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NOG elisa kit :: Mouse Noggin (NOG) ELISA Kit

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Catalog # MBS2021387 (SPECIAL PROMOTION: Get FREE Starbucks gift card ($5 for 48-Wells-Kit or $10 for 96-Wells-Kit. Maximum 5 gift cards/product). Gift card(s) will be included with shipment)
Unit / Price
  24-Strip-Wells  /  $270 +1 FREE 8GB USB
  48-Strip-Wells  /  $505 +1 FREE 8GB USB
  96-Strip-Wells  /  $685 +1 FREE 8GB USB
  5x96-Strip-Wells  /  $2,770 +3 FREE 8GB USB
  10x96-Strip-Wells  /  $5,025 +6 FREE 8GB USB
Typical Testing Data/Standard Curve (for reference only)
Product Name

Noggin (NOG), ELISA Kit

Popular Item
Also Known As

Mouse Noggin (NOG) ELISA Kit

Product Gene Name
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
Request for Current Manual Insert
Sequence Length
232
Chromosome Location
Chromosome: 17; NC_000017.11 (56593699..56595590). Location: 17q22
OMIM
184460
3D Structure
ModBase 3D Structure for Q13253
Species Reactivity
Specificity
This assay has high sensitivity and excellent specificity for detection of Noggin (NOG).
No significant cross-reactivity or interference between Noggin (NOG) and analogues was observed.
Assay Type
Double-antibody Sandwich
Samples
Serum, Plasma, Tissue homogenates, Cell lysates, Cell culture supernates and Other Biological Fluids
Detection Range
0.156-10ng/mL
Sensitivity
< 0.066ng/mL
Application
Enzyme-linked immunosorbent assay for Antigen Detection.
Intra-assay Precision (Precision within an assay)
3 samples with low, middle and high level Noggin (NOG) were tested 20 times on one plate, respectively.
Inter-assay Precision (Precision between assays)
3 samples with low, middle and high level Noggin (NOG) were tested on 3 different plates, 8 replicates in each plate.
CV(%) =
SD/meanX100
Intra-Assay
CV<10%
Inter-Assay
CV<12%
Preparation and Storage
The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition.
To minimize extra influence on the performance, operation procedures and lab conditions, especially room temperature, air humidity, incubator temperature should be strictly controlled. It is also strongly suggested that the whole assay is performed by the same operator from the beginning to the end.
Product Note
Our ELISA Kit assays are dynamic research tools and sometimes they may be updated and improved. If the format of this assay is important to you then please request the current manual or contact our technical support team with a presales inquiry before placing an order. We will confirm the current details of the assay. We cannot guarantee the sample manual posted online is the most current manual.
Other Notes
Small volumes of NOG elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.
Searchable Terms forNOGpurchase
MBS2021387 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Noggin (NOG) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing NOG. The ELISA analytical biochemical technique of the MBS2021387 kit is based on NOG antibody-NOG antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect NOG antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, NOG. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).
Related Product Information for
NOG elisa kit
The test principle applied in this kit is Sandwich enzyme immunoassay. The microtiter plate provided in this kit has been pre-coated with an antibody specific to Noggin (NOG). Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody specific to Noggin (NOG). Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain Noggin (NOG), biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm ± 10nm. The concentration of Noggin (NOG) in the samples is then determined by comparing the O.D. of the samples to the standard curve.

