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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. 再加上，我们可以发Sclerostin 抗体 (98) 和 Sclerostin 蛋白 (18)和数多这个蛋白质的别的产品。
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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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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 (显示 BPIFA1 ELISA试剂盒)
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 (显示 DKK1 ELISA试剂盒) 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 (显示 DKK1 ELISA试剂盒) levels in ossification of the posterior longitudinal ligament of the spine.
chronic TNFalpha (tumor necrosis factor alpha (显示 TNF ELISA试剂盒))-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 (显示 NOTCH1 ELISA试剂盒) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (显示 DMP1 ELISA试剂盒))-Cre;Rosa(Notch (显示 NOTCH1 ELISA试剂盒)) mice hemizygous for the Dmp1 (显示 DMP1 ELISA试剂盒)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (显示 TAZ ELISA试剂盒)-responsive transcriptional activity and TAZ (显示 TAZ ELISA试剂盒)-responsive gene expression, indicating a role for TAZ (显示 TAZ ELISA试剂盒) 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 (显示 LRP6 ELISA试剂盒)) is required for suppression of Sost expression by parathyroid hormone (显示 PTH ELISA试剂盒) (here, human PTH (显示 PTH ELISA试剂盒) peptide 1-34).
These in vivo data support in vitro studies regarding the mechanism of HBM (显示 LRP5 ELISA试剂盒)-causing mutations, and imply that HBM LRP5 (显示 LRP5 ELISA试剂盒) receptors differ in their relative sensitivity to inhibition by SOST and DKK1 (显示 DKK1 ELISA试剂盒).
These findings indicated that AMPK (显示 PRKAA1 ELISA试剂盒) regulated RANKL (显示 TNFSF11 ELISA试剂盒) 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.