Overview

  • Product name

    Anti-Sclerostin antibody - C-terminal
    See all Sclerostin primary antibodies
  • Description

    Goat polyclonal to Sclerostin - C-terminal
  • Host species

    Goat
  • Tested applications

    Suitable for: IHC-Pmore details
  • Species reactivity

    Reacts with: Human
    Predicted to work with: Rat
  • Immunogen

    Synthetic peptide corresponding to Human Sclerostin aa 197-211 (C terminal) (Cysteine residue). NP_079513.1
    Sequence:

    PRARSAKANQAELEN


    Database link: Q9BQB4

  • Positive control

    • Human kidney tissue

Properties

  • Form

    Liquid
  • Storage instructions

    Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
  • Storage buffer

    pH: 7.30
    Preservative: 0.02% Sodium azide
    Constituents: 0.5% BSA, 99% Tris buffered saline
  • Concentration information loading...
  • Purity

    Immunogen affinity purified
  • Purification notes

    ab194940 is purified from Goat serum by ammonium sulphate precipitation followed by antigen affinity chromatography using the immunizing peptide.
  • Clonality

    Polyclonal
  • Isotype

    IgG
  • Research areas

Applications

Our Abpromise guarantee covers the use of ab194940 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P Use a concentration of 4 - 6 µg/ml. Perform heat mediated antigen retrieval with Tris/EDTA buffer pH 9.0 before commencing with IHC staining protocol.

Target

  • Function

    Negative regulator of bone growth.
  • Tissue specificity

    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.
  • Sequence similarities

    Belongs to the sclerostin family.
    Contains 1 CTCK (C-terminal cystine knot-like) domain.
  • Cellular localization

    Secreted.
  • Information by UniProt
  • Database links

  • Alternative names

    • BEER antibody
    • CDD antibody
    • Cortical hyperostosis with syndactyly antibody
    • Sclerosteosis antibody
    • Sclerostin antibody
    • Sost antibody
    • SOST_HUMAN antibody
    • SOST1 antibody
    • UNQ2976/PRO7455/PRO7476 antibody
    • VBCH antibody
    see all

Images

  • Immunohistochemical analysis of paraffin embedded Human kidney tissue labeling Sclerostin with ab194940 at 4 μg/mL using HRP detection.

References

This product has been referenced in:

  • Hruska KA  et al. The chronic kidney disease - Mineral bone disorder (CKD-MBD): Advances in pathophysiology. Bone 100:80-86 (2017). Read more (PubMed: 28119179) »
See 1 Publication for this product

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