Human SOST ELISA Kit (RMEK-0152928)
Cat. No.: RMEK-0152928
Category: ELISA Kits
INQUIRY
1 x 96 tests
Human SOST ELISA Kit is a single-wash 90 min sandwich ELISA designed for the quantitative measurement of SOST protein in cell culture media, cit plasma, edta plasma, and serum. The technology employs capture antibodies conjugated to an affinity tag that is recognized by the monoclonal antibody used to coat our plates. This approach to sandwich ELISA allows the formation of the antibody-analyte sandwich complex in a single step, significantly reducing assay time.
Product Features
| Species Reactivity | Human |
|---|---|
| Detection Method | Colorimetric |
| Assay Duration | One step assay |
| Assay Time | 1.5 h |
| Assay Type | Sandwich (quantitative) |
| Precision | Intra-Assay-Serum-5-4.8%; Inter-Assay-Serum-3-8.6% |
| Sensitivity | 6 pg/mL |
| Range | 31.1 pg/mL - 2000 pg/mL |
| Sample Type | Cell culture media, Cit plasma, EDTA Plasma, Serum |
| Recovery | Serum-106-104% - 109%; Cell culture media-117-113% - 121%; EDTA Plasma-97-95% - 99%; Cit plasma-108-104% - 114% |
| Key Features | One-wash 90 minute protocol; Sensitivity: 6 pg/mL; Range: 31.1 pg/mL - 2000 pg/mL; Sample type: Cell culture media, Cit plasma, EDTA Plasma, Serum; Detection method: Colorimetric; Assay type: Sandwich (quantitative); Reacts with: Human |
Target Information
| Target Symbol | SOST |
|---|---|
| UniProt ID | Q9BQB4 |
| Function | Negative regulator of bone growth. |
| Cellular Localization | Secreted. |
| Involvement in Disease | Defects in SOST are the cause of sclerosteosis (SOST); also known as cortical hyperostosis with syndactyly. SOST is 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. A 52 kb deletion downstream of SOST results in SOST transcription suppression and is a cause of van Buchem disease (VBCH); also known as hyperostosis corticalis generalisata. VBCH is 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. |
Storage & Shipping
| Storage | Store at 2-8°C |
|---|---|
| Shipping | Gel Packs |
| Stability | The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. |
For research use only. Not for clinical use.
