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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 (96) and Sclerostin Kits (44) and many more products for this protein.
Showing 10 out of 18 products:
Rat (Rattus) Sclerostin Protein expressed in Human Cells - ABIN2009022
Brunkow, Gardner, Van Ness, Paeper, Kovacevich, Proll, Skonier, Zhao, Sabo, Fu, Alisch, Gillett, Colbert, Tacconi, Galas, Hamersma, Beighton, Mulligan: Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein. in American journal of human genetics 2001
Show all 5 references for ABIN2009022
Human Sclerostin Protein expressed in Human Cells - ABIN2003109
Balemans, Ebeling, Patel, Van Hul, Olson, Dioszegi, Lacza, Wuyts, Van Den Ende, Willems, Paes-Alves, Hill, Bueno, Ramos, Tacconi, Dikkers, Stratakis, Lindpaintner, Vickery, Foernzler, Van Hul: Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST). in Human molecular genetics 2001
Show all 5 references for ABIN2003109
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 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 levels in ossification of the posterior longitudinal ligament of the spine.
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.
Sclerostin levels are elevated in CKD patients and are associated with inflammation, vascular lesions, uremia and (potentially) mortality.
Our data also demonstrated that vitamin D deficient newborns exhibited lower sclerostin levels than vitamin D sufficient newborns.
the first evidence suggesting that LRP4 (show LRP4 Proteins) is responsible for the retention of sclerostin in the bone environment in humans.
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.
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 Proteins)) is required for suppression of Sost expression by parathyroid hormone (show PTH Proteins) (here, human PTH (show PTH Proteins) peptide 1-34).
These in vivo data support in vitro studies regarding the mechanism of HBM (show LRP5 Proteins)-causing mutations, and imply that HBM LRP5 (show LRP5 Proteins) receptors differ in their relative sensitivity to inhibition by SOST and DKK1 (show DKK1 Proteins).
These findings indicated that AMPK (show PRKAA1 Proteins) regulated RANKL (show TNFSF11 Proteins) and sclerostin expression through the mevalonate pathway in osteocytes.
Sclerostin inhibits bone formation through Lrp5 (show LRP5 Proteins) interaction.
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.