Typical Testing Data/Standard Curve (for reference only)
Human Sclerostin (SOST) ELISA Kit | SOST elisa kit
Human Sclerostin (SOST) ELISA Kit
No significant cross-reactivity or interference between Sclerostin (SOST) and analogues was observed.
To minimize extra influence on the performance, operation procedures and lab conditions, especially room temperature, air humidity, incubator temperature should be strictly controlled. It is also strongly suggested that the whole assay is performed by the same operator from the beginning to the end.
Typical Testing Data/Standard Curve (for reference only)
Typical Testing Data/Standard Curve (for reference only)
NCBI and Uniprot Product Information
NCBI Description
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]
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
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
Research Articles on SOST
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Product Notes
The Human SOST sost (Catalog #AAA2020767) is an ELISA Kit and is intended for research purposes only. The product is available for immediate purchase. The AAA2020767 ELISA Kit recognizes Human SOST. It is sometimes possible for the material contained within the vial of "Sclerostin (SOST), ELISA Kit" to become dispersed throughout the inside of the vial, particularly around the seal of said vial, during shipment and storage. We always suggest centrifuging these vials to consolidate all of the liquid away from the lid and to the bottom of the vial prior to opening. Please be advised that certain products may require dry ice for shipping and that, if this is the case, an additional dry ice fee may also be required.Precautions
All products in the AAA Biotech catalog are strictly for research-use only, and are absolutely not suitable for use in any sort of medical, therapeutic, prophylactic, in-vivo, or diagnostic capacity. By purchasing a product from AAA Biotech, you are explicitly certifying that said products will be properly tested and used in line with industry standard. AAA Biotech and its authorized distribution partners reserve the right to refuse to fulfill any order if we have any indication that a purchaser may be intending to use a product outside of our accepted criteria.Disclaimer
Though we do strive to guarantee the information represented in this datasheet, AAA Biotech cannot be held responsible for any oversights or imprecisions. AAA Biotech reserves the right to adjust any aspect of this datasheet at any time and without notice. It is the responsibility of the customer to inform AAA Biotech of any product performance issues observed or experienced within 30 days of receipt of said product. To see additional details on this or any of our other policies, please see our Terms & Conditions page.Item has been added to Shopping Cart
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