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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 Kits (57) und Sclerostin Proteine (18) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal Sclerostin Primary Antibody für IHC (p), WB - ABIN390193
Semenov, He: LRP5 mutations linked to high bone mass diseases cause reduced LRP5 binding and inhibition by SOST. in The Journal of biological chemistry 2006
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Human Polyclonal Sclerostin Primary Antibody für EIA, IHC (p) - ABIN358751
Ellies, Viviano, McCarthy, Rey, Itasaki, Saunders, Krumlauf: Bone density ligand, Sclerostin, directly interacts with LRP5 but not LRP5G171V to modulate Wnt activity. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2006
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observed an association between sclerostin levels with fasting insulin (zeige INS Antikörper) levels and homoeostatic model assessment-insulin (zeige INS Antikörper) 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 Antikörper). Its involvement with other hormones of mineral homeostasis (FGF23 (zeige FGF23 Antikörper)/Klotho (zeige KL Antikörper) 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 Antikörper) inhibitors DKK1 (zeige DKK1 Antikörper) and sclerostin are unrelated, indicating different sites of origin and/ or different regulatory mechanisms. Sclerostin, as opposed to DKK1 (zeige DKK1 Antikörper), may qualify as a biomarker of chronic kidney disease-mineral and bone and mineral disorder (CKD-MBD (zeige DPEP1 Antikörper)), particularly in dialysis patients.
Vitamin D receptor (zeige VDR Antikörper) 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 Antikörper) receptor and target gene expression via the TGF-beta (zeige TGFB1 Antikörper) signaling pathway. Notch (zeige NOTCH1 Antikörper) signaling participates in TGF-beta (zeige TGFB1 Antikörper)-induced sclerostin expression in periodontal ligament cells.
Dickkopf-1 (zeige DKK1 Antikörper) 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 Antikörper) 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 Antikörper)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 Antikörper) signaling pathway inhibition.
Analysis of SOST expression using large minigenes reveals the MEF2C (zeige MEF2C Antikörper) binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 (zeige TGFB1 Antikörper) 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 Antikörper))-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 Antikörper) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (zeige DMP1 Antikörper))-Cre;Rosa(Notch (zeige NOTCH1 Antikörper)) mice hemizygous for the Dmp1 (zeige DMP1 Antikörper)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (zeige TAZ Antikörper)-responsive transcriptional activity and TAZ (zeige TAZ Antikörper)-responsive gene expression, indicating a role for TAZ (zeige TAZ Antikörper) 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.