. PMID: 27528549
  • In mice, sclerostin deficiency hastened reparative dentinogenesis after pulp injury, suggesting that the inhibition of sclerostin may constitute a promising therapeutic strategy for improving the healing of damaged pulps. PMID: 28571484
  • These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement. PMID: 28081119
  • Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt signaling pathway inhibition. PMID: 28062506
  • Analysis of SOST expression using large minigenes reveals the MEF2C binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 responsiveness. PMID: 26361013
  • removal of sclerostin appears to modestly protect the alveolar bone from resorption in this experimental setting PMID: 27349550
  • chronic TNFalpha (tumor necrosis factor alpha)-dependent arthritis, fibroblast-like synoviocytes constitute a major source of sclerostin and that either the lack of sclerostin or its antibody-mediated inhibition leads to an acceleration of rheumatoid arthritis (RA)-like disease. PMID: 27089204
  • Data show that the phenotype of Notch activation in osteocytes was prevented in matrix protein 1 (Dmp1)-Cre;Rosa(Notch) mice hemizygous for the Dmp1-sclerostin (SOST) transgene. PMID: 26456319
  • Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ-responsive transcriptional activity and TAZ-responsive gene expression, indicating a role for TAZ as a regulator of adipogenesis by sclerostin. PMID: 26553151
  • Our results suggested that sclerostin could be expressed in the liver and sustained successfully at high levels in the blood by using the PhiC31 integrase system, leading to trabecular bone loss. PMID: 26845353
  • Sclerostin depletion enhances tibial fracture healing. PMID: 26608966
  • SOST gene is involved in the regulation of renal interstitial fibrosis (RIF) progression. In obstructive kidney injury, SOST gene deletion would probably enhance renal fibrogenic response and promote the progression of RIF. PMID: 26337453
  • Data (including data from studies in knockout/transgenic mice) suggest that Lrp6 (lipoprotein receptor-related protein 6) is required for suppression of Sost expression by parathyroid hormone (here, human PTH peptide 1-34). PMID: 25847683
  • These in vivo data support in vitro studies regarding the mechanism of HBM-causing mutations, and imply that HBM LRP5 receptors differ in their relative sensitivity to inhibition by SOST and DKK1. PMID: 25808845
  • These findings indicated that AMPK regulated RANKL and sclerostin expression through the mevalonate pathway in osteocytes. PMID: 26713363
  • Sclerostin inhibits bone formation through Lrp5 interaction. PMID: 25640331
  • thyroid hormone-induced changes in bone remodeling are associated with a divergent regulation of DKK1 and sclerostin PMID: 26218891
  • increased sclerostin production achieved by HDAC5 shRNA is abrogated by simultaneous knockdown of MEF2C, indicating that MEF2C is a major target of HDAC5 in osteocytes PMID: 25271055
  • sclerostin is regulated by glutathione, N-acetylcysteine and lipoic acid in osteocytes in a process involving JNK and ERK1/2 PMID: 25660312
  • Estrogen replacement treatment in ovariectomized ER beta KO mice caused a significant increase in Col2 expression, no change in ER alpha expression, and a significant increase in Sost expression. PMID: 25046534
  • Simulated microgravity induces an autonomous up-regulation of sclerostin. PMID: 25953900
  • deleting the Sost gene (a potent inhibitor of WNT signaling) or blocking sclerostin function by using the mAb in a periodontitis model significantly restores bone and periodontal ligament defects PMID: 25757567
  • bony union was not altered by Sclerostin deficiency in externally-fixed closed tibial fractures, but fibrocartilage removal was enhanced and the resultant united bony calluses had increased bone fraction and increased strength. PMID: 25445453
  • Advanced glycation end products increased sclerostin as well as apoptosis, and decreased RANKL in osteocytes. PMID: 25721666
  • long-term Sclerostin deficiency inhibits the bone loss normally induced with decreased mechanical load, but it can augment the increase in bone formation with increased load. PMID: 24821585
  • Findings strongly suggest that Wise and Sost are key modulators of bone development through the ability of their encoded proteins to interact with Lrp5 and control the balance or levels of Wnt signaling. PMID: 24789067
  • the altered bone composition contributes to the increased bone strength of patients with sclerostin deficiency. PMID: 24753092
  • Data indicate that both Dickkopf-1 (DKK1) and sclerostin (SOST) were downregulated in proteoglycan-induced spondylitis (PGISp)-affected mouse spines. PMID: 23171658
  • Data indicate that LRP4 (low-density lipoprotein receptor-related protein 4) deficiency in bone dramatically elevated serum sclerostin levels whereas bone expression of Sost encoding for sclerostin was unaltered. PMID: 25404300
  • importance of the flexible loop and the cystine-knot for Wnt-signaling inhibition PMID: 24312339
  • Evidence is accumulating that sclerostin directly or indirectly reduces renal calcium reabsorption [review]. PMID: 24876121
  • Data indicate that low-dose parathyroid hormone (PTH) decreased the expression of the myocyte enhancer factor 2C (Mef2c) transcription factor, resulting in decreased sclerostin (Sost) expression in osteoblasts/osteocytes. PMID: 25056116
  • Ovariectomy resulted in a substantial decrease in skeletal Sirt1 expression accompanied by an increase in sclerostin. PMID: 24949665
  • results suggest that the lack of sclerostin mainly alters the bone and cementum phenotypes rather than producing abnormalities in tooth structures such as dentin PMID: 24699186
  • Data indicate that sclerostin blockade restored bone mineral density (BMD) and bone volume fraction at all assessed sites but was unable to repair focal erosions. PMID: 24432364
  • In the absence of LRP5, the anabolic effects of SOST depletion can occur via other receptors (such as LRP4/6) PMID: 24225945
  • sclerostin upregulated osteocyte expression of carbonic anhydrase 2. PMID: 23737439
  • these data indicate that enhanced beta-catenin signaling is present in Sost(-/-) mice that demonstrate accelerated healing of bone defects, suggesting that modulation of beta-catenin signaling in bone could be used to promote fracture repair. PMID: 24211207
  • These results support a model in which, in the context of obesity or other inflammatory diseases that increase the production of TNF-alpha, TNF-alpha upregulates the expression of sclerostin through NF-kappaB signaling pathway, thus contributing to bone loss. PMID: 24446199
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