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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. De plus, nous expédions Sclerostin Anticorps (128) et Sclerostin Protéines (18) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 57 products:
Human Sclerostin Kit ELISA pour Sandwich ELISA - ABIN457071
Cidem, Usta, Karacan, Kucuk, Uludag, Gun: Effects of sex steroids on serum sclerostin levels during the menstrual cycle. dans Gynecologic and obstetric investigation 2013
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Human Sclerostin Kit ELISA pour Sandwich ELISA - ABIN415155
Brabnikova Maresova, Pavelka, Stepan: Acute effects of glucocorticoids on serum markers of osteoclasts, osteoblasts, and osteocytes. dans Calcified tissue international 2013
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Mouse (Murine) Sclerostin Kit ELISA pour 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. dans Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2015
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Rat (Rattus) Sclerostin Kit ELISA pour 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. dans Life sciences 2013
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Rat (Rattus) Sclerostin Kit ELISA pour Sandwich ELISA - ABIN585201
Ferreira, Ferrari, Neves, Cavallari, Dominguez, Dos Reis, Graciolli, Oliveira, Liu, Sabbagh, Jorgetti, Schiavi, Moysés: Effects of dietary phosphate on adynamic bone disease in rats with chronic kidney disease--role of sclerostin? dans PLoS ONE 2013
observed an association between sclerostin levels with fasting insulin (Montrer INS Kits ELISA) levels and homoeostatic model assessment-insulin (Montrer INS Kits ELISA) resistance, but there was no clear association with type 2 diabetes risk.
Sclerostin levels in KTR are normal and influenced more by bone turnover than by eGFR (Montrer EGFR Kits ELISA). Its involvement with other hormones of mineral homeostasis (FGF23 (Montrer FGF23 Kits ELISA)/Klotho (Montrer KL Kits ELISA) and Vitamin D) is part of the sophisticated cross-talk between bone and the kidney
In chronic kidney disease, serum levels of the Wnt (Montrer WNT2 Kits ELISA) inhibitors DKK1 (Montrer DKK1 Kits ELISA) and sclerostin are unrelated, indicating different sites of origin and/ or different regulatory mechanisms. Sclerostin, as opposed to DKK1 (Montrer DKK1 Kits ELISA), may qualify as a biomarker of chronic kidney disease-mineral and bone and mineral disorder (CKD-MBD (Montrer DPEP1 Kits ELISA)), particularly in dialysis patients.
Vitamin D receptor (Montrer VDR Kits ELISA) agonism by paricalcitol causes a moderate increase in serum sclerostin in CKD patients, and this effect is modified by circulating pentosidine levels.
SOST is frequently expressed in skeletal bone- and cartilage-forming tumors. The strong spatial correlation with bone formation and the in vitro expression patterns are in line with the known functions of SOST in nonneoplastic bone, as a feedback inhibitor on osteogenic differentiation.
Intermittent compressive stress regulates Notch (Montrer NOTCH1 Kits ELISA) receptor and target gene expression via the TGF-beta (Montrer TGFB1 Kits ELISA) signaling pathway. Notch (Montrer NOTCH1 Kits ELISA) signaling participates in TGF-beta (Montrer TGFB1 Kits ELISA)-induced sclerostin expression in periodontal ligament cells.
Dickkopf-1 (Montrer DKK1 Kits ELISA) and sclerostin were never correlated with each other or with bone turnover markers patients with Paget's disease of bone. Sclerostin was positively correlated with age.
These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.
Circulating sclerostin and Dickkopf-1 (Montrer DKK1 Kits ELISA) levels do not change across the menstrual cycle and do not demonstrate any relationship with estradiol in premenopausal women.
SOST is expressed in the aorta and downregulated in human aortic aneurysms and atheros (Montrer WNT2 Kits ELISA)clerosis, possibly because of epigenetic silencing.
In mice, sclerostin deficiency hastened reparative dentinogenesis after pulp injury, suggesting that the inhibition of sclerostin may constitute a promising therapeutic strategy for improving the healing of damaged pulps.
Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt (Montrer WNT2 Kits ELISA) signaling pathway inhibition.
Analysis of SOST expression using large minigenes reveals the MEF2C (Montrer MEF2C Kits ELISA) binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 (Montrer TGFB1 Kits ELISA) responsiveness.
removal of sclerostin appears to modestly protect the alveolar bone from resorption in this experimental setting
chronic TNFalpha (tumor necrosis factor alpha (Montrer TNF Kits ELISA))-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 (Montrer NOTCH1 Kits ELISA) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (Montrer DMP1 Kits ELISA))-Cre;Rosa(Notch (Montrer NOTCH1 Kits ELISA)) mice hemizygous for the Dmp1 (Montrer DMP1 Kits ELISA)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (Montrer TAZ Kits ELISA)-responsive transcriptional activity and TAZ (Montrer TAZ Kits ELISA)-responsive gene expression, indicating a role for TAZ (Montrer TAZ Kits ELISA) 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.
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.