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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 Kits (49) and Sclerostin Proteins (18) and many more products for this protein.
Showing 10 out of 98 products:
Human Polyclonal Sclerostin Primary Antibody for IHC (p), WB - ABIN390193
Semenov, He: LRP5 mutations linked to high bone mass diseases cause reduced LRP5 binding and inhibition by SOST. in The Journal of biological chemistry 2006
Show all 2 references for ABIN390193
Human Polyclonal Sclerostin Primary Antibody for EIA, IHC (p) - ABIN358751
Ellies, Viviano, McCarthy, Rey, Itasaki, Saunders, Krumlauf: Bone density ligand, Sclerostin, directly interacts with LRP5 but not LRP5G171V to modulate Wnt activity. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2006
Show all 2 references for ABIN358751
Sclerostin is an osteocyte marker that is strongly expressed in human woven and lamellar bone and mineralizing chondrocytes
similar levels in type 1 diabetes patients and controls; decrease concurrent with adolescent growth spurt (show BPIFA1 Antibodies)
Findings indicate that sclerostin expression is closely associated with the degree of joint damage in primary knee osteoarthritis (OA), confirming its involvement in the development of OA.
Results suggest that sclerostin may have a role in the development of or the response to abdominal aortic calcification in chronic kidney disease.
while showing that exercise against bone loss in experimental bed rest results in greater bone formation, could not provide evidence that exercise impeded the rise in serum sclerostin and dickkopf-1 (show DKK1 Antibodies) levels.
serum sclerostin levels were lower in nonalcoholic steatohepatitis patients than in controls.
The aim of this study was to evaluate the renal handling of sclerostin.
Circulating sclerostin and dickkopf-1 (show DKK1 Antibodies) levels in ossification of the posterior longitudinal ligament of the spine.
chronic TNFalpha (tumor necrosis factor alpha (show TNF Antibodies))-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.
Sclerostin levels are elevated in CKD patients and are associated with inflammation, vascular lesions, uremia and (potentially) mortality.
removal of sclerostin appears to modestly protect the alveolar bone from resorption in this experimental setting
Data show that the phenotype of Notch (show NOTCH1 Antibodies) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (show DMP1 Antibodies))-Cre;Rosa(Notch (show NOTCH1 Antibodies)) mice hemizygous for the Dmp1 (show DMP1 Antibodies)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (show TAZ Antibodies)-responsive transcriptional activity and TAZ (show TAZ Antibodies)-responsive gene expression, indicating a role for TAZ (show TAZ Antibodies) 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.
SOST gene is involved in the regulation of renal interstitial fibrosis (RIF) progression. In obstructive kidney injury, SOST gene deletion would probably enhance renal fibrogenic response and promote the progression of RIF.
Data (including data from studies in knockout/transgenic mice) suggest that Lrp6 (lipoprotein receptor-related protein 6 (show LRP6 Antibodies)) is required for suppression of Sost expression by parathyroid hormone (show PTH Antibodies) (here, human PTH (show PTH Antibodies) peptide 1-34).
These in vivo data support in vitro studies regarding the mechanism of HBM (show LRP5 Antibodies)-causing mutations, and imply that HBM LRP5 (show LRP5 Antibodies) receptors differ in their relative sensitivity to inhibition by SOST and DKK1 (show DKK1 Antibodies).
These findings indicated that AMPK (show PRKAA1 Antibodies) regulated RANKL (show TNFSF11 Antibodies) and sclerostin expression through the mevalonate pathway in osteocytes.
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.