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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 53 products:
Human Sclerostin ELISA Kit for Sandwich 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 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 - ABIN426039
Yorgan, Peters, Jeschke, Benisch, Jakob, Amling, Schinke: The Anti-Osteoanabolic Function of Sclerostin Is Blunted in Mice Carrying a High Bone Mass Mutation of Lrp5. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2015
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SOST is expressed in the aorta and downregulated in human aortic aneurysms and atheros (show WNT2 ELISA Kits)clerosis, possibly because of epigenetic silencing.
The level of sclerostin was higher in the female obstructive sleep apnea (OSA) patients than that in female controls. Further, in OSA women with cardiovascular comorbidities, sclerostin was higher than in women without such comorbidities. In men, there were no differences in the serum sclerostin level between the OSA and control subjects, nor was there any relationship with cardiovascular diseases.
Knockdown of SOST in MG-63 cells increases osteogenesis and ratio of OPG/RANKL (show TNFSF11 ELISA Kits) in vitro
The findings confirm that the human SOST gene and sclerostin expression can be considered to be directly 1,25-dihydroxyvitamin D-responsive in osteocytes.
Our study highlighted the high serum levels of DKK-1 (show DKK1 ELISA Kits) and sclerostin in T1DM children and their relationship with altered glycemic control
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.
Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt (show WNT2 ELISA Kits) signaling pathway inhibition.
Analysis of SOST expression using large minigenes reveals the MEF2C (show MEF2C ELISA Kits) binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 (show TGFB1 ELISA Kits) 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 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.
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).
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.