Sheep Sclerostin ELISA Kit | MyBioSource MBS033198 product information

This webpage contains legacy information. The product is either no longer available from the supplier or has been delisted at Labome.

product summary

company name :

MyBioSource

product type :

ELISA/assay

product name :

Sheep Sclerostin ELISA Kit

catalog :

MBS033198

quantity :

48-Strip-Wells

price :

470 USD

product information

catalog number :

MBS033198

products type :

ELISA Kit

products full name :

Sheep Sclerostin ELISA Kit

products short name :

[Sclerostin]

other names :

[sclerostin; Sclerostin; sclerostin; sclerostin]

products gene name :

[SOST]

other gene names :

[SOST; SOST; CDD; VBCH]

uniprot entry name :

SOST_HUMAN

reactivity :

Sheep

specificity :

No significant cross-reactivity or interference between this analyte and analogues is observed.

storage stability :

Store all reagents at 2-8 degree C

image1 heading :

Typical Testing Data/Standard Curve (for reference only)

other info1 :

Samples: Sheep Body Fluids And Tissue Homogenates. Assay Type: Quantitative Sandwich. Detection Range: 0.25ng/ml-8ng/ml. Sensitivity: 0.1ng/ml.

other info2 :

Intra-assay Precision: Intra-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100]. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100]. All CV% should be compared by concentration, not compared by OD values.

products description :

Background/Introduction: This Quantitative Sandwich ELISA kit is for lab reagent/research use only, not for drug, household, therapeutic or diagnostic applications! This kit is intended to be used for determine the level of SOD3 (hereafter termed "analyte") in undiluted original Sheep body fluids and tissue homogenates. This kit is NOT suitable for assaying non-biological sources of substances.

ncbi gi num :

13376846

ncbi acc num :

NP_079513.1

ncbi gb acc num :

NM_025237.2

uniprot acc num :

Q9BQB4

ncbi mol weight :

24,031 Da

ncbi pathways :

Wnt Signaling Pathway (83061); Wnt Signaling Pathway (471)

ncbi summary :

Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Loss-of-function mutations in this gene are associated with an autosomal-recessive disorder, sclerosteosis, which causes progressive bone overgrowth. A deletion downstream of this gene, which causes reduced sclerostin expression, is associated with a milder form of the disorder called van Buchem disease. [provided by RefSeq, Jul 2008]

uniprot summary :

SOST: Negative regulator of bone growth that acts through inhibition of Wnt signaling and bone formation. Defects in SOST are the cause of sclerosteosis type 1 (SOST1). 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. Defects in SOST are a cause of van Buchem disease (VBCH). 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. A 52 kb deletion downstream of SOST results in SOST transcription suppression causing van Buchem disease. Defects in SOST are a cause of 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. Heterozygous mutations located in the secretion signal of the SOST gene prevent sclerostin secretion and can be responsible for craniodiaphyseal dysplasia. Belongs to the sclerostin family. 2 isoforms of the human protein are produced by alternative splicing. Protein type: Secreted; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 17q11.2. Cellular Component: extracellular matrix; Golgi apparatus; proteinaceous extracellular matrix; extracellular space; extracellular region. Molecular Function: heparin binding; protein binding; transcription factor binding. Biological Process: ossification; Wnt receptor signaling pathway; response to mechanical stimulus; positive regulation of transcription, DNA-dependent; negative regulation of ossification; negative regulation of protein complex assembly; negative regulation of BMP signaling pathway. Disease: Sclerosteosis 1; Hyperostosis Corticalis Generalisata; Craniodiaphyseal Dysplasia, Autosomal Dominant

size1 :

48-Strip-Wells

price1 :

470 USD

size2 :

96-Strip-Wells

price2 :

680

size3 :

5x96-Strip-Wells

price3 :

3100

size4 :

10x96-Strip-Wells

price4 :

6095