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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 Kits (57) et Sclerostin Protéines (18) et beaucoup plus de produits pour cette protéine.
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Human Polyclonal Sclerostin Primary Antibody pour IHC (p), WB - ABIN390193
Semenov, He: LRP5 mutations linked to high bone mass diseases cause reduced LRP5 binding and inhibition by SOST. dans The Journal of biological chemistry 2006
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Human Polyclonal Sclerostin Primary Antibody pour 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. dans 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 (Montrer INS Anticorps) levels and homoeostatic model assessment-insulin (Montrer INS Anticorps) 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 Anticorps). Its involvement with other hormones of mineral homeostasis (FGF23 (Montrer FGF23 Anticorps)/Klotho (Montrer KL Anticorps) 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 Anticorps) inhibitors DKK1 (Montrer DKK1 Anticorps) and sclerostin are unrelated, indicating different sites of origin and/ or different regulatory mechanisms. Sclerostin, as opposed to DKK1 (Montrer DKK1 Anticorps), may qualify as a biomarker of chronic kidney disease-mineral and bone and mineral disorder (CKD-MBD (Montrer DPEP1 Anticorps)), particularly in dialysis patients.
Vitamin D receptor (Montrer VDR Anticorps) 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 Anticorps) receptor and target gene expression via the TGF-beta (Montrer TGFB1 Anticorps) signaling pathway. Notch (Montrer NOTCH1 Anticorps) signaling participates in TGF-beta (Montrer TGFB1 Anticorps)-induced sclerostin expression in periodontal ligament cells.
Dickkopf-1 (Montrer DKK1 Anticorps) 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 Anticorps) 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 Anticorps)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 Anticorps) signaling pathway inhibition.
Analysis of SOST expression using large minigenes reveals the MEF2C (Montrer MEF2C Anticorps) binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 (Montrer TGFB1 Anticorps) 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 Anticorps))-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 Anticorps) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (Montrer DMP1 Anticorps))-Cre;Rosa(Notch (Montrer NOTCH1 Anticorps)) mice hemizygous for the Dmp1 (Montrer DMP1 Anticorps)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (Montrer TAZ Anticorps)-responsive transcriptional activity and TAZ (Montrer TAZ Anticorps)-responsive gene expression, indicating a role for TAZ (Montrer TAZ Anticorps) 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.