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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


sclerostin, SOST
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: fibrillin-1, AGE, DKK1, HAD, CAN
Papers using sclerostin antibodies
Inhibition of sclerostin by monoclonal antibody enhances bone healing and improves bone density and strength of non-fractured bones
Shore Paul et al., In Breast Cancer Research : BCR, 2010
... sclerostin from the conditioned media was carried out incubating the media with 4 μg of the sclerostin (Ab63097, Abcam, Cambridge, UK) or Flag ...
Osteocyte Wnt/beta-catenin signaling is required for normal bone homeostasis
Bellido Teresita et al., In Journal of Bone and Mineral Research, 2009
... Generation of DMP1-caPTHR1 and DMP-Sost transgenic mice and crosses with ...
Parathyroid hormone signaling through low-density lipoprotein-related protein 6
Kneissel Michaela et al., In Journal of Bone and Mineral Research, 2007
... SOST bacterial artificial chromosome (BAC) transgenic ( ...
Papers on sclerostin
Early and sustained changes in bone metabolism after severe burn injury.
Muschitz et al., Vienna, Austria. In J Clin Endocrinol Metab, Feb 2016
During the early phase pronounced increases were observed for CTX, P1NP, sclerostin, DKK-1, BALP, FGF23 and iPTH levels, whereas 25-OH vitamin D, albumin, serum and ionized calcium levels decreased.
Rictor is required for optimal bone accrual in response to anti-sclerostin therapy in the mouse.
Long et al., Nanjing, China. In Bone, Feb 2016
Neutralizing antibodies against the secreted Wnt antagonist sclerostin (Scl-Ab) increase bone mass in both animal models and humans.
Effects of a Combination Therapy of Sclerostin Antibody III and Raloxifene on Bone Formation Markers in Ovariectomized Rats.
Gad Allam, Riyadh, Saudi Arabia. In J Coll Physicians Surg Pak, Jan 2016
OBJECTIVE: To determine the systemic effect of sclerostin monoclonal antibody (Scl-AbIII) administration on markers of bone formation and compare it with a combination of sclerostin antibody and raloxifene.
Wnt/β-catenin signaling plays a key role in the development of spondyloarthritis.
Chen et al., Shenyang, China. In Ann N Y Acad Sci, Jan 2016
Recent clinical observations and animal studies demonstrate that Wnt signaling proteins and natural Wnt inhibitors, such as DKK1 and sclerostin, are likely to play important roles in the process of ankylosis in SpA, and could potentially serve as therapeutic targets for the treatment of SpA.
[Newly developed drugs to improve bone strength].
Hagino, Tottori, Japan. In Clin Calcium, Dec 2015
In addition, new drugs with new action mechanisms such as cathepsin K inhibitor or anti-sclerostin antibody are also being developed and it has been reported that they have good potential to increase bone mineral density.
Increased Dickkopf-1 in Recent-onset Rheumatoid Arthritis is a New Biomarker of Structural Severity. Data from the ESPOIR Cohort.
Miceli-Richard et al., Le Kremlin-Bicêtre, France. In Sci Rep, Dec 2015
Here, we investigated Dickkopf-1 (DKK-1) and sclerostin (SOST) serum levels in patients with recent inflammatory arthritis from the ESPOIR cohort.
[Regulation of bone metabolism in osteoporosis : Novel drugs for osteoporosis in development].
Seefried et al., Würzburg, Germany. In Unfallchirurg, Nov 2015
Bone formation can also be stimulated by local administration of BMPs, by systemic treatment with the parathyroid hormone fragment teriparatide and by using antibodies targeting the Wnt inhibitor sclerostin.
Serum and tissue biomarkers in aortic stenosis.
Cokkinos et al., Athens, Greece. In Glob Cardiol Sci Pract, 2014
We prospectively studied the following serum BMs in 60 patients with CAVS and compared them to 20 healthy controls, free from any cardiac disease: Matrix metalloproteinases (MMP) 2 and 9 and tissue inhibitor of metalloproteinase 1 (TIMP1), which regulate collagen turnover, inflammatory factors, i.e. tumor necrosis factor a (TNFa), interleukin 2 (IL2), transforming growth factor β1 (TGF-β1) which regulates fibrosis, fetuin-A (fet-A), osteopontin (OPN), osteoprotegerin (OPG), sclerostin (SOST), and relaxin-2 (RL2) which positively or negatively regulate calcification.
