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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 (93) and Sclerostin Proteins (14) and many more products for this protein.
Showing 10 out of 41 products:
Human Sclerostin ELISA Kit for Sandwich ELISA - ABIN415155
Brabnikova Maresova, Pavelka, Stepan: Acute effects of glucocorticoids on serum markers of osteoclasts, osteoblasts, and osteocytes. in Calcified tissue international 2013
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Rat (Rattus) Sclerostin ELISA Kit for Sandwich 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
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Mouse (Murine) Sclerostin ELISA Kit for Sandwich 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
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.
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 ELISA Kits) is responsible for the retention of sclerostin in the bone environment in humans.
higher serum sclerostin levels are associated with higher bone mineral density, lower aortic calcification scores, and a better survival rate in hemodialysis patients
findings suggest that serum TGF-beta1 (show TGFB1 ELISA Kits) level increases during postmenopause and declines in old age. Sclerostin production is inhibited by TGF-beta1 (show TGFB1 ELISA Kits) during early postmenopause
a cell model of human dermal fibroblasts in order to investigate the functions of sclerostin, is reported.
The aims of this study were to evaluate OCN and sclerostin levels in subjects who underwent coronary artery bypass graft (CABG) surgery compared with those in normal controls.
two affected siblings who carried a novel nonsense mutation of SOST in a consanguineous family from China, is reported.
Sclerostin serum levels are not associated with an adverse metabolic profile during pregnancy in women with GDM and PE
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 inhibits bone formation through Lrp5 (show LRP5 ELISA Kits) 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.