Sclerostin (SOST) ELISA Kits

Human Sclerostin (SOST) interaction partners

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

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

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

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

5. 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%

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

7. 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.

8. SOST gene silencing promotes the proliferation, invasion, and migration, and inhibits apoptosis of osteosarcoma cells by activating Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling pathway

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

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

Mouse (Murine) Sclerostin (SOST) interaction partners

1. The SOST gene inhibited the expression of COL1, OCN, and OPN (show SPP1 ELISA Kits), reduced the activity of alkaline phosphatase, and increased the expression of LPL (show LPL ELISA Kits) and PPARgamma (show PPARG ELISA Kits).

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.

3. A microtubule-dependent mechanotransduction pathway that linked fluid shear stress to reactive oxygen species and calcium (Ca2 (show CA2 ELISA Kits)+) signals that led to a reduction in sclerostin abundance in cultured osteocytes.

4. osteoclast-derived LIF (show LIF ELISA Kits) regulates bone turnover through sclerostin expression.

5. our study provided histological evidences that sclerostin tends to be secreted in osteocytes of remodeled mature bone, while FGF23 (show FGF23 ELISA Kits) would be differently synthesized in osteoblasts and osteocytes according to the developmental stages

6. These results show that osteocytes and/or osteoblasts secrete factors regulating beige (show LYST ELISA Kits) adipogenesis, at least in part, through the Wnt (show WNT2 ELISA Kits)-signaling inhibitor sclerostin.

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 (show GJA1 ELISA Kits)+/-or Sost+/-mice

8. loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL (show TNFSF11 ELISA Kits) and SOST, leading to osteoclast inhibition and Wnt (show WNT2 ELISA Kits) activation together.

9. humanized Multiple Myeloma xenograft mouse model bearing human MM cells (NOD-SCID.CB17 male mice injected intravenously with 2.5 million of MM1 (show PFDN5 ELISA Kits).S-Luc-GFP cells) demonstrated significantly higher concentrations of mouse-derived sclerostin, suggesting a microenvironmental source of sclerostin.

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