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Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Additionally we are shipping Sclerostin Antibodies (128) and Sclerostin Kits (64) and many more products for this protein.
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Positivity of RANKL (show TNFSF11 Proteins) and anti-CCP2 yielded significant risk for progression with negativity for both as reference. No single nucleotide polymorphism encoding TNFSF11 (show TNFSF11 Proteins) or SOST was associated with increased concentrations of the factors.
Osterix (show SP7 Proteins) and RUNX2 (show RUNX2 Proteins) are transcriptional regulators of sclerostin in human bone
Sclerostin But Not Dickkopf-1 has roles in increasing prevalence of osteoporotic fracture and lower bone mineral density in postmenopausal Korean women
An association was found between rs851054 of the SOST promoter and the fracture rate during childhood osteogenesis imperfecta (show COL1A2 Proteins).
High serum levels of sclerostin and Dkk-1 (show DKK1 Proteins) are associated with acute ischaemic stroke
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.
SOST silencing promotes the proliferation, invasion and migration, and decreases the apoptosis of human retinoblastoma cells by activating the Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling pathway.
Sclerostin concentrations in serum significantly decreased and IGF-I (show IGF1 Proteins) significantly increased after 12months of resistance training or JUMP.
observed an association between sclerostin levels with fasting insulin (show INS Proteins) levels and homoeostatic model assessment-insulin (show INS Proteins) resistance, but there was no clear association with type 2 diabetes risk.
Sclerostin levels in KTR are normal and influenced more by bone turnover than by eGFR (show EGFR Proteins). Its involvement with other hormones of mineral homeostasis (FGF23 (show FGF23 Proteins)/Klotho (show KL Proteins) and Vitamin D) is part of the sophisticated cross-talk between bone and the kidney
These results show that osteocytes and/or osteoblasts secrete factors regulating beige adipogenesis, at least in part, through the Wnt (show WNT2 Proteins)-signaling inhibitor sclerostin.
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 Proteins)+/-or Sost+/-mice
loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL (show TNFSF11 Proteins) and SOST, leading to osteoclast inhibition and Wnt (show WNT2 Proteins) activation together.
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 Proteins).S-Luc-GFP cells) demonstrated significantly higher concentrations of mouse-derived sclerostin, suggesting a microenvironmental source of sclerostin.
Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin
Osteocyte-derived molecule sclerostin drives bone marrow adipogenesis.
complete absence of sclerostin has only minor effects on chronic kidney disease-induced bone loss in mice.
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.
These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.
Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt (show WNT2 Proteins) signaling pathway inhibition.
Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Loss-of-function mutations in this gene are associated with an autosomal-recessive disorder, sclerosteosis, which causes progressive bone overgrowth. A deletion downstream of this gene, which causes reduced sclerostin expression, is associated with a milder form of the disorder called van Buchem disease.