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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 (98) und Sclerostin Kits (53) und viele weitere Produktgruppen zu diesem Protein an.
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Human Sclerostin Protein expressed in Human Cells - ABIN2003109
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. in American journal of human genetics 2001
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Rat (Rattus) Sclerostin Protein expressed in Human Cells - ABIN2009022
Balemans, Ebeling, Patel, Van Hul, Olson, Dioszegi, Lacza, Wuyts, Van Den Ende, Willems, Paes-Alves, Hill, Bueno, Ramos, Tacconi, Dikkers, Stratakis, Lindpaintner, Vickery, Foernzler, Van Hul: Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST). in Human molecular genetics 2001
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Circulating sclerostin and Dickkopf-1 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 Proteine)clerosis, possibly because of epigenetic silencing.
The level of sclerostin was higher in the female obstructive sleep apnea (OSA) patients than that in female controls. Further, in OSA women with cardiovascular comorbidities, sclerostin was higher than in women without such comorbidities. In men, there were no differences in the serum sclerostin level between the OSA and control subjects, nor was there any relationship with cardiovascular diseases.
Knockdown of SOST in MG-63 cells increases osteogenesis and ratio of OPG/RANKL (zeige TNFSF11 Proteine) in vitro
The findings confirm that the human SOST gene and sclerostin expression can be considered to be directly 1,25-dihydroxyvitamin D-responsive in osteocytes.
Our study highlighted the high serum levels of DKK-1 (zeige DKK1 Proteine) and sclerostin in T1DM children and their relationship with altered glycemic control
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 (zeige BPIFA1 Proteine)
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.
Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis via wnt (zeige WNT2 Proteine) signaling pathway inhibition.
Analysis of SOST expression using large minigenes reveals the MEF2C (zeige MEF2C Proteine) binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 (zeige TGFB1 Proteine) 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 Proteine))-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 Proteine) activation in osteocytes was prevented in matrix protein 1 (Dmp1 (zeige DMP1 Proteine))-Cre;Rosa(Notch (zeige NOTCH1 Proteine)) mice hemizygous for the Dmp1 (zeige DMP1 Proteine)-sclerostin (SOST) transgene.
Results found that sclerostin enhances adipocyte differentiation in 3T3-L1 cells and reduced TAZ (zeige TAZ Proteine)-responsive transcriptional activity and TAZ (zeige TAZ Proteine)-responsive gene expression, indicating a role for TAZ (zeige TAZ Proteine) 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 (zeige LRP6 Proteine)) is required for suppression of Sost expression by parathyroid hormone (zeige PTH Proteine) (here, human PTH (zeige PTH Proteine) peptide 1-34).
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.