Mouse Sclerostin ELISA Kit | SOST elisa kit

Mouse Sclerostin ELISA Kit

Cat. Num. AAA824629

• Gene Names: Sost; 5430411E23Rik
• Reactivity: Mouse
• Applications: ELISA
• Synonyms: Sclerostin; Mouse Sclerostin ELISA Kit; SOST elisa kit

• Reactivity: Mouse
• Specificity: The Mouse Sclerostin ELISA Kit allows for the detection and quantification of endogenous levels of natural and/or recombinant Mouse Sclerostin proteins within the range of 15.6 pg/ml - 1000 pg/ml.
• Sequence Length: 211

• Applicable Applications for SOST elisa kit: Sandwich ELISA (SE)
• Samples: Cell Culture Supernatants, Serum, Plasma.
• Sensitivity: 10 pg/ml.
• Preparation and Storage: Shipped and store at 4 degree C for 6 months, store at -20 degree C for one year. Avoid freeze/thaw cycles.

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for SOST elisa kit

Principle of the Assay: The Mouse Sclerostin ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of Mouse Sclerostin in Cell Culture Supernatants, Serum, Plasma. This assay employs an antibody specific for Mouse Sclerostin coated on a 96-well plate. Standards and samples are pipetted into the wells and Sclerostin present in a sample is bound to the wells by the immobilized antibody. The wells are washed and biotinylated anti-Mouse Sclerostin antibody is added. After washing away unbound biotinylated antibody, HRP-conjugated streptavidin is pipetted to the wells. The wells are again washed, a TMB substrate solution is added to the wells and color develops in proportion to the amount of Sclerostin bound. The Stop Solution changes the color from blue to yellow, and the intensity of the color is measured at 450 nm.

Background: 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

NCBI and Uniprot Product Information

• NCBI GI #: 567316045
• NCBI GeneID: 74499
• NCBI Accession #: NP_077769.4
• NCBI GenBank Nucleotide #: NM_024449.6
• UniProt Accession #: Q99P68; Q9D3L7
• Molecular Weight: 23,443 Da
• NCBI Official Full Name: sclerostin
• NCBI Official Synonym Full Names: sclerostin
• NCBI Official Symbol: Sost
• NCBI Official Synonym Symbols: 5430411E23Rik
• NCBI Protein Information: sclerostin
• UniProt Protein Name: Sclerostin
• Protein Family: Sclerostin
• UniProt Gene Name: Sost
• UniProt Entry Name: SOST_MOUSE

Uniprot Description

SOST: Negative regulator of bone growth that acts through inhibition of Wnt signaling and bone formation. Defects in SOST are the cause of sclerosteosis type 1 (SOST1). An autosomal recessive sclerosing bone dysplasia characterized by a generalized hyperostosis and sclerosis leading to a markedly thickened skull, with mandible, ribs, clavicles and all long bones also being affected. Due to narrowing of the foramina of the cranial nerves, facial nerve palsy, hearing loss and atrophy of the optic nerves can occur. Sclerosteosis is clinically and radiologically very similar to van Buchem disease, mainly differentiated by hand malformations and a large stature in sclerosteosis patients. Defects in SOST are a cause of van Buchem disease (VBCH). An autosomal recessive sclerosing bone dysplasia characterized by endosteal hyperostosis of the mandible, skull, ribs, clavicles, and diaphyses of the long bones. Affected patients present a symmetrically increased thickness of bones, most frequently found as an enlarged jawbone, but also an enlargement of the skull, ribs, diaphysis of long bones, as well as tubular bones of hands and feet. The clinical consequence of increased thickness of the skull include facial nerve palsy causing hearing loss, visual problems, neurological pain, and, very rarely, blindness as a consequence of optic atrophy. Serum alkaline phosphatase levels are elevated. A 52 kb deletion downstream of SOST results in SOST transcription suppression causing van Buchem disease. Defects in SOST are a cause of craniodiaphyseal dysplasia autosomal dominant (CDD). A severe bone dysplasia characterized by massive generalized hyperostosis and sclerosis, especially involving the skull and facial bones. The sclerosis is so severe that the resulting facial distortion is referred to as 'leontiasis ossea' (leonine faces) and the bone deposition results in progressive stenosis of craniofacial foramina. Respiratory obstruction due to choanal stenosis compromises the clinical outcomes of affected patients. Heterozygous mutations located in the secretion signal of the SOST gene prevent sclerostin secretion and can be responsible for craniodiaphyseal dysplasia. Belongs to the sclerostin family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Secreted; Secreted, signal peptide

Cellular Component: extracellular matrix; Golgi apparatus; extracellular space; proteinaceous extracellular matrix; extracellular region

Molecular Function: heparin binding; protein binding; transcription factor binding

Biological Process: ossification; Wnt receptor signaling pathway; negative regulation of Wnt receptor signaling pathway; positive regulation of transcription, DNA-dependent; negative regulation of ossification; negative regulation of protein complex assembly; negative regulation of BMP signaling pathway