Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
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.
Showing 10 out of 21 products:
In our cohort of pregnant women, sclerostin and DKK1 (zeige DKK1 Proteine) were not associated with any adverse metabolic profile, and possibly do not play relevant roles in the pathophysiology of gestational diabetes mellitus.
Sclerostin increased after exercise in comparison to baseline (mean +/- SEM: 410 +/- 27 vs. 290 +/- 19 pg/mL; p < 0.001) corresponding to an increase of +44.3 +/-5.5%
serum sclerostin levels correlated positively with carotid intima-media thickness and inversely with the augmentation index, a marker of arterial stiffness
The difference of serum sclerostin levels in Ankylosing Spondylitis and Rheumatoid Arthritis patients was not significantly different from HC, indicating that the sclerostin may not associate with the development of Ankylosing Spondylitis and Rheumatoid Arthritis.
SOST gene silencing promotes the proliferation, invasion, and migration, and inhibits apoptosis of osteosarcoma cells by activating Wnt (zeige WNT2 Proteine)/beta-catenin (zeige CTNNB1 Proteine) signaling pathway
No difference was found in the serum sclerostin levels between the hyperthyroidism patients and healthy control.
Positivity of RANKL (zeige TNFSF11 Proteine) and anti-CCP2 yielded significant risk for progression with negativity for both as reference. No single nucleotide polymorphism encoding TNFSF11 (zeige TNFSF11 Proteine) or SOST was associated with increased concentrations of the factors.
Osterix (zeige SP7 Proteine) and RUNX2 (zeige RUNX2 Proteine) are transcriptional regulators of sclerostin in human bone
Sclerostin But Not Dickkopf-1 has roles in increasing prevalence of osteoporotic fracture and lower bone mineral density in postmenopausal Korean women
An association was found between rs851054 of the SOST promoter and the fracture rate during childhood osteogenesis imperfecta (zeige COL1A2 Proteine).
A microtubule-dependent mechanotransduction pathway that linked fluid shear stress to reactive oxygen species and calcium (Ca2 (zeige CA2 Proteine)+) signals that led to a reduction in sclerostin abundance in cultured osteocytes.
osteoclast-derived LIF (zeige LIF Proteine) regulates bone turnover through sclerostin expression.
our study provided histological evidences that sclerostin tends to be secreted in osteocytes of remodeled mature bone, while FGF23 (zeige FGF23 Proteine) would be differently synthesized in osteoblasts and osteocytes according to the developmental stages
These results show that osteocytes and/or osteoblasts secrete factors regulating beige adipogenesis, at least in part, through the Wnt (zeige WNT2 Proteine)-signaling inhibitor sclerostin.
In vivo muCT analysis of cortical bone at age 1 and 3 months confirmed increased thickness in Sost-/-mice, but revealed no cortical abnormalities in single Gja1 (zeige GJA1 Proteine)+/-or Sost+/-mice
loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL (zeige TNFSF11 Proteine) and SOST, leading to osteoclast inhibition and Wnt (zeige WNT2 Proteine) 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 Proteine).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.
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.