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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. Zusätzlich bieten wir Ihnen Sclerostin Antikörper (128) und Sclerostin Proteine (18) und viele weitere Produktgruppen zu diesem Protein an.
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Human Sclerostin ELISA Kit für 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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Human Sclerostin ELISA Kit für 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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Mouse (Murine) Sclerostin ELISA Kit für 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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Rat (Rattus) Sclerostin ELISA Kit für 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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Rat (Rattus) Sclerostin ELISA Kit für 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? in PLoS ONE 2013
observed an association between sclerostin levels with fasting insulin (zeige INS ELISA Kits) levels and homoeostatic model assessment-insulin (zeige INS ELISA Kits) 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 (zeige EGFR ELISA Kits). Its involvement with other hormones of mineral homeostasis (FGF23 (zeige FGF23 ELISA Kits)/Klotho (zeige KL ELISA Kits) and Vitamin D) is part of the sophisticated cross-talk between bone and the kidney
In chronic kidney disease, serum levels of the Wnt (zeige WNT2 ELISA Kits) inhibitors DKK1 (zeige DKK1 ELISA Kits) and sclerostin are unrelated, indicating different sites of origin and/ or different regulatory mechanisms. Sclerostin, as opposed to DKK1 (zeige DKK1 ELISA Kits), may qualify as a biomarker of chronic kidney disease-mineral and bone and mineral disorder (CKD-MBD (zeige DPEP1 ELISA Kits)), particularly in dialysis patients.
Vitamin D receptor (zeige VDR ELISA Kits) 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 (zeige NOTCH1 ELISA Kits) receptor and target gene expression via the TGF-beta (zeige TGFB1 ELISA Kits) signaling pathway. Notch (zeige NOTCH1 ELISA Kits) signaling participates in TGF-beta (zeige TGFB1 ELISA Kits)-induced sclerostin expression in periodontal ligament cells.
Dickkopf-1 (zeige DKK1 ELISA Kits) 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 (zeige DKK1 ELISA Kits) 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 (zeige WNT2 ELISA Kits)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 (zeige WNT2 ELISA Kits) signaling pathway inhibition.
Analysis of SOST expression using large minigenes reveals the MEF2C (zeige MEF2C ELISA Kits) binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 (zeige 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 (zeige 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 (zeige NOTCH1 ELISA Kits) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (zeige DMP1 ELISA Kits))-Cre;Rosa(Notch (zeige NOTCH1 ELISA Kits)) mice hemizygous for the Dmp1 (zeige DMP1 ELISA Kits)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (zeige TAZ ELISA Kits)-responsive transcriptional activity and TAZ (zeige TAZ ELISA Kits)-responsive gene expression, indicating a role for TAZ (zeige 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.
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.