New insights into treatment of osteoporosis in postmenopausal women.
Geusens, Maastricht, Netherlands. In Rmd Open, 2014
New potential drugs for fracture prevention that uncouple bone resorption from bone formation include odanacatib, a specific inhibitor of cathepsin-K, the enzyme that degrades bone collagen type I, that inhibits bone resorption and only temporarily bone formation, and monoclonal antibodies against sclerostin (romosozumab, blosozumab), that stimulate bone formation and decrease bone resorption.
Role of Irisin on the bone-muscle functional unit.
Grano et al., Bari, Italy. In Bonekey Rep, 2014
Low-dose r-Irisin also increases osteopontin and decreases sclerostin synthesis but did not affect Uncoupling protein 1 expression in white adipose tissue, whose upregulation is known to cause browning of fat, when Irisin is administered at a higher dose.
Removing the bone brake.
Bozec et al., Erlangen, Germany. In Cell Metab, 2014
Recently, McClung et al. (2014) found that neutralization of sclerostin, a potent inhibitor of bone formation, effectively increased bone mass in postmenopausal women.
Romosozumab in postmenopausal women with low bone mineral density.
Bone et al., Thousand Oaks, United States. In N Engl J Med, 2014
BACKGROUND: Sclerostin is an osteocyte-derived inhibitor of osteoblast activity.
Strongly enhanced levels of sclerostin during human fracture healing.
Aharinejad et al., Vienna, Austria. In J Orthop Res, 2012
local and systemic involvement during fracture healing
Sclerostin and Dickkopf-1 as therapeutic targets in bone diseases.
Ominsky et al., Thousand Oaks, United States. In Endocr Rev, 2012
The Wnt pathway plays an important role in bone formation and regeneration, and expression of two Wnt pathway inhibitors, sclerostin and Dickkopf-1 (DKK1), appears to be associated with changes in bone mass.
Characterization of the interaction of sclerostin with the low density lipoprotein receptor-related protein (LRP) family of Wnt co-receptors.
Robinson et al., Slough, United Kingdom. In J Biol Chem, 2012
peptide derived from the loop 2 region of sclerostin blocked the interaction of sclerostin with LRP5/6 and also inhibited Wnt1 but not Wnt3A or Wnt9B signaling. This suggests that these Wnts interact with LRP6 in different ways
TNF-α mediates the stimulation of sclerostin expression in an estrogen-deficient condition.
Kim et al., Seoul, South Korea. In Biochem Biophys Res Commun, 2012
these results suggest that TNF-alpha originating from T cells may be at least in part responsible for stimulating the sclerostin expression observed in an estrogen-deficient condition.
Serum sclerostin levels in Paget's disease and prostate cancer with bone metastases with a wide range of bone turnover.
Papapoulos et al., Leiden, Netherlands. In Bone, 2012
Circulating sclerostin levels are significantly increased in patients with increased bone turnover, regardless of underlying pathology.
Circulating sclerostin and Dickkopf-1 (DKK1) in predialysis chronic kidney disease (CKD): relationship with bone density and arterial stiffness.
Hampson et al., London, United Kingdom. In Calcif Tissue Int, 2012
Sclerostin was higher in men than women (p = 0.013). Following correction for age and gender, there was a negative association between GFR and sclerostin
Osteoporosis: now and the future.
Hofbauer et al., Dresden, Germany. In Lancet, 2011
The most promising novel treatments include: denosumab, a monoclonal antibody for receptor activator of NF-κB ligand, a key osteoclast cytokine; odanacatib, a specific inhibitor of the osteoclast protease cathepsin K; and antibodies against the proteins sclerostin and dickkopf-1, two endogenous inhibitors of bone formation.
New sequence variants associated with bone mineral density.
Stefansson et al., Reykjavík, Iceland. In Nat Genet, 2009
These are near the SOST gene at 17q21, the MARK3 gene at 14q32, the SP7 gene at 12q13 and the TNFRSF11A (RANK) gene at 18q21.
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