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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 (57) and many more products for this protein.
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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
In chronic kidney disease, serum levels of the Wnt (show WNT2 Proteins) inhibitors DKK1 (show DKK1 Proteins) and sclerostin are unrelated, indicating different sites of origin and/ or different regulatory mechanisms. Sclerostin, as opposed to DKK1 (show DKK1 Proteins), may qualify as a biomarker of chronic kidney disease-mineral and bone and mineral disorder (CKD-MBD (show DPEP1 Proteins)), particularly in dialysis patients.
Vitamin D receptor (show VDR Proteins) agonism by paricalcitol causes a moderate increase in serum sclerostin in CKD patients, and this effect is modified by circulating pentosidine levels.
SOST is frequently expressed in skeletal bone- and cartilage-forming tumors. The strong spatial correlation with bone formation and the in vitro expression patterns are in line with the known functions of SOST in nonneoplastic bone, as a feedback inhibitor on osteogenic differentiation.
Intermittent compressive stress regulates Notch (show NOTCH1 Proteins) receptor and target gene expression via the TGF-beta (show TGFB1 Proteins) signaling pathway. Notch (show NOTCH1 Proteins) signaling participates in TGF-beta (show TGFB1 Proteins)-induced sclerostin expression in periodontal ligament cells.
Dickkopf-1 (show DKK1 Proteins) and sclerostin were never correlated with each other or with bone turnover markers patients with Paget's disease of bone. Sclerostin was positively correlated with age.
These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.
Circulating sclerostin and Dickkopf-1 levels do not change across the menstrual cycle and do not demonstrate any relationship with estradiol in premenopausal women.
SOST is expressed in the aorta and downregulated in human aortic aneurysms and atheros (show WNT2 Proteins)clerosis, possibly because of epigenetic silencing.
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.
Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt (show WNT2 Proteins) signaling pathway inhibition.
Analysis of SOST expression using large minigenes reveals the MEF2C (show MEF2C Proteins) binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 (show TGFB1 Proteins) responsiveness.
removal of sclerostin appears to modestly protect the alveolar bone from resorption in this experimental setting
chronic TNFalpha (tumor necrosis factor alpha (show TNF Proteins))-dependent arthritis, fibroblast-like synoviocytes constitute a major source of sclerostin and that either the lack of sclerostin or its antibody-mediated inhibition leads to an acceleration of rheumatoid arthritis (RA)-like disease.
Data show that the phenotype of Notch (show NOTCH1 Proteins) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (show DMP1 Proteins))-Cre;Rosa(Notch (show NOTCH1 Proteins)) mice hemizygous for the Dmp1 (show DMP1 Proteins)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (show TAZ Proteins)-responsive transcriptional activity and TAZ (show TAZ Proteins)-responsive gene expression, indicating a role for TAZ (show TAZ Proteins) as a regulator of adipogenesis by sclerostin.
Our results suggested that sclerostin could be expressed in the liver and sustained successfully at high levels in the blood by using the PhiC31 integrase system, leading to trabecular bone loss.
Sclerostin depletion enhances tibial fracture healing.
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.