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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 (63) und Sclerostin Proteine (18) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal Sclerostin Primary Antibody für EIA, IHC (p) - ABIN358751
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 IHC (p), WB - ABIN390193
Lin, Lin, Chang, Wang, Lai: Single-pulsed electromagnetic field therapy increases osteogenic differentiation through Wnt signaling pathway and sclerostin downregulation. in Bioelectromagnetics 2015
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High serum levels of sclerostin and Dkk-1 (zeige DKK1 Antikörper) are associated with acute ischaemic stroke
The increased expression of sclerostin in the liver and the association with histologic cholangitis may explain the high serum levels of this protein in patients with primary biliary cirrhosis.
SOST silencing promotes the proliferation, invasion and migration, and decreases the apoptosis of human retinoblastoma cells by activating the Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling pathway.
Sclerostin concentrations in serum significantly decreased and IGF-I (zeige IGF1 Antikörper) significantly increased after 12months of resistance training or JUMP.
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.
loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL (zeige TNFSF11 Antikörper) and SOST, leading to osteoclast inhibition and Wnt (zeige WNT2 Antikörper) activation together.
humanized Multiple Myeloma xenograft mouse model bearing human MM cells (NOD-SCID.CB17 male mice injected intravenously with 2.5 million of MM1 (zeige PFDN5 Antikörper).S-Luc-GFP cells) demonstrated significantly higher concentrations of mouse-derived sclerostin, suggesting a microenvironmental source of sclerostin.
Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin
Osteocyte-derived molecule sclerostin drives bone marrow adipogenesis.
complete absence of sclerostin has only minor effects on chronic kidney disease-induced bone loss in mice.
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.
These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.
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
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.