Rat Sclerostin (SOST) Antibody Pair - BSA and Azide free (RMAB-0252295)
Cat. No.: RMAB-0252295
Category: Antibody Pair
INQUIRY
10 x 96 tests
The Antibody Pair can be used to quantify Rat Sclerostin. BSA and Azide free antibody pairs include unconjugated capture and detector antibodies suitable for sandwich ELISAs. The antibodies are provided at an approximate concentration of 1 mg/mL as measured by the protein A280 method. The recommended antibody orientation is based on internal optimization for ELISA-based assays. Antibody orientation is assay dependent and needs to be optimized for each assay type. Both capture and detector antibodies are rabbit monoclonal antibodies delivering consistent, specific, and sensitive results._x000D_
Product Features
| Conjugate | Unconjugated capture and detector antibodies |
|---|---|
| Species Reactivity | Rat |
| Range | 15.625 pg/mL - 1000 pg/mL |
| Applications | Sandwich ELISA |
| Key Features | Unconjugated capture and detector antibodies; Adaptable to any antibody pair-based assay format; Antibody concentration ~ 1 mg/mL; BSA and azide free buffer - ready for conjugation; Reacts with: Rat |
Target Information
| Target Symbol | SOST |
|---|---|
| Target Name | Sclerostin |
| UniProt ID | Q9BQB4 |
| Cellular Localization | Secreted. |
| Function | Negative regulator of bone growth. |
| 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.Note=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. |
| Sequence Similarities | Belongs to the sclerostin family. Contains 1 CTCK (C-terminal cystine knot-like) domain. |
Storage & Shipping
| Storage & Shipping | Store at 4°C. Please refer to protocols. |
|---|
For research use only. Not for clinical use.
