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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 (98) et Sclerostin Protéines (18) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 49 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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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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Mouse (Murine) Sclerostin Kit ELISA pour Sandwich ELISA - ABIN1889353
Brunkow, Gardner, Van Ness, Paeper, Kovacevich, Proll, Skonier, Zhao, Sabo, Fu, Alisch, Gillett, Colbert, Tacconi, Galas, Hamersma, Beighton, Mulligan: Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein. dans American journal of human genetics 2001
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Sclerostin is an osteocyte marker that is strongly expressed in human woven and lamellar bone and mineralizing chondrocytes
similar levels in type 1 diabetes patients and controls; decrease concurrent with adolescent growth spurt (Montrer BPIFA1 Kits ELISA)
Findings indicate that sclerostin expression is closely associated with the degree of joint damage in primary knee osteoarthritis (OA), confirming its involvement in the development of OA.
Results suggest that sclerostin may have a role in the development of or the response to abdominal aortic calcification in chronic kidney disease.
while showing that exercise against bone loss in experimental bed rest results in greater bone formation, could not provide evidence that exercise impeded the rise in serum sclerostin and dickkopf-1 (Montrer DKK1 Kits ELISA) levels.
serum sclerostin levels were lower in nonalcoholic steatohepatitis patients than in controls.
The aim of this study was to evaluate the renal handling of sclerostin.
Circulating sclerostin and dickkopf-1 (Montrer DKK1 Kits ELISA) levels in ossification of the posterior longitudinal ligament of the spine.
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.
Sclerostin levels are elevated in CKD patients and are associated with inflammation, vascular lesions, uremia and (potentially) mortality.
removal of sclerostin appears to modestly protect the alveolar bone from resorption in this experimental setting
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.
SOST gene is involved in the regulation of renal interstitial fibrosis (RIF) progression. In obstructive kidney injury, SOST gene deletion would probably enhance renal fibrogenic response and promote the progression of RIF.
Data (including data from studies in knockout/transgenic mice) suggest that Lrp6 (lipoprotein receptor-related protein 6 (Montrer LRP6 Kits ELISA)) is required for suppression of Sost expression by parathyroid hormone (Montrer PTH Kits ELISA) (here, human PTH (Montrer PTH Kits ELISA) peptide 1-34).
These in vivo data support in vitro studies regarding the mechanism of HBM (Montrer LRP5 Kits ELISA)-causing mutations, and imply that HBM LRP5 (Montrer LRP5 Kits ELISA) receptors differ in their relative sensitivity to inhibition by SOST and DKK1 (Montrer DKK1 Kits ELISA).
These findings indicated that AMPK (Montrer PRKAA1 Kits ELISA) regulated RANKL (Montrer TNFSF11 Kits ELISA) and sclerostin expression through the mevalonate pathway in osteocytes.
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.