The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/1000. Detects a band of approximately 24 kDa (predicted molecular weight: 24 kDa).
1/10 - 1/50.
Negative regulator of bone growth.
Widely expressed at low levels with highest levels in bone, cartilage, kidney, liver, bone marrow and primary osteeoblasts differentiated for 21 days.
Involvement in disease
Defects in SOST are the cause of sclerosteosis (SOST) [MIM:269500]; 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) [MIM:239100]; 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.
Belongs to the sclerostin family. Contains 1 CTCK (C-terminal cystine knot-like) domain.
ab63097 staining Sclerostin in Human liver tissue sections by Immunohistochemistry (IHC-P - paraformaldehyde-fixed, paraffin-embedded sections). Tissue was fixed with formaldehyde and blocked with 3% BSA for 30 minutes at room temperature; antigen retrieval was by heat mediation in a citrate buffer. Samples were incubated with primary antibody (1/25) for 1 hour at 37°C. An undiluted Biotin-conjugated Goat polyclonal was used as the secondary antibody.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Sclerostin antibody (ab63097)Image courtesy of an anonymous Abreview.
Immunohistochemical analysis of PFA-fixed paraffin-embedded rat femural tissue, labelling sclerostin with ab63097 at a dilution of 1/50 incubated for 13 hours at 4°C in 1% BSA in TBS. Heat mediated antigen retrival was performed via Tris-EDTA pH 9.0. Blocking was via ab93695 ABC kit incubated at 1% for 20 minutes at room temperature. A sexondary was not used, but ab93695 detection kit was used for signal amplification.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human breast carcinoma tissue labelling Sclerostin with ab63097. Tissue was fixed with formaldehyde and blocked with 3% BSA for 0.5 hours at 38°C; antigen retrieval was by heat mediation with a citrate buffer (pH6). Samples were incubated with primary antibody (1/25) for 1 hours at 37°C. A peroxidase-conjugated goat anti-rabbit polyclonal (ready to use) was used as the secondary antibody.
Hopper N et al. Increased sclerostin associated with stress fracture of the third metacarpal bone in the Thoroughbred racehorse. Bone Joint Res7:94-102 (2018).
Read more (PubMed: 29363519) »
Wu J et al. Wnt-ß-catenin signaling pathway inhibition by sclerostin may protect against degradation in healthy but not osteoarthritic cartilage. Mol Med Rep15:2423-2432 (2017).
Read more (PubMed: 28259981) »