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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 (98) and Sclerostin Proteins (18) and many more products for this protein.
Showing 10 out of 49 products:
Human Sclerostin Primary Antibody for ELISA - ABIN457071
Cidem, Usta, Karacan, Kucuk, Uludag, Gun: Effects of sex steroids on serum sclerostin levels during the menstrual cycle. in Gynecologic and obstetric investigation 2013
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Rat (Rattus) Sclerostin Primary Antibody for ELISA - ABIN416496
Kim, Lee, Jo, Song, Lim, Park, Bonewald, Kim: Exendin-4 increases bone mineral density in type 2 diabetic OLETF rats potentially through the down-regulation of SOST/sclerostin in osteocytes. in Life sciences 2013
Show all 2 references for ABIN416496
Mouse (Murine) Sclerostin Primary Antibody for ELISA - ABIN1889353
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 2 references for ABIN1889353
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 ELISA Kits)
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 ELISA Kits) 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 ELISA Kits) levels in ossification of the posterior longitudinal ligament of the spine.
chronic TNFalpha (tumor necrosis factor alpha (show TNF ELISA Kits))-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 ELISA Kits) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (show DMP1 ELISA Kits))-Cre;Rosa(Notch (show NOTCH1 ELISA Kits)) mice hemizygous for the Dmp1 (show DMP1 ELISA Kits)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (show TAZ ELISA Kits)-responsive transcriptional activity and TAZ (show TAZ ELISA Kits)-responsive gene expression, indicating a role for TAZ (show TAZ ELISA Kits) 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 ELISA Kits)) is required for suppression of Sost expression by parathyroid hormone (show PTH ELISA Kits) (here, human PTH (show PTH ELISA Kits) peptide 1-34).
These in vivo data support in vitro studies regarding the mechanism of HBM (show LRP5 ELISA Kits)-causing mutations, and imply that HBM LRP5 (show LRP5 ELISA Kits) receptors differ in their relative sensitivity to inhibition by SOST and DKK1 (show DKK1 ELISA Kits).
These findings indicated that AMPK (show PRKAA1 ELISA Kits) regulated RANKL (show TNFSF11 ELISA Kits) 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.