Anti-Sclerostin antibody [MM0556-9N13] (ab89733)
Key features and details
- Mouse monoclonal [MM0556-9N13] to Sclerostin
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG2
Overview
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Product name
Anti-Sclerostin antibody [MM0556-9N13]
See all Sclerostin primary antibodies -
Description
Mouse monoclonal [MM0556-9N13] to Sclerostin -
Host species
Mouse -
Tested applications
Suitable for: WBmore details -
Species reactivity
Reacts with: Human -
Immunogen
Recombinant full length Human Sclerostin
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Positive control
- WB: Human placenta tissue lysate
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General notes
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
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Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles. -
Storage buffer
Constituent: PBS -
Concentration information loading...
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Purity
Protein G purified -
Purification notes
The IgG fraction of culture supernatant was purified by Protein G affinity chromatography and filtered through a 0.2 µm filter. -
Clonality
Monoclonal -
Clone number
MM0556-9N13 -
Isotype
IgG2 -
Research areas
Associated products
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Compatible Secondaries
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Recombinant Protein
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab89733 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 |
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WB |
1/500 - 1/1000. Predicted molecular weight: 24 kDa.
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Notes |
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WB
1/500 - 1/1000. Predicted molecular weight: 24 kDa. |
Target
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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
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Database links
- Entrez Gene: 50964 Human
- Omim: 605740 Human
- SwissProt: Q9BQB4 Human
- Unigene: 349204 Human
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Alternative names
- BEER antibody
- CDD antibody
- Cortical hyperostosis with syndactyly antibody
see all
Images
Datasheets and documents
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Datasheet download
References (0)
ab89733 has not yet been referenced specifically in any publications.