Mouse Sclerostin (SOST) ELISA kit; VBCH; sclerostin; sclerosteosis

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

This assay has high sensitivity and excellent specificity for detection of mouse SOST. No significant cross-reactivity or interference between mouse SOST and analogues was observed.

Unopened test kits should be stored at 2 to 8 degree C upon receipt. Please refer to pdf manual for further storage instructions.

Manufactured in an ISO 13485:2003 and EN ISO 13485:2012 Certified Laboratory.

Select online data sheet information is drawn from bioinformatics databases, occasionally resulting in ambiguous or non-relevant product information. It is the responsibility of the customer to review, verify, and evaluate the information to make sure it matches their requirements before purchasing the kit. Our ELISA Kit assays are dynamic research tools and sometimes they may be updated and improved. If the format of this assay is important to you then please request the current manual or contact our technical support team with a presales inquiry before placing an order. We will confirm the current details of the assay. We cannot guarantee the sample manual posted online is the most current manual.

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.

MBS926429 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the sclerosteosis (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 MBS926429 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(%).

Principle of the assay: This assay employs the quantitative sandwich enzyme immunoassay technique. Antibody specific for SOST has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and any SOST present is bound by the immobilized antibody. After removing any unbound substances, a biotin-conjugated antibody specific for SOST is added to the wells. After washing, avidin conjugated Horseradish Peroxidase (HRP) is added to the wells. Following a wash to remove any unbound avidin-enzyme reagent, a substrate solution is added to the wells and color develops in proportion to the amount of SOST bound in the initial step. The color development is stopped and the intensity of the color is measured.

23,443 Da

sclerostin

sclerostin

Sclerostin

SOST_MOUSE

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, signal peptide; Secreted

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

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