For Research Use Only. Not for use in diagnostic procedures.

Chromosome: 17; NC_000017.10 (41831099..41836156, complement). Location: 17q11.2

No significant cross-reactivity or interference between Human SOST and analogues was observed.

Store all reagents at 2-8 degree C

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Small volumes of SOST elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS015699 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Sclerostin (SOST) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing SOST. The ELISA analytical biochemical technique of the MBS015699 kit is based on SOST antibody-SOST antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect SOST antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, SOST. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

Background: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated SOST concentrations in Human serum, plasma and other body fluids. Using Purified Human SOST antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add SOST and SOST antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of SOST in the samples is then determined by comparing the O.D. of the samples to the standard curve.

24,031 Da

sclerostin

sclerostin

Sclerostin

SOST_HUMAN

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]

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

Chromosomal Location of Human Ortholog: 17q11.2

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; response to mechanical stimulus; positive regulation of transcription, DNA-dependent; negative regulation of ossification; negative regulation of protein complex assembly; negative regulation of BMP signaling pathway

Disease: Sclerosteosis 1; Hyperostosis Corticalis Generalisata; Craniodiaphyseal Dysplasia, Autosomal Dominant

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