Sclerostin (SOST) ELISA Kits

Human Sclerostin (SOST) interaction partners

1. 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%

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

3. 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.

4. 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

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

6. 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.

7. Osterix (show SP7 ELISA Kits) and RUNX2 (show RUNX2 ELISA Kits) are transcriptional regulators of sclerostin in human bone

8. Sclerostin But Not Dickkopf-1 (show DKK1 ELISA Kits) has roles in increasing prevalence of osteoporotic fracture and lower bone mineral density in postmenopausal Korean women

9. An association was found between rs851054 of the SOST promoter and the fracture rate during childhood osteogenesis imperfecta (show COL1A2 ELISA Kits).

10. High serum levels of sclerostin and Dkk-1 (show DKK1 ELISA Kits) are associated with acute ischaemic stroke

Mouse (Murine) Sclerostin (SOST) interaction partners

1. 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.

2. 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

3. 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.

4. 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.

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

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

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

8. 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.

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

10. Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt (show WNT2 ELISA Kits) signaling pathway inhibition.