Typical Testing Data/Standard Curve (for reference only) of NOG elisa kit
NOG elisa kit Typical Testing Data/Standard Curve (for reference only) image
Sample Manual Insert of MBS2021387. Click to request current manual
NCBI/Uniprot data below describe general gene information for NOG. It may not necessarily be applicable to this product.
NCBI GI #
NCBI GeneID
NCBI Accession #
NCBI GenBank Nucleotide #
UniProt Primary Accession #
UniProt Related Accession #
Molecular Weight
25,774 Da
NCBI Official Full Name
noggin
NCBI Official Synonym Full Names
noggin
NCBI Official Symbol
NCBI Official Synonym Symbols
SYM1; SYNS1
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NCBI Protein Information
noggin; symphalangism 1 (proximal)
UniProt Protein Name
Noggin
Protein Family
UniProt Gene Name
UniProt Entry Name
NOGG_HUMAN
NCBI Summary for NOG
The secreted polypeptide, encoded by this gene, binds and inactivates members of the transforming growth factor-beta (TGF-beta) superfamily signaling proteins, such as bone morphogenetic protein-4 (BMP4). By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, this protein may have a principal role in creating morphogenic gradients. The protein appears to have pleiotropic effect, both early in development as well as in later stages. It was originally isolated from Xenopus based on its ability to restore normal dorsal-ventral body axis in embryos that had been artificially ventralized by UV treatment. The results of the mouse knockout of the ortholog suggest that it is involved in numerous developmental processes, such as neural tube fusion and joint formation. Recently, several dominant human NOG mutations in unrelated families with proximal symphalangism (SYM1) and multiple synostoses syndrome (SYNS1) were identified; both SYM1 and SYNS1 have multiple joint fusion as their principal feature, and map to the same region (17q22) as this gene. All of these mutations altered evolutionarily conserved amino acid residues. The amino acid sequence of this human gene is highly homologous to that of Xenopus, rat and mouse. [provided by RefSeq, Jul 2008]
UniProt Comments for NOG
NOG: Essential for cartilage morphogenesis and joint formation. Inhibitor of bone morphogenetic proteins (BMP) signaling which is required for growth and patterning of the neural tube and somite. Defects in NOG are a cause of symphalangism proximal syndrome (SYM1). SYM1 is characterized by the hereditary absence of the proximal interphalangeal (PIP) joints (Cushing symphalangism). Severity of PIP joint involvement diminishes towards the radial side. Distal interphalangeal joints are less frequently involved and metacarpophalangeal joints are rarely affected whereas carpal bone malformation and fusion are common. In the lower extremities, tarsal bone coalition is common. Conducive hearing loss is seen and is due to fusion of the stapes to the petrous part of the temporal bone. Defects in NOG are the cause of multiple synostoses syndrome type 1 (SYNS1); also known as synostoses, multiple, with brachydactyly/symphalangism-brachydactyly syndrome. SYNS1 is characterized by tubular-shaped (hemicylindrical) nose with lack of alar flare, otosclerotic deafness, and multiple progressive joint fusions commencing in the hand. The joint fusions are progressive, commencing in the fifth proximal interphalangeal joint in early childhood (or at birth in some individuals) and progressing in an ulnar-to-radial and proximal- to-distal direction. With increasing age, ankylosis of other joints, including the cervical vertebrae, hips, and humeroradial joints, develop. Defects in NOG are the cause of tarsal-carpal coalition syndrome (TCC). TCC is an autosomal dominant disorder characterized by fusion of the carpals, tarsals and phalanges, short first metacarpals causing brachydactyly, and humeroradial fusion. TCC is allelic to SYM1, and different mutations in NOG can result in either TCC or SYM1 in different families. Defects in NOG are a cause of stapes ankylosis with broad thumb and toes (SABTS); also known as Teunissen- Cremers syndrome. SABTS is a congenital autosomal dominant disorder that includes hyperopia, a hemicylindrical nose, broad thumbs, great toes, and other minor skeletal anomalies but lacked carpal and tarsal fusion and symphalangism. Defects in NOG are the cause of brachydactyly type B2 (BDB2). BDB2 is a subtype of brachydactyly characterized by hypoplasia/aplasia of distal phalanges in combination with distal symphalangism, fusion of carpal/tarsal bones, and partial cutaneous syndactyly. Belongs to the noggin family.

Protein type: Secreted; Secreted, signal peptide

Chromosomal Location of Human Ortholog: 17q22

Cellular Component: extracellular space; extracellular region

Molecular Function: protein binding; protein homodimerization activity; cytokine binding

Biological Process: limb development; wound healing; somatic stem cell maintenance; embryonic skeletal development; motor axon guidance; negative regulation of transcription from RNA polymerase II promoter; middle ear morphogenesis; negative regulation of BMP signaling pathway; BMP signaling pathway; notochord morphogenesis; cell differentiation in hindbrain; negative regulation of cardiac muscle cell proliferation; axial mesoderm development; negative regulation of osteoblast differentiation; negative regulation of cell migration; skeletal development; nervous system development; neural plate morphogenesis; in utero embryonic development; osteoblast differentiation; mesoderm formation; dorsal/ventral pattern formation; endoderm formation; pituitary gland development; spinal cord development; cartilage development; negative regulation of astrocyte differentiation; neural tube closure; epithelial to mesenchymal transition; positive regulation of transcription from RNA polymerase II promoter; embryonic digit morphogenesis; positive regulation of epithelial cell proliferation

Disease: Stapes Ankylosis With Broad Thumb And Toes; Symphalangism, Proximal, 1a; Brachydactyly, Type B2; Tarsal-carpal Coalition Syndrome; Multiple Synostoses Syndrome 1
Precautions
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Disclaimer
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