Sclerostin (SOST) ELISA Kits

Human Sclerostin (SOST) interaction partners

1. Sclerostin is degraded by cathepsin K in vitro. Cathepsin K degradation of sclerostin is affected by hypoxia.

2. Study found that sclerostin concentrations were not significantly higher in patients with bone metastases compared to non-metastatic prostate cancer (PC) but they were significantly higher in patients with CRPC. Sclerostin levels were significantly higher in patients with advanced disease and increased bone turnover due to a compensatory response to the increased number of osteoblasts.

3. Patients with Latent autoimmune diabetes in Adults (LADA) presented lower bone resorption than did controls, similar to patients with T2 diabetes (T2D). Sclerostin is increased in T2D but not in LADA, suggesting possible roles on bone metabolism in T2D only.

4. Higher Sclerostin/SOST expression is associated with lower percentage of circulatory blasts and better prognosis in patients with myelofibrosis.

5. Sclerosteosis is caused by loss-of-function mutations in the SOST gene which encodes a secreted glycoprotein, sclerostin--{REVIEW}

6. Serum sclerostin level was not an independent predictor of mortality in Maintenance Hemodialysis Patients

7. these results suggest a possible role of sclerostin in the identification of ankylosing spondylitis patients

8. important role for SOST SNP rs1877632 and VDR SNPs rs10735810 and rs731236 in the pathophysiology of stress fracture

9. In our cohort of pregnant women, sclerostin and DKK1 were not associated with any adverse metabolic profile, and possibly do not play relevant roles in the pathophysiology of gestational diabetes mellitus.

10. Sclerostin increased after exercise in comparison to baseline (mean +/- SEM: 410 +/- 27 vs. 290 +/- 19 pg/mL; p < 0.001) corresponding to an increase of +44.3 +/-5.5%

11. serum sclerostin levels correlated positively with carotid intima-media thickness and inversely with the augmentation index, a marker of arterial stiffness

12. The difference of serum sclerostin levels in Ankylosing Spondylitis and Rheumatoid Arthritis patients was not significantly different from HC, indicating that the sclerostin may not associate with the development of Ankylosing Spondylitis and Rheumatoid Arthritis.

13. SOST gene silencing promotes the proliferation, invasion, and migration, and inhibits apoptosis of osteosarcoma cells by activating Wnt/beta-catenin signaling pathway

14. No difference was found in the serum sclerostin levels between the hyperthyroidism patients and healthy control.

15. Positivity of RANKL and anti-CCP2 yielded significant risk for progression with negativity for both as reference. No single nucleotide polymorphism encoding TNFSF11 or SOST was associated with increased concentrations of the factors.

16. Osterix and RUNX2 are transcriptional regulators of sclerostin in human bone

17. Sclerostin But Not Dickkopf-1 has roles in increasing prevalence of osteoporotic fracture and lower bone mineral density in postmenopausal Korean women

18. An association was found between rs851054 of the SOST promoter and the fracture rate during childhood osteogenesis imperfecta.

19. High serum levels of sclerostin and Dkk-1 are associated with acute ischaemic stroke

20. The increased expression of sclerostin in the liver and the association with histologic cholangitis may explain the high serum levels of this protein in patients with primary biliary cirrhosis.

Mouse (Murine) Sclerostin (SOST) interaction partners

1. Study demonstrated that sclerostin is expressed in chondrocytes and upregulates the early stage of chondrogenic differentiation in vitro. Furthermore, sclerostin downregulates the expression of markers associated with the late stage of chondrogenic differentiation.

2. Oxygen sensing by PHD2 in osteocytes negatively regulates bone mass through epigenetic regulation of sclerostin and targeting PHD2 elicits an osteo-anabolic response in osteoporotic mouse models.

3. Findings establish mechanical loading-induced attenuation of sclerostin expression and elevation of bone formation along the subchondral bone plate surface as the major mechanisms characterizing subchondral bone phenotypes associated with severe late-stage osteoarthritis in mice

4. 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.

5. Since adipocytes do not produce sclerostin, these findings suggest an unexplored endocrine function for sclerostin that facilitates communication between the skeleton and adipose tissue.

6. 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.

7. osteoclast-derived LIF regulates bone turnover through sclerostin expression.

8. 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

9. These results show that osteocytes and/or osteoblasts secrete factors regulating beige adipogenesis, at least in part, through the Wnt-signaling inhibitor sclerostin.

10. 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

11. 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.

12. 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.

13. Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin

14. Osteocyte-derived molecule sclerostin drives bone marrow adipogenesis.

15. complete absence of sclerostin has only minor effects on chronic kidney disease-induced bone loss in mice.

16. 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.

17. These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.

18. Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt signaling pathway inhibition.

19. 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.

20. removal of sclerostin appears to modestly protect the alveolar bone from resorption in this experimental setting