Mouse Sclerostin(SOST) ELISA kit

Instructions
Code CSB-EL022415MO
Size 96T,5×96T,10×96T
See More Details 24T ELISA kits trial application
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Product Details

Target Name sclerosteosis
Alternative Names Sost ELISA Kit; Sclerostin ELISA Kit
Abbreviation SOST
Uniprot No. Q99P68
Species Mus musculus (Mouse)
Sample Types serum, plasma, tissue homogenates
Detection Range 93.75 pg/mL-6000 pg/mL
Sensitivity 23.4 pg/mL
Assay Time 1-5h
Sample Volume 50-100ul
Detection Wavelength 450 nm
Research Area Signal Transduction
Assay Principle quantitative
Measurement Sandwich
Precision
Intra-assay Precision (Precision within an assay): CV%<8%        
Three samples of known concentration were tested twenty times on one plate to assess.    
Inter-assay Precision (Precision between assays): CV%<10%        
Three samples of known concentration were tested in twenty assays to assess.      
               
Linearity
To assess the linearity of the assay, samples were spiked with high concentrations of mouse SOST in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.  
  Sample Serum(n=4)    
1:1 Average % 86    
Range % 82-91    
1:2 Average % 101    
Range % 98-105    
1:4 Average % 87    
Range % 84-91    
1:8 Average % 100    
Range % 95-105    
Recovery
The recovery of mouse SOST spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.  
 
Sample Type Average % Recovery Range    
Serum (n=5) 89 85-94    
EDTA plasma (n=4) 107 103-110    
               
               
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.  
 
pg/ml OD1 OD2 Average Corrected    
6000 2.904 2.869 2.887 2.720    
3000 2.282 2.301 2.292 2.125    
1500 1.507 1.536 1.522 1.355    
750 0.921 0.902 0.912 0.745    
375 0.607 0.612 0.610 0.443    
187.5 0.356 0.362 0.359 0.192    
93.75 0.248 0.268 0.258 0.091    
0 0.165 0.169 0.167      
Troubleshooting
and FAQs
ELISA kit FAQs
Storage Store at 2-8°C. Please refer to protocol.
Lead Time 5-7 working days

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Target Data

Function Negative regulator of bone growth that acts through inhibition of Wnt signaling and bone formation.
Gene References into Functions
  1. The SOST gene inhibited the expression of COL1, OCN, and OPN, reduced the activity of alkaline phosphatase, and increased the expression of LPL and PPARgamma. PMID: 30041240
  2. 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
  3. 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
  4. osteoclast-derived LIF regulates bone turnover through sclerostin expression. PMID: 28543818
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin PMID: 27163932
  11. Osteocyte-derived molecule sclerostin drives bone marrow adipogenesis. PMID: 28460416
  12. complete absence of sclerostin has only minor effects on chronic kidney disease-induced bone loss in mice. PMID: 27528549
  13. 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
  14. These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement. PMID: 28081119
  15. Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt signaling pathway inhibition. PMID: 28062506
  16. 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
  17. removal of sclerostin appears to modestly protect the alveolar bone from resorption in this experimental setting PMID: 27349550
  18. 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
  19. 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
  20. 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
  21. 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
  22. Sclerostin depletion enhances tibial fracture healing. PMID: 26608966
  23. 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
  24. 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
  25. 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
  26. These findings indicated that AMPK regulated RANKL and sclerostin expression through the mevalonate pathway in osteocytes. PMID: 26713363
  27. Sclerostin inhibits bone formation through Lrp5 interaction. PMID: 25640331
  28. thyroid hormone-induced changes in bone remodeling are associated with a divergent regulation of DKK1 and sclerostin PMID: 26218891
  29. 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
  30. sclerostin is regulated by glutathione, N-acetylcysteine and lipoic acid in osteocytes in a process involving JNK and ERK1/2 PMID: 25660312
  31. 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
  32. Simulated microgravity induces an autonomous up-regulation of sclerostin. PMID: 25953900
  33. 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
  34. 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
  35. Advanced glycation end products increased sclerostin as well as apoptosis, and decreased RANKL in osteocytes. PMID: 25721666
  36. 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
  37. 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
  38. the altered bone composition contributes to the increased bone strength of patients with sclerostin deficiency. PMID: 24753092
  39. Data indicate that both Dickkopf-1 (DKK1) and sclerostin (SOST) were downregulated in proteoglycan-induced spondylitis (PGISp)-affected mouse spines. PMID: 23171658
  40. 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
  41. importance of the flexible loop and the cystine-knot for Wnt-signaling inhibition PMID: 24312339
  42. Evidence is accumulating that sclerostin directly or indirectly reduces renal calcium reabsorption [review]. PMID: 24876121
  43. 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
  44. Ovariectomy resulted in a substantial decrease in skeletal Sirt1 expression accompanied by an increase in sclerostin. PMID: 24949665
  45. 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
  46. 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
  47. In the absence of LRP5, the anabolic effects of SOST depletion can occur via other receptors (such as LRP4/6) PMID: 24225945
  48. sclerostin upregulated osteocyte expression of carbonic anhydrase 2. PMID: 23737439
  49. 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
  50. 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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Subcellular Location Secreted, extracellular space, extracellular matrix
Protein Families Sclerostin family
Database Links

KEGG: mmu:74499

STRING: 10090.ENSMUSP00000001534

UniGene: Mm.265602

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