Rat Recombinant SOST protein, His Tag (V2LY-0526-LY9594)
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Basic Information
Formulations & Storage [For reference only, actual COA shall prevail!]
Target
Biological Process canonical Wnt signaling pathwayIEA:Ensembl
Biological Process cellular response to parathyroid hormone stimulusManual Assertion Based On ExperimentIDA:UniProtKB
Biological Process localizationManual Assertion Based On ExperimentIEP:DisProt
Biological Process negative regulation of BMP signaling pathwayManual Assertion Based On ExperimentIDA:MGI
Biological Process negative regulation of canonical Wnt signaling pathwayManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process negative regulation of ossification2 PublicationsNAS:UniProtKB
Biological Process negative regulation of protein-containing complex assemblyManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process negative regulation of Wnt signaling pathwayManual Assertion Based On ExperimentIBA:GO_Central
Biological Process ossificationManual Assertion Based On ExperimentIBA:GO_Central
Biological Process positive regulation of DNA-templated transcriptionManual Assertion Based On ExperimentIMP:UniProtKB
Biological Process response to mechanical stimulusManual Assertion Based On ExperimentIEP:UniProtKB
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.
Van Buchem disease (VBCH):
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.
Craniodiaphyseal dysplasia autosomal dominant (CDD):
A severe bone dysplasia characterized by massive generalized hyperostosis and sclerosis, especially involving the skull and facial bones. The sclerosis is so severe that the resulting facial distortion is referred to as 'leontiasis ossea' (leonine faces) and the bone deposition results in progressive stenosis of craniofacial foramina. Respiratory obstruction due to choanal stenosis compromises the clinical outcomes of affected patients.
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Please try the standard protocols which include: protocols, troubleshooting and guide.
Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols
Alternative Versions
Human Recombinant SOST protein, Biotin Conjugated, AVI & His Tag (CAT#: V2LY-0526-LY6917)
Human Recombinant SOST protein, His Tag (CAT#: V2LY-0526-LY6919)
Human Recombinant SOST protein, Biotin Conjugated, His Tag (CAT#: V2LY-0526-LY6920)
Mouse Recombinant SOST protein, hFc Tag (CAT#: V2LY-0526-LY8925)
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Human Recombinant SOST protein, Biotin Conjugated, His Tag (CAT#: V2LY-0526-LY6920)
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Custom Antibody Labeling
We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).
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