SOST

(redirected from Sclerostin)
Also found in: Medical, Wikipedia.
AcronymDefinition
SOSTSclerostin
SOSTSclerosteosis
SOSTSpecial Operations Science and Technology (ammunition)
SOSTSymphony of Southeast Texas
SOSTSpecial Operator Service Treatment
SOSTSpecial Operations Surgical Team
SOSTSite Operator Specific Training
SOSTStandard Operations Solutions Team
References in periodicals archive ?
High circulating sclerostin is present in patients with thalassemia-associated osteoporosis and correlates with bone mineral density.
NMR based studies have shown that sclerostin, like the cytokine, is characterised by regions that show significant flexibility.
Sclerostin antibody prevents particle-induced implant loosening by stimulating bone formation and inhibiting bone resorption in a rat model.
Hypoxia decreases sclerostin expression and increases Wnt signaling in osteoblasts.
The Wnt pathway inhibitor sclerostin has been also discussed as a therapeutic target for cancer-related bone disease.
We hypothesize that low bone turnover associated with low levels of serum OC (caused by low formation), in the presence of high serum sclerostin, is also associated with poor glycemic control in older Hispanic patients suffering from T2D.
Jones et al., "Serum leptin, parathyroid hormone, 1,25-dihydroxyvitamin D, fibroblast growth factor 23, bone alkaline phosphatase, and sclerostin relationships in obesity," The Journal of Clinical Endocrinology & Metabolism, vol.
Garcia-Ibarbia et al., "Osterix and RUNX2 are transcriptional regulators of sclerostin in human bone," Calcified Tissue International, vol.
Recently, the role of the Wnt/[beta]-catenin pathway and its inhibitors, Dikkopf and sclerostin, has been evaluated in AS pathogenesis to identify a possible link with bone formation [9-11].
PTH would increase bone mass by increasing the recruitment and activation of BMU (basic multicellular units), which operates in conjunction with the osteoblast precursors to promote their differentiation, inhibiting apoptosis of osteoblasts and osteocytes (Jilka, 2007) and the production of the bone formation inhibitor sclerostin (Keller & Kneissel, 2005).
Pathologic bone formation in AS might be due to molecular dysfunction of certain other protein biomarkers, for example, Sclerostin and Dkk-1, at the cellular level [54].
Carboxyterminal type I collagen cross links (CTX-I) for bone degradation products, human type I procollagen amino terminal propeptide (P1NP, Sunred Biological Technology) for bone formation, sclerostin (SOST), osteoprotegerin (OPG), Dickkopf-related protein-1 (DKK1), and soluble RANKL (ampli-sRANKL, Biomedica Gruppe) were analyzed with enzyme-linked immunosorbent assay [14] in serum samples according to the manufacturer's instructions.