ELISA/assay

Rat Noggin (NOG) ELISA Kit

MBS2022549

48-Strip-Wells

595 USD

ELISA Kit

Rat Noggin (NOG) ELISA Kit

Noggin (NOG)

noggin; Noggin; noggin; symphalangism 1 (proximal); noggin

NOG

NOG; NOG; SYM1; SYNS1

NOGG_HUMAN

Rat

232

This assay has high sensitivity and excellent specificity for detection of noggin. No significant cross-reactivity or interference between noggin and analogues was observed.

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.

Samples: Rat serum, plasma, tissue homogenates and other biological fluids. Detection Range: 0.156-10ng/mL. Sensitivity: The minimum detectable dose of noggin is typically less than 0.063ng/mL. The sensitivity of this assay, or Lower Limit of Detection (LLD) was defined as the lowest protein concentration that could be differentiated from zero. It was determined by adding two standard deviations to the mean optical density value of twenty zero standard replicates and calculating the corresponding concentration.

Intra-assay Precision: Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level noggin were tested 20 times on one plate, respectively. Intra-Assay: CV<10%. Inter-assay Precision: Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level noggin were tested on 3 different plates, 8 replicates in each plate. CV(%) = SD/meanX100. Inter-Assay: CV<12%. Intended Uses: The kit is a sandwich enzyme immunoassay for in vitro quantitative measurement of noggin in rat serum, plasma, tissue homogenates and other biological fluids.

Principle of the assay: The microtiter plate provided in this kit has been pre-coated with an antibody specific to noggin. Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody specific to noggin. 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, 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 in the samples is then determined by comparing the O.D. of the samples to the standard curve.

4885523

NP_005441.1

NM_005450.4

Q13253

25,774 Da

BMP Receptor Signaling Pathway (137948); BMP Signalling And Regulation Pathway (198910); Cardiac Progenitor Differentiation Pathway (712094); Signal Transduction Pathway (477114); Signaling By BMP Pathway (106336); TGF Beta Signaling Pathway (198810); TGF-beta Signaling Pathway (83064); TGF-beta Signaling Pathway (475)

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]

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, signal peptide; Secreted. 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; middle ear morphogenesis; negative regulation of transcription from RNA polymerase II promoter; 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; dorsal/ventral pattern formation; mesoderm formation; spinal cord development; pituitary gland development; endoderm formation; 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

48-Strip-Wells

595 USD

96-Strip-Wells

810

5x96-Strip-Wells

3220

10x96-Strip-Wells

5795