Sclerostin (SOST) ELISA Kits

Human Sclerostin (SOST) interaction partners

1. Serum levels of sclerostin, but not Dickkopf-1, are positively correlated with carotid-femoral pulse wave velocity and independently predict aortic stiffness in patients with type 2 diabetes mellitus.

2. natural variation in SOST gene is not a major contributor to the observed variability in peak BMD in Chinese male-offspring nuclear families.

3. the expressions of serum DKK-1 and sclerostin in ankylosing spondylitis patients were independent of disease activity. Sclerostin was negatively correlated with the mSASSS, which suggests that sclerostin may be a potential marker indicating the spine ossification process in ankylosing spondylitis.

4. sclerostin promotes breast cancer cell migration, invasion and bone osteolysis. Inhibition of sclerostin may serve as an efficient strategy for interventions against breast cancer bone metastasis or osteolytic bone diseases.

5. Elevated serum sclerostin levels were found to be independent risk factors for the development of arterial stiffness in hypertensive patients.

6. Study showed no significant response in serum concentrations of sclerostin and biochemical markers of bone formation and resorption related to an acute bout of plyometric jump exercise.

7. the addition of whole-body vibration exposures prior to high intensity resistance exercise (RE) did not alter sclerostin and PTH responses to RE in young women.

8. high sclerostin levels are related to mortality due to cardiovascular causes.

9. These findings uncover the biological consequences of four independent genetic variants in the SOST region.

10. Serum was analyzed for sclerostin, cross linked telopeptide of type I collagen (CTXI), and procollagen type I amino-terminal propeptide (PINP). A significant time effect was found for sclerostin, which increased from pre-exercise to 5 min after exercise in both trials

11. Declining serum SOST levels are associated with greater carotid intima-media thickness (CIMT) in patients with chronic kidney disease-mineral and bone disorder (CKD-MBD).

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

13. 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.

14. 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.

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

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

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

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

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

20. 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.

Mouse (Murine) Sclerostin (SOST) interaction partners

1. Sost deficiency led to a greater cortical bone formation response to mechanical loading and altered gene expression

2. 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.

3. 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.

4. 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

5. 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.

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

7. 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.

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

9. 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

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

11. 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

12. 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.

13. 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.

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

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

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

17. 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.

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

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

20. 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.