Abcam, ab213889, Mouse Sclerostin ELISA Kit (SOST)

Size: 1 x 96Tests
Mouse Sclerostin ELISA Kit (SOST) is a Sandwich (quantitative) ELISA for the measurement of Mouse Sclerostin (SOST) in Mouse in Cell/Tissue Extracts, Cell Culture Media, Biofluids samples.
Key facts
Detection method:Colorimetric,
Sample types:Cell Lysate, Cell culture supernatant, EDTA Plasma, Heparin Plasma, Serum,
Reacts with:Mouse,
Assay type:Sandwich (quantitative),
Sensitivity:< 10 pg/mL,
Range:15.6 - 1000 pg/mL,
Assay time:3h 30m,
Assay Platform:Pre-coated microplate (12 x 8 well strips)

Product details:
The Mouse Sclerostin Enzyme-Linked Immunosorbent Assay (ELISA) kit (SOST) (ab213889) is designed for the quantitative detection of Mouse Sclerostin in cell culture supernatants, cell lysates, serum and plasma (heparin, EDTA).
The ELISA kit is based on standard sandwich enzyme-linked immunosorbent assay technology. A monoclonal antibody from rat specific for Sclerostin/SOST has been precoated onto 96-well plates. Standards (Expression system for standard: NSO; Immunogen sequence: Q24-Y211) and test samples are added to the wells, a biotinylated detection polyclonal antibody from goat specific for Sclerostin/SOST is added subsequently and then followed by washing with PBS or TBS buffer. Avidin-Biotin-Peroxidase Complex was added and unbound conjugates were washed away with PBS or TBS buffer. HRP substrate TMB was used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the Mouse Sclerostin/SOST amount of sample captured in plate.
Sclerostin is a protein that in humans is encoded by the SOST gene. 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. Sclerostin is produced by the osteocyte and has anti-anabolic effects on bone formation. The SOST gene maps to chromosome 17q12-q21.

Properties and Storage Information:
Shipped at conditions-Blue Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Storage information--20°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Sclerostin also known as SOST is a glycoprotein weighing approximately 22 kDa. It is predominantly expressed in osteocytes the most abundant cells found in bone. Sclerostin is an extracellular molecule that plays a role in bone metabolism by inhibiting the Wnt signaling pathway which is important for bone formation. This protein acts as a negative regulator of bone growth by binding to the LRP5/6 receptors. Inhibitors such as 'anti-sclerostin' antibodies have been developed to block its function and promote bone formation.
Biological function summary
Sclerostin inhibits osteoblastic activity and formation by interfering with bone morphogenetic proteins. It doesn’t form part of a large protein complex but interacts directly with cell surface receptors. Its expression decreases in response to mechanical loading on bones which is an important part of regulating bone density and remodeling. By controlling osteoblast function sclerostin contributes to skeletal homeostasis an essential process for maintaining bone strength and integrity.
Pathways
Several mechanisms regulate sclerostin activity. In the canonical Wnt/β-catenin signaling pathway it serves as an important checkpoint that ensures controlled bone formation. Sclerostin acts by preventing the activation of LRP5/6 receptors pivotal components in this pathway. Additionally it shares a regulatory network with dickkopf-1 (DKK1) another Wnt inhibitor both of which have an influence on bone metabolism and development.
Two primary conditions associated with sclerostin are osteoporosis and sclerosteosis. Osteoporosis arises from excessive inhibition of bone formation and is characterized by fragile bones due to decreased bone mass. On the other hand sclerosteosis results from mutations in the SOST gene leading to excessive bone growth. Sclerostin's interaction with proteins like DKK1 clarifies its role in bone density management and highlights its relevance in therapeutic strategies targeting these conditions.